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Symposium
IIa
Symposium organizer:
Milos
Pekny
Department of Clinical Neuroscience and
Rehabilitation Institute of Neuroscience and
Physiology Sahlgrenska Academy at
Medicinaregatan 9A
Sweden
Symposium title:
Astrocyte dynamics in health and disease
Outline
Astrocytes are increasingly viewed as crucial cells
in supporting and integrating the brain function.
Neuronal transmission is closely
coupled
to neuron-astrocyte signalling and gliotransmitters
released from astrocytes further shape
astrocyte-astrocyte and
astrocyte-neuronal
communication. Here, neurotransmitter and
gliotransmitter signalling, such as glutamate and
ATP signalling, play
the imperative role. ATP acts as a transmitter or a
co-transmitter in most nerves in the peripheral and
central nervous system, in
neurons
and glia. Transmitters are released from astrocytes
through several mechanisms, such as membrane
channels, transporters or
exocytosis from membrane-bound vesicles. Exocytotic
release has been recently described for glutamate,
neuroactive peptides and
ATP.
Prior release, exocytotic membrane-bound vesicles
need to be adequately transported through the
cytoplasm and to the
plasma
membrane. Trafficking of astrocyte vesicles (glutamatergic,
peptidergic, ATP) and their detailed
characterization are being
increasingly
studied in recent years, including the basic
characteristics of vesicle traffic and role of the
cytoskeleton in this traffic. In
acute
and chronic CNS pathological states the expression
of several astrocytic proteins changes, developing
alterations in astrocyte
physiology,
as well as in morphology. Such astrocytes are termed
reactive astrocytes. These alterations may induce
responses in
the
neighbouring tissue and the exact consequences and
mechanisms through which these changes are evoked
are yet to be
determined.
Reactive astrocytes upregulate also the expression
of cytoskeletal intermediate filament proteins,
glial fibrillary acidic
protein
and vimentin and the role of this upregulation seem
to be implicated in the outcome of brain ischemia.
Yet, the underlying
mechanisms
remain to be elucidated. Profound discoveries about
Ca2+-dependent signalling, membrane vesicle traffic
and the role of
intermediate filaments on the outcome of CNS
pathological states open wide research opportunities
in the development of
improved
strategies for their treatment. This symposium will
aim at elucidating and discussing the most up to
date results on
astrocyte
exocytosis, purinergic signalling, vesicle transport
and the role of the cytoskeleton in health and
disease.
Speaker 1:
Milos
Pekny
Speaker 2: Yang
(Ted) D. Teng
Speaker 3:
Elly
Hol
Speaker 4:
Marko
Kreft
Symposium
IIb
Symposium organizer:
Frits
Prinzen
Maastricht University
P.O. Box 616, 6200 MD Maastricht
The Netherlands
Symposium title:
Assessment and consequences of asynchronous
activation of the ventricles.
Outline
Asynchronous activation occurs during ventricular
pacing and during conduction abnormalities, such as
bundle branch block.
Asynchronous
activation leads to dyscoordinate contraction, with
pronounced differences in mechanical loading
conditions within
the
same ventricle. This not only has important clinical
consequences, it can also lead to changes in
electrophysiology and gene
expression,
even leading to myocardial protection.
In this symposium the presentations will illustate
the various aspects of asynchronous activation. The
first two talks will be on
measuring
electrical conduction and mechanical contraction in
asynchronous hearts. The final two presentations
will provide
examples
of myocardial adaptations to the asynchronous
activation, in the area of electrical remodeling and
myocardial protection.
Speaker 1:
F.
Prinzen
Dept. of Physiology, Maastricht University (NL)
Speaker 2:
B.
Kirn
School of Medicine, University of Ljubljana,
Institute of Physiology (SLO)
Speaker 3:
R.
Coronel
Academic Medical Center, Amsterdam (NL)
Speaker 4:
E.
Radatz
Dept. of Physiology, Univ. Hospital Lausanne (CH)
Symposium
IIc
Symposium organizer:
Marjan
Rupnik
Faculty of Medicine, University of Maribor
Slomskov trg 15
Slovenia
Symposium title:
The physiology of endocrine pancreas
Outline
The endocrine pancreas, primarily as beta-cells of
rodents, has been intensively studied during the
last decades. The major goal is to
find
a way to stop or at least limit the spread of
diabetes mellitus and establish adequate treatment
strategies for the disease.
Biochemical
and electrophysiological pieces of evidence started
to complete parts of a puzzle; though it is clear we
lack big
segments
of the complete image and, maybe even more
frustrating, that we have been too aggressive in
placing pieces together that
actually
do not fit. The symposium will address some latest
news on the physiology of rodent beta-cells, the
importance of cellulo-
social context and cell swelling. In addition, it
will add novel aspects on the role of peripheral
serotonin for insulin release. We shall
end
the symposium with a “glass of pure wine” regarding
use of mice endocrine pancreas to understand human
diabetes mellitus.
Speaker 1:
Marjan
Rupnik
see above
Speaker 2:
Patrik
Rorsman
Oxford Centre for Diabetes, Endocrinology and
Metabolism
The Churchill Hospital
Headington
Oxford
OX3 7LJ
Speaker 3:
Diego
J Walther
Max-Planck Institute for Molecular Genetics
Ihnestrasse 73
14195 Berlin
Speaker 4:
Martin
Jakab
Institute of Physiology and Pathophysiology,
Paracelsus Medical University, Salzburg, Austria
Symposium
IId
Symposium organizer:
Margarethe
Geiger
Center for Biomolecular Medicine and Pharmacology,
Medical University of Vienna
Schwarzspanierstrasse 17, A-1090 Vienna
Austria
Symposium title:
Serpins: a family of proteins regulating a variety
of physiological processes
Outline
Serpins (acronym for serine protease inhibitors) are
large superfamily of proteins, which not only
includes inhibitors of proteases,
but
also non-inhibitory members such as the hormone
precursor angiotensinogen, the hormone transporters
CBG and TBG,
molecular
chaperons, and tumor suppressors. Serpins are widely
distributed in nature. They have been identified in
animals, viruses,
plants, and bacteria. Most inhibitory serpins
inhibit serine proteases, but some inhibit caspases
and papain-like cysteine proteases.
Well
known are the functions of serpins regulating
processes such as blood coagulation (e.g.
antithrombin III, heparin cofactor II), or
fibrinolysis (Plasmin inhibitor, plasminogen
activator inhibitors). Studies analyzing the roles
of different intra- and extracellular
serpins
in other physiological processes (e.g. in embryonic
development, in inflammation and immunity, in
protein secretion, in
tumor
development and metastasis) have been performed only
during the last few years.
The inhibitory mechanism of serpins has been
identified on the molecular level. It involves a
major conformational change of the
serpin
molecule upon interaction with the protease. Serpins
are therefore very vulnerable , and point mutations
in serpin molecules
can
cause so called "serpinopathies". The molecular
basis of serpinopathies is the formation of serpin
polymers, which can cause
tissue
damage by intra- or extracellular accumulation
(resulting in e.g. dementia or cirrhosis) and "overactivity"
of proteolytic
activity
(resulting in e.g. emphysema).
Speaker 1:
Wei
Li (proposed title: Serpin structure and
function)
University of Cambridge, Department of Hematology,
Hills Road, Cambridge CB2 OXY, UK
Speaker 2:
Stephen
P. Bottomley (proposed title: Serpin polymerization
and its role in disease)
Department of Biochemistry and Molecular Biology,
Monash University, Clayton, Australia
Speaker 3:
Margarethe
Geiger (proposed title: Serpins in reproduction)
Center for Biomolecular Medicine and Pharmacology,
Medical University of Vienna, Austria
Speaker 4:
Ming
Zhang (proposed title: Serpins and cancer)
Northwestern University, Feinberg School of
Medicine, Chicago, USA
Symposium
IIe
Symposium organizer:
Tina
Pangrsic
InnerEarLab, Department of Otolaryngology and Center
for Molecular Physiology of the Brain, University of
Goettingen
Robert-Koch-Str. 40, 37099 Göttingen
Germany
Symposium title:
Molecular Physiology of Hearing
Outline
Analyzing the mechanisms of auditory processing
along the afferent pathway, identifying and
functionally characterizing involved
molecules
is essential for understanding hearing and deafness.
During last years major progress has been achieved
in elucidating
molecular
mechanisms of cochlear function. For example, most
ion channels and pumps mediating the cochlear
potassium cycle,
important
components of the nanomachineries underlying
mechanoelectrical transduction, outer hair cell
electromotility and inner
hair
cell transmitter release have been identified. With
the help of functional genomics, cellular and
systems physiology and
modeling,
roles of many hearing related proteins have now been
described and a more comprehensive scheme of
cochlear processing
has
evolved. In parallel, elaborate exploration of
synapses in the central auditory system, in
particular of the calyx of Held, has
greatly
broadened not only our knowledge of auditory
processing but also of synaptic transmission in
general. At this symposium
we
aim to discuss the current understanding of
molecular and cellular mechanisms of hearing and
indicate future goals.
Speaker 1:
Tobias
Moser
InnerEarLab, Department of Otolaryngology and Center
for Molecular Physiology of the Brain, University of
Goettingen,
Goettingen, Germany
Speaker 2:
Thomas
Jentsch
Leibniz-Institut für Molekulare Pharmakologie (FMP)
and Max-Delbrück-Centrum für Molekulare Medizin (MDC),
Berlin, Germany
Speaker 3:
Ian
Russell
School of Life Sciences,
University of Sussex,
Falmer, Brighton, UK
Speaker 4:
Ralf
Schneggenburger
Laboratory of Synaptic Mechanisms,
Ecole Polytechnique Fédérale de Lausanne, Brain-Mind
Institute,
Lausanne, Switzerland
Symposium
Va
Symposium organizer:
José Julio
Rodríguez Arellano
Faculty of Life Sciences, The University of
Manchester
AV Hill Building, Room 2.002, Oxford Road, M13 9PT
Umited Kingdom
Symposium title:
Glia in neurodegenerative processes
Outline
Neuroglia cells (represented by astrocytes,
oligodendrocytes and microglial cells), the most
numerous cells in the brain, act as the
main
element of the homeostatic system of the brain.
Recent advances in gliology emphasised the role of
glia in the progression and
handling
of the insults to the nervous system. The brain
pathology, is, to a very great extent, a pathology
of glia, which, when
falling
to function properly, determines the degree of
neuronal death, the outcome and the scale of
neurological deficit. The neuroglia
appears as a brain warden, and as such it is
intrinsically endowed with two opposite features: it
protects the nervous tissue as long
as
it can, but it also can rapidly assume the guise of
a natural killer, trying to eliminate and seal the
damaged area, to save the whole
at
the expense of the part.
The proposed symposium is dedicated to the state-of
the-art overview of the pathological potential of
glial cells in various forms of
neurological
and neurodegenerative conditions. We shall
concentrate on pathological potential of astroglia (J.J.
Rodríguez and E.
Sykova),
oligodendroglia (C. Matute) and microglia (F.
Kirchoff).
Speaker 1:
Dr.
José Julio Rodríguez Arellano
Faculty of Life Sciences, The University of
Manchester, Manchester, UK
Speaker 2:
Prof.
Eva Sykova
Institute of Experimental Medicine, Academy of
Sciences of the Czech Republic, Prague, Czech
Republic
Speaker 3:
Dr.
Carlos Matute
Departamento de Neurociencias, Universidad del País
Vasco, Leioa, Spain
Speaker 4:
Prof.
Frank Kirchhoff
Max Planck Institute of Experimental Medicine and
DFG Research Center for Molecular Physiology of the
Brain, Göttingen,
Germany
Symposium
Vb
Symposium organizer:
Alexei
Verkhratsky
The University of Manchester
Oxford Road, Manchester M13 9PT
UK
Ole
H.Petersen
The Physiological Laboratory
Crown Street
University of Liverpool
Liverpool L69 3BX, UK
Symposium title:
Calcium signals in cell death and disease
Outline
Most leaving creatures have one thing in common:
they all undergo the process of death. Evolution
based on simple cell division
required
extinction of unfit cells and selection of those
endowed with environmental adaptation. The most
obvious example of a
primordial
death mechanism is the failure of ion homeostasis
when the environmental changes strained ion
compartmentalisation
between
the intra- and extracellular space. These mechanisms
of cell and tissue damage are universally operative
among all forms of
life.
In mammalian cells both Ca2+ and Na+ overloads are
one of the major causes of tissue damage. Imbalances
in Ca2+ are the
most
common examples of death routines using
physiological signalling systems. Deregulation of
Ca2+ signalling is involved in
many
types of cell death: it triggers excitotoxicity in
neurones and muscle cells, it initiates apoptosis in
many excitable and non-
excitable tissues, and it acts as activator and
executor of necrotic cell death. All these death
subroutines use existing molecular
systems,
which are responsible for physiological Ca2+
signalling. As tissue plasticity and remodelling
became a fundamental step in
evolution of complex organisms, biochemical
programmes involving complex cascades leading to
cell disassembly have also
developed.
Speaker 1:
O.H.Petersen
The Physiological Laboratory
Crown Street
University of Liverpool
Liverpool L69 3BX, UK
Speaker 2: Daniele
Bano
University of Leicester,
Leicester, UK
Speaker 3: Julian
Grosskreutz,
University hospital Jena, Germany
Speaker 4:
A.
Verkhratsky
The University of Manchester, Manchester M13 9PT, UK
Symposium
Vc
Symposium organizer:
Stephen
Smith
Oregon Health & Science University
3181 SW Sam Jackson Park Drive, UHN-67, Portland,OR
97239
USA
Symposium title:
Regulation of synaptic transmission
Outline
Synaptic transmission is the major pathway through
which neuron to neuron communication occurs and is
vital for normal brain
function.
Thus advancing our knowledge about how synapses
function is crucial if we are to fully understand
information transfer
between
neurons. Pre- and post synaptic factors combine to
modulate synaptic efficacy and there is growing
appreciation of how
deficits
may lead to various neurological disorders. Recently
there has been substantial progress in our
understanding of the
mechanisms
by which synaptic strength is regulated. Mounting
appreciation of the complexity of vesicle pools and
their
heterogeneity
has promoted interest in this presynaptic form of
regulation. Dr
Jessica
Raingo will discuss the
multiple forms of
synaptic
vesicle trafficking and their impact on
neurotransmission. Synaptic transmission is
exquisitely sensitive to external [Ca]
since
its entry through Ca channels triggers exocytosis.
Dr Stephen Smith will discuss how external [Ca]
signaling via the Ca-sensing
receptor also impacts transmitter release. At the
calyx of Held tight coupling between action
potential firing and exocytosis is
necessary
to permit rapid sound localization. Dr Henrique von
Gersdorff will describe how a fast Na/K-ATPase-mediated
post-
tetanic hyperpolarization controls the probability
and precision of subsequent firing at this synapse.
Interference with the ubiquitin
proteasome system, through either proteasome
blockers or environmental pesticides rapidly alters
neurotransmission. Dr Felix
Schweizer
will discuss the molecular mechanisms underlying
this regulation. These four talks will present new
work on synaptic
regulation
in neurons from brainstem, hippocampus and neocortex.
To enhance the possibility that there is maximal
interest
associated
with the session presenters will be encouraged to
present exciting new results. This session will
serve as a forum for
discussing
new developments in this highly interdisciplinary
area of brain research. Consequently we expect
interest for students
and
scientists in neuroscience, as well as for anyone
interested in nervous system physiology.
Speaker 1:
Stephen
Smith
OHSU, Oregon, USA.
Speaker 2:
Ege
Kavalali
/ Jessica Raingo
University of Texas,
Southwestern Medical Center,
Dallas,
Texas,
USA.
Speaker 3:
Henrique
von Gersdorff
Vollum Institute, Oregon, USA.
Speaker 4:
Felix
Schweizer
University of California, Los Angeles, USA.
Symposium
Vd
Symposium organizer:
Mojca
Kr¾an
Department of Pharmacology and Experimental
Toxicology, faculty of Medicine
Korytkova 2, Si-1000 Ljubljana
Slovenia
Symposium title:
Histamine and CNS
Outline
Histamine acts as a central neurotransmitter and
neuroimmunomodulator. In the CNS, it regulates
neurovegetative, neuroendocrine
and
neuroimmune functions. Recently, the role of
histamine in the processes of learning and memory
has been found, as well as its
important
contribution in the regulation of sleep waking cycle
and a feeding behavior. Due to good living
conditions in the Western
hemisphere
the life expectancy is significantly longer and
proportion of older people in society is constantly
increasing. The quality
of life of elderly people can be significantly
affected because of decreased cognitive and memory
function. So, there is a big niche
for
the drugs with nootropic, memory enhancing effects.
On the other site sedentary life style as well as
medical treatment with
antidepressant
and antipsychotic drugs which stimulate appetite
calls for design of safer appetite suppressing
drugs.
The main goal of the symposia is to present the new
knowledge regarding the role and function of
histamine in central nervous
system
(invited lecture by Patrizio Blandina or Pertti
Panula), followed by the presentation of possible
interplay of histamine with
other
neurotransmitters especially with endocannabinoids
(invited lecture by Maria Beatrice Passani). Since
histamine does not
affect
just the targets on neuronal cells, Metoda Lipnik
©tangelj will present some ways how histamine
modulates the function of
astrocytes
which represent one of the main targets of the
central histaminergic neurons in the CNS.
The symposium will be closed by new facts on the
participation of astrocytes in the inactivation of
histamine (lecture by Mojca
Krzan).
The new knowledge on histamine physiology function
will not just enrich the scientific literature, but
is also a good foundation for
future
design of new sedative/hypnotic, nootropic and
appetite suppressing drugs.
Speaker 1:
Pertti
Panula
Neuroscience Center and Institute of
Biomedicine/Anatomy, Biomedicum Helsinki, University
Helsinki, Finland
Speaker
2:
Patrizio Blandina
Department of Preclinical and Clinical Pharmacology,
University of Florence, Italy
Speaker
3:
Maria
Beatrice Passani
Department of Preclinical and Clinical Pharmacology,
University of Florence, Italy
Speaker
4:
Metoda
Lipnik-©tangelj
Department of Pharmacology and Experimental
Toxicology, Faculty of Medicine, University of
Ljubljana, Slovenia and Department
of Pharmacology and Toxicology, Faculty of
Medicine, University of Maribor, Slovenia
Speaker
5:
Mojca
Kr¾an
Department of Pharmacology and Experimental
Toxicology, Faculty of Medicine, University of
Ljubljana, Slovenia
Symposium
Ve
Symposium organizer:
M.-Saadeh
Suleiman
Faculty of Medicine & Dentistry, University of
Bristol
Level 7, Bristol Royal Infirmary, Bristol BS2 8HW
United Kingdom
Symposium title:
Obesity and cardiac cellular physiology
Outline
Overweight and obesity are on the increase and are
associated with increased risk of cardiovascular
disease. High-fat diet and
sedentary
lifestyle are the main causes of obesity. There will
be metabolic and physiological cardiac remodelling
which will be
triggered
initially by a shift to high fat energy production
(acute) followed by changes triggered by
overweight/obesity
(hypertension,
hypertrophy etc). Understanding the cellular changes
in the myocardium as a result of changing energy
provisions
and/or
in response to overweight/obesity is important for
dealing with ensuing cardiomypathies and for disease
prevention. The aim
of this symposium is to enable experts in this
field to present their work and provide valuable
advice to other physiologists who
are
working in this important and emerging area of
research.
Speaker 1:
Professor
Kieran Clarke
University of Oxford, UK
Speaker 2:
Dr.
Anabelle Chase
Medical School University Walk Bristol,
UK
Speaker 3:
Jatin
Burniston
Liverpool John Moores
University, UK
Speaker 4:
Professor
Saadeh Suleiman
University of Bristol, UK
Symposium
VIa
Symposium organizer:
A. Mark
Evans
University of Edinburgh
EH8 9XD
UK
Symposium title:
AMP-activated protein kinase: Regulation of energy
supply at cellular and whole body level
Outline
AMP-activated protein kinase (AMPK) is has long been
recognized as molecular fuel gauge that plays a key
role in regulating
cellular
energy balance. AMPK is activated by an increase in
the AMP / ATP ratio that occurs following a fall in
ATP supply and
maintains
energy supply by switching on catabolic processes
and switching of ATP consuming pathways. However,
there is a
growing
body of evidence now suggests that AMPK is a key
player in the regulation of energy supply at the
level of the whole
organism.
In the hypothalamus, AMPK is inhibited by leptin and
insulin, hormones which suppress feeding, whilst
ghrelin, a
hormone
that increases food intake, activates AMPK.
Furthermore, AMPK mediates hypoxia response coupling
in the carotid
body
and pulmonary arteries, thereby regulating
respiratory function and, therefore, oxygen supply.
Thus, AMPK provides a
mechanism
for monitoring changes in energy metabolism within
individual cells and at the level of the whole
body. Activation of
AMPK,
either in response to exercise or to pharmacological
agents, has considerable potential to reverse the
pathophysiologies
associated
with sleep apnea, type 2 diabetes and the metabolic
syndrome. The proposed symposium is therefore timely
and will be
of
general interest to the physiological community, as
it will address the key questions on the role of
AMPK in regulating those
physiological
systems that determine energy supply to the body by
modulating oxygen supply (Speaker 1: Evans), feeding
(Speaker
2: Lopez), fertility (Speaker 3: Dupont)
and autophagy (Speaker
4:
Hoyer-Hansen).
Speaker 1:
A.
Mark Evans
University of Edinburgh, Edinburgh, UK
Speaker 2:
Miguel
Lopez
University of Santiago de Compostela, Spain
Speaker 3:
Joelle
Dupont
Unite de Physiologie de la Reproduction et des
Comportement, INRA Centre de Tours, Nouzilly, France
Speaker 4:
Maria
Helena
Hoyer-Hansen
Danish Cancer Society, Copenhagen, Denmark
Symposium
VIb
Symposium organizer:
Markus
Ritter
Institute of Physiology and Pathophysiology,
Paracelsus Medical University
Strubergasse 21, 5020 Salzburg
Austria
Symposium title:
Ion Transporters in Cell Migration and Apoptosis
Outline
Ion transport mechanisms are critically involved in
the regulation of cell migration, cell proliferation
and programmed cell death and
therefore
essential for normal cell-, tissue- and organ
function. Disturbances of their functionallity can
lead to severe disorders like
tumor-
and metastasis formation. The symposium will (i)
give an overview on the functional importance of ion
channels as part of
the
cellular migration machinery and present general
principles by which channels can affect cell
migration, as ion and water flow is
required
for optimal migration, and the inhibition or genetic
ablation of channels impairs migration as well as
cell-matrix interactions;
(ii) focus on the role of the ubiquitously
expressed NHE1 isoform of the plasma membrane
Na+/H+-exchanger, which is regulating
migration
via affecting cell volume, intracellular pH,
cytoskeletal elements, cell signaling and gene
expression, and which extrudes
cellular
protons leading to local, extracellular
acidification necessary for cell/matrix interaction
and adhesion at the cell front; (iii)
highlight
the role of the non-gastric H+/K+ ATPase ATP12A,
which is essential for cell migration of
polymorphonuclear
leucocytes,
and which is transcriptionally und functionally
upregulated during induction of apoptosisin
myeolomonocytic leukemic
HL60
cells and insulinoma cells, thereby excerting
antiapoptotic activity presumably by protecting
cells from K+-loss, intracellular
acidosis, caspase activation and by counteracting
cell shrinkage during apoptotic volume decrease;
(iv) highlight the role of the
potassium
channel Kv1.3 which has recently been shown to be
located to the inner mitochondrial membrane of
lymphocytes and
which
plays an essential role in lymphocyte apoptosis by
directly interacting with proapoptotic Bax and which
is mediating Bax-
induced apoptosis.
Speaker 1:
Christian
Stock, M.D., Professor of Physiology
Institute of Physiology II, University of Muenster,
Germany
Speaker 2:
Schwab
Albrecht, M.D. - Professor of Physiology
Institute of Physiology II, University of Muenster,
Germany
Speaker 3:
Ritter
Markus, M.D. - Professor of Physiology
Institute of Physiology and Pathophysiology,
Paracelsus Medical University Salzburg, Austria
Speaker 4:
Ildikò
Szabò Ph.D. - Professor in Biochemistry
Department of Biology, University of Padova, Italy
Symposium
VIc
Symposium organizer:
Ludwig
Aigner
Institute of Molecular Regenerative Medicine,
Paracelsus Medical University Salzburg, Salzburg,
Austria
Strubergasse 21, 5020 Salzburg
Austria
Symposium title:
The physiology of neural stem cells in the healthy
and diseased brain
Outline
Since the discovery of the existence of
undifferentiated progenitor cells in the adult
brain, much effort has been undertaken to
understand
the identity and the mechanisms regulating the
proliferation and the fate of these cells. Neural
stem cells and adult
neurogenesis
are currently developing as a prime target for cell
therapy and drug development in neurodegenerative
and psychiatric
disorders.
Here, the aim is to promote neurogenesis and
functional integration of newly generated neurons.
Moreover, there are
approaches
on the way that aim to generate neurons out of glial
cells. Most of the studies were focusing on stem
cell regulation by
growth
factors and by genetic and epigenetic programs.
Cellular physiology of neural stem cells has been,
with the exception of
electrophysiological
aspects, underrepresented in the field. The fact,
however, that neural stem cells do not only provide
a cellular
pool
for cell replacement and regeneration, but are
probably the cellular source of tumor stem cells
generating brain tumors, has
generated
a revival of physiology in the stem cell field, not
least because the metabolic status of the tumor stem
cell niche seems to
regulate
its outcome.
Speaker 1:
Ludwig
Aigner
Insitute of Molecular Regenerative Medicine,
Paracelsus Medical University Salzburg. Salzburg.
Austria
Speaker 2:
Juergen
Winkler
Institute of Molecular Neurology, Department of
Neurology,
University of Erlangen, Germany
Speaker 3:
Peter
Hau
Department of Neurology, University of Regensburg,
Germany
Speaker 4:
Josef
Bischofberger
Department of Physiology, University of Freiburg,
Germany
Symposium
VId
Symposium organizer:
Igor
Mekjavic
Jozef Stefan Institute
Jamova 39, SI-1000 Ljubjana
Slovenia
Symposium title:
Physiology of deconditioning
(European Space Agency (ESA) meeting)
Outline
Inactivity-induced deconditioning coupled with poor
nutrition exacerbates age-related muscle weakness,
bone osteoporosis, and
causes
a reduction in aerobic capacity. Since, physical
performance capacity is a key factor in quality of
life, maintenance of optimal
physical performance is essential, and it is
therefore not surprising that the prevention and
treatment of deconditioning are key FP7
priorities covered by the Health Work Programme
2008 (HEALTH-2007-2.2.2-2: Termination of
developmental processes and
their
reactivation in adult life; HEALTH-2007-2.4.5-3:
Osteoporosis: signalling pathways in bone formation;
HEATLH-2007-2.4.5-
6: Innovative concepts in chronic obstructive
pulmonary disease pathogenesis (COPD);
HEALTH-2007-2.4.5-10: Understanding
and
combating age-related muscle weakness) and the
Health Work Programme 2009 (HEALTH-2009-4.3.3-2:
Mechanisms of
diabetic
and weight-related comorbidity in heart failure).
The Symposium will review innovative and integrative
approaches to
prevention
and treatment of deconditioning, so that optimal
functional capacities of the cardiorespiratory,
musculoskeletal,
thermoregulatory
and neurohumoural systems are maintained.
Speaker 1:
Ola
Eiken
Swedish Defence Research Agency
Karolinska Institutet
Bezelius v. 13, S-17177 Stockholm, Sweden
Speaker 2:
Per
Tesch
Mittuniversitetet
Radgusgatan 15, S-83141 Ostersund, Sweden
Speaker 3:
Joern
Rittweger
Manchester metropolitan University Cheshire
Hassall Road, Aslager, Stoke-on-Trent, UK
Speaker 4:
Ian
MacDonald
School of Medicine
University of Nottingham
Nottingham, UK
Symposium
VIe
Symposium organizer:
Francois
Darchen
Institut de Biologie Physico-Chimique - CNRS
13 rue Pierre et Marie Curie 75005 Paris
France
Symposium title:
Exocytosis and fusion pore physiology
Outline
The process of neurotransmitter and hormone release
represents a major topic in cell physiology and a
highly dynamic field for
scientists
from different communities (neurophysiology,
endocrinology, membrane biophysics, intracellular
traffic). This
symposium
will cover several important aspects of this process
and should be of interest for a broad audience. In
particular, we
will
address the role of SNARE proteins, that constitute
the core of the fusion apparatus and describe how
SNAREs activity is
linked
to the dynamics of the fusion pore. Opening of a
fusion pore does not terminate the fusion proces. We
will show that the
fusion
pore can enlarge, flicker or close with important
consequences for the release process. We will
discuss how membrane
retrieval
is affected by fusion pore dynamics (the 30-year old
debate on kiss and run vs full fusion is still
active!) and which
parameters
controls this dynamics.
Henrique
von Gersdorff (Portland, USA), a well-known
electrophysiologist, will talk about compound and
cumulative exocytosis at
a ribbon synapse. These synapses can sustain
synaptic transmission at high frequencies, which
poses interesting questions in term
of
vesicle recycling and fusion pore dynamics (kiss and
run vs slow retrieval).
Jakob Soerensen (Copenhagen) has been conducting for
several years an in-depth analysis of the role of
SNAREs (and SNARE-
associated proteins) in membrane fusion. He will
present his recent work in hippocampal neurons.
Robert Zorec (Ljubljana) has used advanced
electrophysiological techniques to monitor fusion
pore dynamics and will present data
demonstrating
an unsuspected importance of fusion pore flickering
in endocrine cells.
François Darchen (Paris) analysed fusion pores in
endocrine cells by carbon fibre amperometry. He will
show that the mode of
fusion
(fast vs slow pore dilation) depends on the
tightness of SNARE assemblies.
Speaker 1:
Francois
Darchen
Laboratory of Membrane Dynamics, CNRS FRE 3146,
Institut de Biologie Physico-Chimique
Paris, France
Speaker 2:
Jakob
Sorensen
Max Planck Institute for biophysical Chemistry
Göttingen, GERMANY
moving to the University of Copenhagen, Denmark
Speaker 3:
Takeshi
Sakaba
Speaker 4:
Robert
Zorec
Laboratory of Neuroendocrinology-Molecular Cell
Physiology, Institute of Pathophysiology, University
of Ljubljana, Slovenia
Symposium
IXa
Symposium organizer:
Helena
Lenasi
Institute of Physiology, Medical Faculty, University
of Ljubljana, Slovenia
Zaloska 4, 1000 Ljubljana
Slovenia
Symposium title:
Human cutaneous microcirculation in health and
disease
Outline
The cutaneous circulation is the main effector organ
for human thermoregulation and as such is under the
control of competing
thermoregulatory
and nonthermoregulatory mechanisms. It is easily
accessible and has been used as a model vascular bed
to
investigate
the mechanisms of microcirculatory function and
dysfunction. Skin blood flow is regulated by a
complex interplay of
centrally
mediated neural mechanisms and humoral and metabolic
factors. The endothelium plays a crucial role by
releasing
vasoconstrictors
and vasodilators such as nitric oxide,
prostaglandins and endothelium-derived
hyperpolarizing factor. The exact
interplay
of these mechanisms remains to be elucidated. Skin
microcirculation is important also from the clinical
point of view as
early
detectable endothelial dysfunction might precede
clinical manifestation of the disease states (as
diabetes, hypertension, heart
failure,
metabolic disorders, peripheral vascular diseases
etc., and ageing) and also reflects changes in other
parts of the circulation.
On
the other hand, endurance training leads to an
enhancement of endothelium-dependent vasodilatation
in human microcirculation.
Using laser Doppler flowmetry, cutaneous
microvascular responses to physiological and
pharmacological stimuli are currently being
investigated as indices of vascular function and
to monitor responses to therapy.
The
session would present some new insights in the
physiology, pharmacology and pathophysiology of skin
microcirculation with
emphasis
on endothelial function as well as some clinical
experiences, as altered microvascular function in
scleroederma, diabetes and
hypertension.
Speaker 1:
Wouter
van Marken Lichtenbelt
Department of Human Biology, NUTRIM, Maastricht
University Medical Centre, The Netherlands
Speaker 2:
asist.
dr. Helena Lenasi
Institut za fiziologijo, Mediciska fakulteta v
Ljubljani
Speaker 3:
Prof.
Dr. Marco Rossi
Dipartimento Medicina Interna, Universita di Pisa
Speaker 4:
doc.
dr. Vilma Urbancic-Rovan
Univerzitetni klinièni center Ljubljana, KO za
endokrinologijo, diabetes in presnovne bolezni
Symposium
IXb
Symposium organizer:
Andrea
Nistri
International School for Advanced Studies (SISSA)
Via Beirut 4, 34014 Trieste
Italy
Symposium title:
Rhythmic oscillations of spinal networks in health
and disease models
Outline
Periodic electrical discharges of neuronal ensembles
in the brain are an important process for
physiological activities like network
development,
rhythmic motor discharges, sensory and memory
processing. Spinal cord networks also generate
electrical oscillations
through
which rhythmic activation of discrete neuronal
populations enables walking or sensory signalling.
In certain neurological
diseases
of the spinal cord, either oscillations are lost,
like for example during motor paralysis, or they are
aberrantly generated like
in
neuropathic pain. Hence, studying rhythmic
oscillations might clarify the operation of spinal
networks in health and disease and
outline
new strategies to restore lost function.
The
present symposium will address these issues by
pooling together the expertise of international
leaders in this field to discuss
how
in vivo and in vitro models help to advance our
understanding of oscillations. This subject is at
the forefront of the integration
of
spinal cord neurophysiology, pathology and
rehabilitation and thus offers exciting new
perspectives.
What
are the elementary mechanisms supporting
oscillations? J. Streit will show, with organotypic
spinal cultures and combining
multiple
recording of neuronal firing with patch clamping,
the origin of rhythmic bursting, the relative
contribution by intrinsic and
network
mechanisms, and its spatio-temporal organization.
Recording from single neurons in vitro and from the
dorsal horn of
anaesthetized
animals. Taccola will
discuss how a chemically
produced
lesion of a restricted region of the spinal cord in
vitro can block the motor oscillations typical of
locomotion not only
locally
but also in distant segments. A. Nistri will discuss
the pathophysiology of experimental spinal injury in
vitro by comparing
the
electrophysiological consequences of excitotoxicity
with those of anoxia/aglycemia as paradigms of an
acute spinal lesion.
Speaker 1:
Prof.
Andrea Nistri
International School for Advanced Studies, Trieste,
Italy
Speaker 2:
Prof.
Juerg Streit
Department of Physiology
University of Bern, Bern, Switzerland
Speaker 3:
Laura
Ballerini,
Trieset, Italy
Speaker 4:
Dr.
Giuliano Taccola
SPINAL Laboratory
Institute of Physical Medicine and Rehabilitation,
Udine, Italy
Symposium
IXc
Symposium organizer:
Govindan
Dayanithi
Institute of Experimental Medicine, Department of
Cellular Neurophysiology
AS CR, v.v.i., Videnska 1083, Prague 4
Czech Republic
Symposium title:
Vasopressin and Oxytocin receptors: looking for new
tools, pharmacology, physiology and therapeutic
agents.
Outline
The vasopressin (AVP) oxytocin (OT) mediate their
biological actions by acting on their own receptors:
the AVP (V1a;
vasopressor),
(V1b; pituitary), (V2; renal) (V1c; vasodilating?)
and the OT (uterine) receptors. Activation of these
receptors are
directly
or indirectly involve a change in the in the
intracellular calcium concentrations
This symposium is planned:
i) to summarize some highlights of the recent
progress, in the design and synthesis of selective
peptide agonists, antagonists,
radioiodinated
ligands, fluorescent ligands and bivalent ligands
for these receptors.
ii) to focus on how to make selection of the most
appropriate ligand for a given study. The current
status of non-peptide AVP and
OT
antagonists and agonists will be highlighted.
iii) the relative merits of peptide and non-peptide
AVP and OT agonists and antagonists as: (1) research
tools and (2) therapeutic
agents
will be evaluated. Promising new non-peptide (V1b)
and OT antagonists, as well as non-peptide (V2) and
OT agonists are
now
in pre-clinical development.
iv) many of the receptor selective peptide agonists
and antagonists from a few laboratories are far more
widely used as
pharmacological
tools for studies on the peripheral and central
effects of AVP and OT than their non-peptide
counterparts mainly
focusing
on the variations intracellular calcium concentions
under physiological actions
Speaker 1:
1)
Govindan Dayanithi,
Institute of Experimental Medicine, AV CR, v.v.i,
Videnska 1083 Prague 4, Czech Republic
Speaker 2:
2)
Gilles Guillon
Institut de Génomique Fonctionnelle, 141 Rue de la
Cardonille, 34094 Montpellier cedex 05, France.
Speaker 3:
3)
Bichi Chini
Cellular and Molecular Pharmacology Section, CNR
Institute of Neuroscience, 20129, Italy
Speaker 4:
4)
Hans H. Zingg,
Department of Pharmacology & Therapeutics,
McGill University in Montreal, Canada
Symposium
IXd
Symposium organizer:
Jørgen
Jensen
National Institute of Occupational Health
Pb 8149 Dep, Gydaa vei 8, 0033 Oslo
Norway
Symposium title:
Muscle and fat: Molecular mechanisms of signaling
and crosstalk
COST BM0602 WG3-meeting
Outline
Skeletal muscles are the specialized tissue which
makes movement possible. However, skeletal muscles
also have a key role for
whole
body metabolic regulation. Skeletal muscles in the
human body make 30-40 % of the body, and account for
the majority of
insulin-stimulated
glucose disposal. There are still many questions to
be answered about the mechanism that regulate
glucose uptake
in skeletal muscles and the defects occurring in
type 2 diabetes. Normally, fat cells do not take up
much glucose during insulin
stimulation.
However, fat cell secretes many hormone like
substances (adipokines) and adipose tissue has an
important role in
determination
of insulin sensitivity in skeletal muscles and other
organs. In the present symposium, mechanism for
crosstalk
between
muscle and fat cells will be discussed and mechanism
for regulation glucose uptake and insulin
sensitivity in skeletal
muscles
will be reviewed.
Speakers and titles of talks:
Juergen
Eckel: Molecular mechanisms of the fat and muscle
crosstalk
Antonio Zorzano: Bridging mitochondrial dynamics and
metabolism in muscle.
Jørgen Jensen: PIKfyve in regulation of
glucose uptake in muscles
Sebastian Beck Jørgensen: AMPK in obesity and
insulin actions
Speaker 1:
Juergen
Eckel
German Diabetes Center, Duesseldorf
Germany
Speaker 2:
Antonio
Zorzano
University of Barcelona, Barcelona
Spain
Speaker 3:
Jorgen
Jensen
National Institute of Occupational Health, Oslo,
Norway
Speaker 4:
Sebastian
Beck Jørgensen
University of Copenhagen, Copenhagen
Denmark
Short communications
(19.00-20.00):
Tarja Kokkola, Finland
Helena Chowdhury, Slovenia
Didier Vertommen, Belgium
Symposium
IXe
Symposium organizer:
Wolfgang
Graier
Institute of Molecular Biology & Biochemistry,
Medical University Graz
Harrachgasse 21/III
Austria
Symposium title:
Ca2+, a miraculous messenger - an update
Outline
It is still fascinating that Ca2+, a single ion,
serves as a high selective intracellular mediator
for a multitude of cellular functions. In
many
cells, Ca2+ initiates acute cell functions such like
contraction or the secretion of hormones. Moreover,
Ca2+ also affects long-
term adaptation of the cells by triggering
activation and binding of transcription factors
(e.g. NFkB, CREB), controlling the activity
of
mitogenic enzymes (e.g. src), and counteracting or
initiating apoptosis. Such multiple, sometimes
oppositional actions of the
Ca2+
signal emphasize Ca2+ to serve as universal
activator for cells. However, in order to accomplish
specificity in the Ca2+-
regulation of such multitude of cell functions,
Ca2+-sensitive mechanisms essentially needs to be
controlled in a very sophisticated
manner.
The "Ca2+ paradox" of Ca2+ to be probably the most
versatile but still highly specific intracellular
messenger is proposed
to
be achieved by localized Ca2+ signaling. In respect
to such central role and outstanding importance of
cellular Ca2+, it is not
surprising
that cells express a vast number of Ca2+-shuttling
proteins (i.e. ryanodine-/IP3- receptors, SERCA,
Na+/Ca2+ exchange,
plasma
membrane Ca2+ ATPase, TRPs, ORAI, etc.), numerous
Ca2+-sensitive ion channels for Ca2+/Na+, K+ or Cl-
and four
Ca2+-handling
organelles (i.e. endoplasmic reticulum,
mitochondria, golgi, nucleus) that concertedly
control Ca2+ signaling. This
symposium
is designed to provide an update on: store operated
Ca2+ entry in non-excitable cells, the ER -
mitochondria connection
and mitochondrial motility, the mitochondrial Ca2+
signaling, the regulation and function of Ca2+
oscillations, and, the spatial
Ca2+
signaling in cardiac myocytes.
Speaker 1:
Maud
Frieden
Department of cell Physiology and Metabolism
University of Geneva
Geneva, Switzerland
Speaker 2:
Gyorgy
Szabadkai
Department of Physiology,
University College London,
London, UK
Speaker 3:
Roland
Malli
Institute of Molecular Biology & Biochemistry
Medical University Graz
Graz, Austria
Speaker 4:
Marko
Marhl
Faculty of Natural Sciences and Mathematics
University of Maribor
Maribor, Slovenia
Speaker
5:
Jens Kockskaemper
Department of Cardiology
Medical University of Graz
Graz, Austria
Symposium
XIa
Symposium organizer:
Helmut Hinghofer-Szalkay,
Nandu
Goswami
Prof Helmut Hinghofer-Szalkay
Medical University of Graz, Austria
Harrachgasse 21/5
Austria
Symposium title:
Gravitational Physiology
Outline
This symposium provides a comprehensive and
potentially interdisciplinary link between physical
stressors such as orthostatic
stress
and mental stressors/relaxants (such as Yoga). The
interplay between sensory inputs, central nervous
signal processing and
cardiovascular
/ autonomic stimulus response patterns is complex.
Cardiovascular responses to orthostatic stress may
be influenced
by
additional stimuli, like mental challenge, exercise
or "alternative" approaches such as meditation. This
would have practical value,
as carefully chosen stressors might increase
orthostatic capacity or resilience in people prone
to rapid development of syncope,
particularly
in "early fainters".
Interestingly,
the mechanisms of cardiovascular regulation have
been reported to be different in the two
(orthostatic and mental)
forms
of stress: Cardiopulmonary baroreceptor unloading
due to central hypovolemia occurs with orthostatic
stress while an
increase
in central command and arterial baroreceptor loading
is noticed under mental stress . Furthermore, mental
stress increases
sympathetic-nerve
activity and arterial-pressure despite stimulation
of arterial baroreceptors.
Specifc topics included here would be the response
changes due to these complex stimuli in different
sexes, ages, healthy/non-
healthy subjects, etc. Presentations included here
will be those from established researchers from all
over the world but as well as
selected
ones from emerging young physiologists.
Speaker 1:
Prof
Helmut Hinghofer-Szalkay
Institute of Physiology, Medical University of Graz;
Institute of Adaptive and Spaceflight Physiology,
Graz, Austria
Speaker 2:
Prof.
Niels Secher
Muscle Research Center, Rigshospitalet, University
of Copenhagen, Denmark
Speaker 3:
Prof.
Dag Linnarsson
Karolinska Institutet, Stockholm, Sweden
Speaker 4:
Prof.
Daniela Jezova
Institute of Experimental Endocrinology, Slovak
Academy of Science,
Bratislava, Slovakia
Symposium
XIb
Symposium organizer:
Markus
Ritter
Institute of Physiology and Pathophysiology,
Paracelsus Medical University
Strubergasse 21, 5020 Salzburg
Austria
Symposium title:
Osmoregulation, Osmosensing and Mechanotransduction
Outline
Prof. E.K. Hoffmann: Ion and Water Channels involved
in Cell Volume Control: Regulation and Physiological
Roles
Prof. Frank Wehner: Hypertonicity-Induced Cation
Channels(HICCs): Molecular Correlate and Role in
Proliferation vs. Apoptosis
Prof. Dieter Häussinger: Osmosignaling in the Liver
Prof. Joachim P. Spatz: The Role of Cell Adhesion
and Mechanics in Regulating Cellular Functions
Speaker 1:
Prof.
Else K. Hoffmann
Department of Biology, University of Copenhagen,
Denmark
Speaker 2:
Prof.
Frank Wehner
Department of Systemic Cell Biology, Max Planck
Institute of Molecular Physiology, Dortmund, Germany
Speaker 3:
Prof.
Dieter Häussinger
Clinic for Gastroenterology, Hepatology and
Infectiology, Heinrich-Heine-University, Düsseldorf,
Germany
Speaker 4:
Prof.
Joachim P. Spatz
Max Planck Institute for Metals Research, Department
of New Materials and Biosystems & University of
Heidelberg, Department
of Biophysical Chemistry
Symposium
XIc
Symposium organizer:
Elsa
Fabbretti
University of Nova Gorica
Vipavska 13, PO Box 301 Ro¾na Dolina SI-5000 Nova
Gorica
Slovenia
Symposium title:
Physiology and Pathophysiology of Purinergic
Signalling
Outline
Extracellular ATP interacts with specific membrane
receptors (ionotropic, P2X or metabotropic, P2Y)
having different molecular
characteristics,
namely selective agonist-gated channel properties
and/or intracellular G-protein coupled responses.
Discrete cell-
specific expression of various subtypes of ATP
receptors allows specificity and selectivity of
purinergic responses in many body
organs.
At single cell level, the ATP effects are
susceptible to modulation by crosstalk with other
receptors and by intracellular
molecular
pathways, allowing refinement and plasticity of cell
responses. ATP and related nucleotides are now
recognized key
players
in many tissue and cell responses during
physiological states or disease conditions, like in
chronic pain, inflammation,
neurologic
disorders and cancer. Thus, it is highly desirable
to identify novel pharmacological approaches to
block pathological
purinergic
effects in many chronic diseases. This aim is better
attained once the molecular mechanisms of purinergic
signalling
become
fully clear and is the subject of intensive research
world-wide. In particular, recent studies have
indicated distinct
mechanisms
regulating the expression and function of ATP
receptors like P2X3 receptors of sensory neurons
involved in pain,
P2X7
receptors in inflammation and neurodegeneration, or
P2Y receptors in the control of microcirculation.
Strong focus on
purinergic
signalling in the process of neuro-inflammation
suggests for example, aberrant ATP-mediated
communication amongst
different
cell types as a potential factor to express disease
chronicity. The present symposium proposes to
critically discuss the
role
of the extracellular ATP in physiological responses
and its modification and contribution to disease: in
this sense, the
symposium
plans to present the latest original research data,
drawing from the state-of-the art experience of
world leaders in this
field.
Speaker 1:
Prof.
Geoffrey Burnstock - "Overview of the
pathophysiology of purinergic signalling".
President of Autonomic Neuroscience Centre
Royal Free and University College Medical School,
Rowland Hill Street, University College London -
Gower Street - London -
WC1E 6BT
London NW3 2PF, UK
Speaker 2:
Dr.
Elsa Fabbretti - "ATP-mediated signalling in
trigeminal neurons in a migraine animal model".
University of Nova Gorica
Vipavska 13, PO Box 301
Roµna Dolina SI-5000 Nova Gorica Slovenia
Speaker 3:
Prof.
Stefan Boehm - "Nucleotide receptors at the neuro-vascular
interface".
Medical University of Vienna, Center of Physiology
and Pharmacology, Department of Pharmacology,
Waehringerstrasse 13a, A-
1090 Vienna, Austria
Speaker 4:
Prof.
Dirk Adriaensen
- "Purinergic signaling in the
pulmonary neuroepithelial body microenvironment
unraveled by live cell
University of Antwerp, Middelheimlaan 1
Dept. Diergeneeskundige Wet.
Middelheimcampus G.U.102
Groenenborgerlaan 171
2020 Antwerp, Belgium
Speaker
5:
Prof.
Francesco
Di Viriglio -
"Extracellular
ATP and P2 receptors in neurodegenerative diseases"
University of Ferrara,
Italy
Symposium
XId
Symposium organizer:
Marcella MOTTA
Valerio MAGNAGHI
Dept. of Endocrinology, Physiopathology and Applied
Biology
Via Balzaretti, 9 - 20133 Milano
Italy
Symposium title:
Pain: role of glutamate and GABA metabotropic
receptors
Outline
Pain is an increasing emergent issue in western
countries. Physiologically, it is considered as a
sensory system that under normal
conditions
is protective and adaptive, inducing changes to
facilitate wound healing and recovery. Glutamate and
GABA
(respectively
two major excitatory and inhibitory
neurotransmitters of the adult nervous system) are
two interesting candidates
among
the different mechanisms that are involved in pain
circuitries. These neurotransmitters exert their
action also through
metabotropic
receptors, that belong to the superfamily of
G-protein coupled receptors GPCRs. Metabotropic
glutamate receptors
(mGluRs)
and metabotropic GABA receptors (GABA-B) are present
at different levels of the pain neuraxis where they
regulate
nociceptive
transmission and pain. The first talk will introduce
the mechanisms of metabotropic glutamate modulation
in pain,
focusing
on new therapeutic aspects. The second talk will
address fresh evidence on the role of spinal pre-
and post-synaptic
metabotropic
GABA-B receptors in nociceptive circuitries. The
third talk will focus on the novel role of GABA-B
receptors in glial
cells, emphasizing the GABA-B contribution to the
peripheral myelination process and pain sensitivity.
The last talk will deal
with
the latter acquisition on the molecular features of
group III metabotropic mGluRs and on the development
of new
antinociceptive
drugs.
Speaker 1:
Prof.
Ferdinando NICOLETTI
Dept. Human Physiology and Pharmacology - University
"La Sapienza" Rome, Italy
Speaker 2:
Prof.
Marc LANDRY
Univ. Bordeaux 2, and INSERM U862, Institut François
Magendie - Bordeaux Cedex, France
Speaker 3:
Dr.
Valerio MAGNAGHI
Dept. of Endocrinology, Physiopathology and Applied
Biology - University of Milan - Italy
Speaker 4:
Dr.
Cyril GOUDET
Univ Montpellier I and II, CNRS UMR5203, Institut de
Génomique Fonctionnelle, and INSERM U661 -
Montpellier Cedex 5, F-
34094, France |
