Munkatársaink részvétele (abstract-ok):
Title: Nucleus accumbens subregions: hodological and immunohistochemical study in the domestic chick (Gallus domesticus)
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Sunday, Oct 15, 2006, 10:00 AM -11:00 AM
Authors: *A. CSILLAG, E. BALINT;
1st Dept Anatomy, Semmelweis Univ Med, Budapest, HUNGARY.
The nucleus accumbens has been identified in avian species for some
time. However, the precise localization and extent of this nucleus is still
a matter of controversy. The present study is an attempt to further clarify
the position and subdivisions of nucleus accumbens, as compared to the
situation established in the mammalian brain. We used immunolabeling against
calbindin, neuropeptide Y and DARPP-32 for selective marking of putative
accumbens subdivisions, as well as anterograde transport of biotinylated
dextran amine, injected to the nucleus tractus solitarii region, in order to
study the distribution of afferent fibers in the nucleus accumbens and
surrounding ventrobasal forebrain areas of 7-day-old domestic chicks.
Biotinylated dextran amine was also injected to the putative subdivisions of
nucl. accumbens for selective projections. We found that the nucleus
accumbens extending between the rostrocaudal atlas coordinates A 10.6 and A
8.8 can be subdivided into core and shell, the core corresponding to
ventromedial and juxtaventricular medial striatum laterodorsal to the bed
nucleus of stria terminalis pars lateralis, and the shell representing an
arched region situated ventrally and ventrolaterally to the core.
Immunoreactivity to both calbindin and neuropeptide Y was more intense in
the shell than in the core division. DARPP-32 immunolabeling did not differ
in the two divisions but it was markedly weaker in the bed nucleus of stria
terminalis, enabling separation of this nucleus from surrounding accumbens
subdivisions. Fibers from nucleus solitarius predominantly terminate in the
shell division, similar to the situation described in mammals. While the
suggested core lies entirely within the boundary of medial striatum, the
shell seems to partially overlap the ventral pallidum. The remaining part of
accumbens lying rostral to A 10.6 cannot be subdivided into putative shell
and core by any of the methods used in the present study. This region is
likely to correspond to the rostral pole of nucleus accumbens.
Disclosures: A. Csillag , None; E. Balint, None.
Support: OTKA 43462
Semmelweis Univ. Sch. of Doctoral Studies
Title: Hetereogeneous appearance of immunohistochemical markers in ependyma
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Tuesday, Oct 17, 2006, 8:00 AM – 9:00 AM
Authors: I. ADORJAN, A. SZABO, *K. MIHALY;
1st Dept Anat, Semmelweis Univ Med, H-1450 Budapest, HUNGARY.
In ‘lower’ vertebrates as well as in the immature brains of mammals
and birds the radial ependymoglia take the tasks of both lining the
ventricles and enmeshing the brain wall. In the latter groups during brain
maturation radial cells transform into two very different cell types:
process-bearing free astrocytes for the ‘enmeshing’ function, and
epithelium-like ependymal cells for lining the ventricles. The ependyma has
its own immunohistochemical markers, few of them different from that of
astrocytes. These changes arise the following questions:
1) Do the appearances of these markers (the ‘biochemical maturation’)
precede the loss of long processes (the morphological transformation)?
2) Are the biochemical alterations synchronous in the ventricular
system?
3) Are there persistent local immunohistochemical differences?
Present study therefore compares the distribution of several
immunohistochemical markers in the ependyma, both in developing (E14-P10)
and mature rat brain. The following markers were used: aquaporin-4,
cadherin, dystrophin-71f, glutamin-synthetase, S-100 protein, nestin,
laminin. The results suggest that the biochemical maturation appears at
first in the third ventricle, near the hypothalamic groove, from E17. In
development, the third ventricle and the cerebral aqueduct precede the
lateral and fourth ventricles, in which the alterations occur about P0-P2.
The disappearance of the radial glia and nestin immunopositivity occurs
considerably later (about P0-P2 and P7-P10, respectively). Circumventricular
organs had different immunohistochemical pattern, not only during
development but also in the mature brain.
Disclosures: I. Adorjan, None; A. Szabo, None; K. Mihaly , None.
Support: Ph.D. School of the Semmelweis Univ.
Title: Immunohistochemical milestones of cerebrovascular maturation
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Monday, Oct 16, 2006, 4:00 PM –
5:00 PM
Authors: *I. ADORJAN, A. SZABO, M. KALMAN;
Anatomy, Histology and Embryology, Semmelweis University,
Budapest, HUNGARY.
Immunopositivity of cerebral vessels to the basal lamina marker
laminin, loose connective tissue marker fibronectin, laminin receptor
components of beta-dystroglycan and dystrophin 71d, and blood-brain barrier
marker aquaporin-4 were investigated during brain development or
post-lesion. Embryos were obtained from dated matings, removed in deep
ketamine-xylazine anaesthesia. Postnatal rats were transcardially perfused
in sublethal ether narcosis. Brains were fixed by immersion in 4%
paraformaldehyde in 0.1 M phosphate buffer (pH 7.4). Vibratome sections were
processed for fluorescent immunohistochemical reactions. The following
assemblies were found (although timing was different in different areas),
suggesting developmental stages:
Fibronectin +, laminin +, dystroglycan -: vessels are free of
glial connections.
Fibronectin +-, laminin +, dystroglycan +-: glial connections,
not yet generalized.
Fibronectin -, laminin +, dystroglycan +: glial connections are
generalized, but basal laminae not yet fused.
Fibronectin -, laminin +-, dystroglycan +: fusion of glial and
vascular basal laminae is in progress.
Fibronectin -, laminin -, dystroglycan +: common, fused
gliovascular lamina.
Appearance of aquaporin-4 and dystrophin 71d was approximately
parallel to that of beta-dystroglycan. The adult vascular immunopattern had
developed until the period of the replacement of radial glia by astrocytes.
There was, however, no coincidence with either the disappearance of nestin,
or the appearance of GFAP. Similar phenomena followed the post-lesion
rearrangement of vessels and reorganization of the gliovascular basal
lamina. The operations were performed in ketamine-xylazin anesthesia.
Following postoperative days (POD) 2 to 35, rats were overdosed with ether,
perfused transcardially with 4% phosphate-buffered paraformaldehyde
solution, and processed for immunohistochemistry, as above. Transitorily the
dystroglycan immunoreactivity disappeared from the territory of the lesion,
whereas laminin immunopositivity re-appeared, suggesting the desintegration
of the common gliovascular basal lamina. In this model the most frequent
integrin subunits, alphaV and beta1 were also investigated, but not detected
in the intact tissue, whereas alphaV appeared in a stage of the glial
reaction (at POD 4), and in the near vessels (POD 4 to 12). Therefore,
immunoreactivities of laminin receptors can characterise the stages of the
glial reaction as well.
Disclosures: I. Adorjan , None; A. Szabo, None; M. Kalman,
None.
Support: OTKA K60930/2006
Title: Origin and targets of cocaine–amphetamine-regulated transcript peptide immunoreactive fibers in lamina I of the rat spinal cord
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Saturday, Oct 14, 2006, 4:00
PM – 5:00 PM
Authors: M. KOZSUREK1, G. WITTMANN2, *G. GERBER1, C.
FEKETE2,3, Z. PUSKÁR1;
1Dept Anat, Histol, & Embryol, Semmelweis Univ Budapest,
Budapest 1094, HUNGARY, 2Department of Endocrine Neurobiology, Institute of
Experimental Medicine of the Hungarian Academy of Sciences, Budapest,
HUNGARY, 3Dept. of Medicine, Div. of Endocrinology, Diabetes and
Metabolism,, Tupper Research Inst. and New England Medical Center, Boston,
MA.
Cocaine and amphetamine regulated transcript (CART)
peptides are widely distributed in the central nervous system and have been
implicated in the regulation of several physiological functions including
pain modulation. The anatomical relationship of the CART-containing neuronal
elements and the spinal nociception, however, is unknown yet. We used
immunohistochemistry with antibody against CART(55-102) together with
markers for various populations of primary afferents, local interneurons and
descending axons to study the distribution and origin of CART-containing
fibres in the rat spinal cord.
Dense plexus of CART positive axons were located in lamina
I and the lateral spinal nucleus. A few weakly stained cells and scattered
terminals were also found in lamina II. CART cells and fibres also appeared
around the central canal and in the lateral horn of the upper thoracic cord.
This distribution could be followed from the cervical to the sacral
segments. The majority of CART-erg axons contained both SP and CGRP in
lamina I. Many of them were also labeled with galanin. In the dorsal root
ganglions about 10% of small cells expressed CART. Many of them also
contained both SP and CGRP. These results suggest that the majority of CART
positive axons in the superficial laminae have primary afferent origin.
We also investigated the postsynaptic targets of CART
positive axons in the superficial laminae. Many CART terminals showed
synaptophysin positivity and formed close appositions with NK1
immunoreactive dendrites. Projection neurons in lamina I have been
identified by injection of retrograde tracer Cholera-toxin β-subunit into
the lateral parabrachial nucleus where the majority of them terminate. Many
of the identified projection cells received contacts from CART positive
terminals that also contained SP.
Our data suggest that the majority of CART-erg axons in
lamina I originate from nociceptive primary afferents and terminate on
supraspinally projecting cells. These results provide morphological evidence
for the involvement of CART peptide in pain processing at the spinal level.
Disclosures: M. Kozsurek, None; G. Wittmann, None; G.
Gerber , None; C. Fekete, None; Z. Puskár, None.
Title: A role for the bone alkaline phosphatase in cortex myelination
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Tuesday, Oct 17, 2006, 2:00 PM –
3:00 PM
Authors: J. S. XIAO1, L. NEGYESSY2, J. BARNA2, L. RENAUD1, J. L.
MILLAN3, *C. FONTA1;
1Ctre de Recherche Cerveau et Cog, UMR5549, Toulouse cedex 9,
FRANCE, 2Neurobiology Research Group, Semmelweis University, Budapest,
HUNGARY, 3Oncodevelopmental Biology Program, Burnham Institute, La Jolla,
CA.
We recently found that alkaline phosphatase activity is
developmentally regulated in the primate cerebral cortex. We observed a
down-regulation correlated with myelination in the white matter, resulting
in the presence of alkaline phosphatase limited to the nodes of Ranvier in
the adult monkey (Fonta et al., JCN, 2005). In order to clarify the role of
this enzyme during central nervous system myelination, we used Tissue
Non-specific Alkaline Phosphatase (TNAP) knockout mice ( Narisawa et al.,
Dev Dyn 1997). These mice die at around 10 postnatal days and manifest
severe epileptic seizures. We compared myelination progress at various
developmental ages in WT and TNAP-/- mice in the cerebellum, spinal cord and
cerebral cortex, by using histological Gallyas staining method and electron
microscopic investigations. Histological examination indicates a lower
myelin content in the spinal cord and the cerebellum in the KO mice. By TEM,
two abnormal configurations are observed in the TNAP-/- cerebrum : from the
one hand, axons enveloped in a thin sheath of myelin, and on the other hand,
anomalous small irregular-shaped structures composed of several sheaths of
myelin surrounding a swelling axon. This result confirms our previous
hypothesis on the tied link between formation of myelin sheaths and the
developmental expression of alkaline phosphatase in the mammal brain.
Disclosures: J.S. Xiao, None; L. Negyessy, None; J. Barna,
None; L. Renaud, None; J.L. Millan, None; C. Fonta , None.
Support: French Embassy in Beijing
Hypophosphatasie Europe
Title: Succinate-sensitive and GABABR-independent gamma-hydroxybutyrate-binding sites in brain synaptic membranes
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Monday, Oct 16, 2006,
2:00 PM – 3:00 PM
Authors: T. MOLNAR1, E. F. KUTINE1, *J. KARDOS2,1,
E. SIMON-TROMPLER3, M. PALKOVITS4, Z. EMRI1;
1Dept of Neurochemistry, Inst of Biomolecular
Chemistry, Chem Res Center, HAS, Budapest, HUNGARY, 2Neurochemistry Group,
Cent Res Inst Chem Hungarian, H-1025 Budapest, HUNGARY, 3Group for
Radiosyntheses, Inst of Biomolecular Chemistry, Chem Res Center, HAS,
Budapest, HUNGARY, 4Laboratory of Neuromorphology, Semmelweis University and
HAS, Budapest, HUNGARY.
Gamma-hydroxybutyrate (GHB), a metabolite of
gamma-aminobutyric acid (GABA) has been known as a drug of abuse. The
nucleus accumbens is responsible for the development of reward properties of
different drugs. In many brain areas GHB acts on its own receptor (GHBR) and
also binds to GABAB receptor (GABABR). Succinate-sensitive and
GABABR-independent GHBR has been revealed in synaptic membranes isolated
from the rat forebrain or human basal ganglia areas nucleus accumbens and
globus pallidus, however, [3H]GHB and [3H]succinate binding has not been
compared yet.
Binding of GHB, the GHBR antagonist NCS-382 and the
metabolite succinate to [3H]GHB-labelled sites in rat forebrain synaptic
fractions was characterized by micromolar inhibition constants, in the order
of NCS-382 ≈ GHB << succinate. There was no significant binding interaction
between GABABR agonist (R)-baclofen and these [3H]GHB-labelled sites.
Synaptic GHBR sites of human nucleus accumbens and globus pallidus samples
showed similar binding profile. Similarly, (R)-baclofen did not bind to
[3H]succinate-labelled sites in rat forebrain synaptic fractions. In
contrast, succinate was found to be more effective than GHB in displacing
specifically bound [3H]succinate in rat forebrain synaptic fractions.
These findings suggest that succinate can mimic some
of the actions of GHB.
Disclosures: T. Molnar, None; E.F. Kutine, None; J.
Kardos , None; E. Simon-Trompler, None; M. Palkovits, None; Z. Emri, None.
Support: Wellcome Grant 068690/Z/02/Z
MediChem2 1/A/005/2004 NKFP
Transporter Explorer AKF-050068
Title: High-fidelity short-term memory for facial expressions
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Tuesday, Oct 17, 2006,
10:00 AM -11:00 AM
Authors: E. BANKO1, *Z. VIDNYANSZKY2;
1Faculty of Information Technology, Peter Pazmany
Catholic University, Budapest, HUNGARY, 2Neurobiol Res Grp, Hungarian
Academy of Sciences – Semmelweis University, Budapest, HUNGARY.
Increasing the delay between subsequently presented
visual stimuli can affect humans’ ability to discriminate some of their
basic visual dimensions: orientation but not spatial frequency
discrimination is impaired when stimuli are separated by several seconds.
However, whether discrimination of more complex visual attributes – such as
facial expressions – is affected by the delay between the stimuli to be
compared is still an open question.
We addressed this question using a delayed facial
emotion discrimination task (inter-stimulus intervals, ISI: 1-3-6-9 s). We
also recorded event related potentials (ERP) to characterize the neural
correlates of visual short-term memory for facial emotions. Our behavioral
results revealed that face emotion discrimination accuracy is not affected
by ISI. The results of the control experiments exclude the possibility that
faces were compared based on their low level visual attributes (i.e.
contrast, color etc.), since discrimination performance was significantly
impaired when face stimuli were presented upside-down. However, reaction
times (RT) increased with ISI: there was a significant (150-200 ms)
difference in RT between the shortest and the longest ISI. This RT
difference was not due to an impaired ability to estimate the onset of the
second stimuli at long delays, since adding a temporal cue before the onset
of the second stimulus did not eliminate the RT difference between the short
and long ISIs. Our ERP experiments revealed that the amplitude of the
face-evoked N170 component is significantly increased in the conditions with
long (6 s) ISI as compared to that with short (1 s) ISI and that the ISI
effect on N170 cannot be explained by adaptation to the first face stimulus.
These findings provide evidence that facial emotions
can be stored in visual memory without loss for up to several seconds and
that the face-specific N170 component represents the primary ERP correlate
of short-term visual memory for facial emotions.
Disclosures: E. Banko, None; Z. Vidnyanszky , None.
Support: Hungarian Scientific Research Fund (OTKA)
T048949
Title: Alteration in urocortin 1 and BDNF-expression in the human Edinger-Westphal nucleus in depression
Location: Georgia World Congress Center: Halls B3-B5
Presentation Start/End Time: Wednesday, Oct 18,
2006, 9:00 AM -10:00 AM
Authors: *T. L. KOZICZ1, N. DERKS1, D.
TILBURG-OUWENS1, M. PALKOVITS2, E. W. ROUBOS1;
1Dept Cell Animal Physiol, Radboud Univ Nijmegen,
Nijmegen, THE NETHERLANDS, 2Department of Anatomy, Semmelweis University,
Budapest, HUNGARY.
Failed adaptation to stress underlies certain forms
of stress-related neuropathology, such as anxiety and major depression.
Successful stress adaptation requires the activation of various brain
centers, such as the hypothalamic pituitary adrenal (HPA) axis and the
Edinger-Westphal (EW) urocortin 1 system. Both brain centers undergo
conspicuous activity changes in response to stress. The HPA-axis is
hyperactive in patients suffering from depression and CRF is strongly
elevated in the brain and in the cerebrospinal fluid in major depression. We
have recently demonstrated that in mice over-expressing neuronal CRF (an
animal model for depression), EW-Ucn1 mRNA is strongly down-regulated. This
finding suggests that an altered activity of the EW-Ucn1 system may
contribute to the pathogenesis of major depression, and led us to
hypothesize a chronically down-regulated level of EW-Ucn1 mRNA in patients
suffering from major depression. To test this hypothesis we measured the
Ucn1 mRNA level in the EW of seven male suicide victims, and compared these
data with those obtained from eight healthy male controls.
Contrary to our expectations, however, we found that
EW-Ucn1-mRNA levels were significantly higher (p<0.039) in suicide victims,
since EW-Ucn1 mRNA expression was 13.4ą7.03 higher in patients with major
depression than in healthy subjects. To further elucidate mechanism(s)
underlying this phenomenon, we examined the expression of brain-derived
neurotrophic factor (BDNF) in the human EW. BDNF has been implicated in the
pathogenesis of major depression, and in rats Ucn1 and BDNF co-exist in EW
neurons. We found a 25% lower (p<0.041) BDNF mRNA expression in suicide
victims than in controls.
On the basis of these results we conclude that
altered expression of EW Ucn1 and of BDNF may play a role in the
pathogenesis of major depression, and propose that the EW-Ucn1 system plays
an important role in stress-induced mood disorders.
Disclosures: T.L. Kozicz, None; N. Derks, None; D.
Tilburg-Ouwens, None; M. Palkovits, None; E.W. Roubos, None.
Support: Nederlands Organisation for Scientific
Research (#864.05.008).