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Article: Neuropeptide-mediated excitability: a key triggering mechanism for seizure generation in the developing brain.

Baram, T Z / Hatalski, C G

1998 Volume 21, Issue 11, Page(s) 471–476

Abstract: Most human seizures occur early in life,consistent with established excitability-promoting features of the developing brain. Surprisingly, the majority of developmental seizures are not spontaneous but are provoked by injurious or stressful stimuli. What ...

Abstract	Most human seizures occur early in life,consistent with established excitability-promoting features of the developing brain. Surprisingly, the majority of developmental seizures are not spontaneous but are provoked by injurious or stressful stimuli. What mechanisms mediate'triggering' of seizures and limit such reactive seizures to early postnatal life? Recent evidence implicates the excitatory neuropeptide, corticotropin-releasing hormone (CRH). Stress activates expression of the CRH gene in several limbic regions, and CRH-expressing neurons are strategically localized in the immature rat hippocampus, in which this neuropeptide increases the excitability of pyramidal cells in vitro. Indeed, in vivo, activation of CRH receptors--maximally expressed in hippocampus and amygdala during the developmental period which is characterized by peak susceptibility to 'provoked' convulsions--induces severe, age-dependent seizures. Thus, converging data indicate that activation of expression of CRH constitutes an important mechanism for generating developmentally regulated, triggered seizures, with considerable clinical relevance.
MeSH term(s)	Animals ; Brain/growth & development ; Brain/metabolism ; Brain/physiopathology ; Brain Chemistry/physiology ; Child, Preschool ; Epilepsy/metabolism ; Epilepsy/physiopathology ; Humans ; Infant ; Infant, Newborn ; Neuropeptides/metabolism ; Neurotoxins/metabolism
Chemical Substances	Neuropeptides ; Neurotoxins
Language	English
Publishing date	1998-11
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	282488-7
ISSN	1878-108X ; 0166-2236 ; 0378-5912
ISSN (online)	1878-108X
ISSN	0166-2236 ; 0378-5912
DOI	10.1016/s0166-2236(98)01275-2
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Zs.MG 53: Show issues

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Article: Stress-induced transcriptional regulation in the developing rat brain involves increased cyclic adenosine 3',5'-monophosphate-regulatory element binding activity.

Hatalski, C G / Baram, T Z

Molecular endocrinology (Baltimore, Md.)

1997 Volume 11, Issue 13, Page(s) 2016–2024

Abstract: The cAMP-regulatory element (CRE) binding protein (CREB) functions as a trans-acting regulator of genes containing the CRE sequence in their promoter. These include a number of critical genes, such as CRF, involved in the hypothalamic response to ... ...

Abstract	The cAMP-regulatory element (CRE) binding protein (CREB) functions as a trans-acting regulator of genes containing the CRE sequence in their promoter. These include a number of critical genes, such as CRF, involved in the hypothalamic response to stressful stimuli in the adult. The ability of the developing rat (during the first 2 postnatal weeks) to mount the full complement of this stress response has been questioned. We have previously demonstrated the stress-induced up-regulation of the transcription of hypothalamic CRF during the second postnatal week in the rat. The focus of the current study was to explore the mechanism of transcriptional regulation in response to stress through the physiological induction of transcriptional trans-activators that bind to the CRE in the developing rat brain. CRE-binding activity was detected via gel shift analysis in extracts from both the hypothalamus and the cerebral cortex of the developing rat. CREB was identified in these extracts by Western blot analysis and was shown to be the major contributor to the CRE-binding activity by gel shift analysis with two specific antibodies directed against CREB. After acute hypothermic stress, the abundance of CRE-binding activity (but not of total immunoreactive CREB), increased in hypothalamic extracts. This enhanced CRE-binding activity was blocked by an antiserum directed against CREB and was accompanied by an apparent increase in CREB phosphorylation. These results indicate that posttranslational enhancement of CRE-binding activity is likely to constitute an important mechanism for up-regulation of genes possessing the CRE sequence in the developing rat hypothalamus by adverse external signals.
MeSH term(s)	Animals ; Animals, Newborn ; Blotting, Western ; Brain/growth & development ; Brain/metabolism ; Cerebral Cortex/chemistry ; Cerebral Cortex/metabolism ; Cold Temperature ; Corticosterone/blood ; Cyclic AMP/genetics ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/analysis ; Cyclic AMP Response Element-Binding Protein/physiology ; Female ; Gene Expression Regulation, Developmental ; Hypothalamus, Anterior/chemistry ; Hypothalamus, Anterior/metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Regulatory Sequences, Nucleic Acid ; Stress, Physiological/genetics ; Stress, Physiological/metabolism
Chemical Substances	Cyclic AMP Response Element-Binding Protein ; Cyclic AMP (E0399OZS9N) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	1997-12
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/mend.11.13.0042
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Article: Corticotropin releasing factor mRNA expression in the hypothalamic paraventricular nucleus and the central nucleus of the amygdala is modulated by repeated acute stress in the immature rat.

Hatalski, C G / Guirguis, C / Baram, T Z

Journal of neuroendocrinology

1998 Volume 10, Issue 9, Page(s) 663–669

Abstract: Age-appropriate acute stress, such as cold exposure, provokes the secretion of corticotropin releasing factor (CRF) from the hypothalamus, leading to a robust increase of plasma corticosterone in the immature rat. This activation of the hypothalamic- ... ...

Abstract	Age-appropriate acute stress, such as cold exposure, provokes the secretion of corticotropin releasing factor (CRF) from the hypothalamus, leading to a robust increase of plasma corticosterone in the immature rat. This activation of the hypothalamic-pituitary-adrenal system is accompanied by a stress-induced increase of steady-state CRF-mRNA expression in the hypothalamic paraventricular nucleus (PVN). In the current study, we analysed changes in CRF-mRNA expression in the PVN and the central nucleus of the amygdala (ACe) in the immature rat in response to a single episode of cold stress and three repeated exposures to this same stressor. CRF-mRNA expression in the PVN increased after a single, but not repeated exposures to cold stress, while repeated acute stress increased the content of the CRF peptide in the anterior hypothalamus. In the ACe, repeated episodes of cold stress resulted in increased expression of CRF-mRNA. These findings indicate a differential regulation of CRF gene expression in the PVN and ACe of the immature rat by single and repeated acute stress.
MeSH term(s)	Acute Disease ; Amygdala/metabolism ; Animals ; Cold Temperature ; Corticotropin-Releasing Hormone/blood ; Corticotropin-Releasing Hormone/genetics ; Corticotropin-Releasing Hormone/metabolism ; Hypothalamus/metabolism ; Paraventricular Hypothalamic Nucleus/metabolism ; RNA, Messenger/metabolism ; Rats ; Recurrence ; Stress, Physiological/genetics ; Stress, Physiological/metabolism
Chemical Substances	RNA, Messenger ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	1998-09
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1007517-3
ISSN	1365-2826 ; 0953-8194
ISSN (online)	1365-2826
ISSN	0953-8194
DOI	10.1046/j.1365-2826.1998.00246.x
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Zs.A 2634: Show issues

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Article: Humoral immunity in the central nervous system of Lewis rats infected with Borna disease virus.

Hatalski, C G / Hickey, W F / Lipkin, W I

Journal of neuroimmunology

1998 Volume 90, Issue 2, Page(s) 128–136

Abstract: The aim of this study was to investigate the humoral immune response to Borna disease (BD) virus in the brain of experimentally infected Lewis rats. Abundant IgG was detected in BD-rat brain with isotype variation throughout infection. IgG was locally ... ...

Abstract	The aim of this study was to investigate the humoral immune response to Borna disease (BD) virus in the brain of experimentally infected Lewis rats. Abundant IgG was detected in BD-rat brain with isotype variation throughout infection. IgG was locally produced as indicated by an intact blood-brain barrier, Ig kappa light chain mRNA-containing cells in brain and accumulation of virus-specific antibodies in cerebrospinal fluid. Treatment with BD-rat serum altered viral gene expression in persistently infected cultured rat glioblastoma cells. These data suggest that antibodies, produced in the brain, may influence viral gene expression.
MeSH term(s)	Animals ; Antibodies, Viral/biosynthesis ; Antibodies, Viral/physiology ; Blood-Brain Barrier ; Borna Disease/immunology ; Borna disease virus/genetics ; Borna disease virus/immunology ; Brain/immunology ; Gene Expression Regulation, Viral ; Immunoglobulin G/biosynthesis ; Immunoglobulin Isotypes/biosynthesis ; Immunoglobulin kappa-Chains/genetics ; RNA, Messenger/analysis ; Rats ; Rats, Inbred Lew
Chemical Substances	Antibodies, Viral ; Immunoglobulin G ; Immunoglobulin Isotypes ; Immunoglobulin kappa-Chains ; RNA, Messenger
Language	English
Publishing date	1998-10-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/s0165-5728(98)00066-6
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Zs.A 1646: Show issues

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Article: Evolution of the immune response in the central nervous system following infection with Borna disease virus.

Hatalski, C G / Hickey, W F / Lipkin, W I

Journal of neuroimmunology

1998 Volume 90, Issue 2, Page(s) 137–142

Abstract: Borna disease virus infection of Lewis rats results in an immune-mediated disease associated with transient meningoencephalitis and persistent viral infection. In the acute phase of disease, perivascular immune cell infiltrates consisted of CD4 + and CD8 ...

Abstract	Borna disease virus infection of Lewis rats results in an immune-mediated disease associated with transient meningoencephalitis and persistent viral infection. In the acute phase of disease, perivascular immune cell infiltrates consisted of CD4 + and CD8 + T cells, macrophages and NK cells with peak expression of mRNAs encoding the cytokines IL1alpha, IL2, IL6, TNFalpha, and IFNgamma. In the chronic phase of disease, numbers of NK cells, B cells and activated microglia increased in the brain parenchyma with peak expression of IL4 mRNA. These data were consistent with a switch from a Th1-like, cellular immune response to a Th2-like, humoral immune response.
MeSH term(s)	Animals ; Antibodies, Viral/blood ; Apoptosis ; Borna Disease/immunology ; Borna Disease/pathology ; Brain/immunology ; Brain/pathology ; Cytokines/genetics ; Immunoglobulin E/blood ; Male ; RNA, Messenger/analysis ; Rats ; Rats, Inbred Lew ; T-Lymphocytes/immunology
Chemical Substances	Antibodies, Viral ; Cytokines ; RNA, Messenger ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	1998-10-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/s0165-5728(98)00076-9
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Article: Neurobiology of Borna disease virus.

Lipkin, W I / Hatalski, C G / Briese, T

Journal of neurovirology

1997 Volume 3 Suppl 1, Page(s) S17–20

MeSH term(s)	Animals ; Borna Disease/physiopathology ; Borna disease virus/pathogenicity ; Borna disease virus/physiology ; Brain/virology ; Central Nervous System/virology ; Genes, Viral ; Humans ; Neurons/virology ; Viral Proteins/analysis
Chemical Substances	Viral Proteins
Language	English
Publishing date	1997-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
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Zs.A 4426: Show issues

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Article: Borna disease.

Hatalski, C G / Lewis, A J / Lipkin, W I

Emerging infectious diseases

1997 Volume 3, Issue 2, Page(s) 129–135

Abstract: Borna disease virus, a newly classified nonsegmented negative-strand RNA virus with international distribution, infects a broad range of warm-blooded animals from birds to primates. Infection causes movement and behavioral disturbances reminiscent of ... ...

Abstract	Borna disease virus, a newly classified nonsegmented negative-strand RNA virus with international distribution, infects a broad range of warm-blooded animals from birds to primates. Infection causes movement and behavioral disturbances reminiscent of some neuropsychiatric syndromes. The virus has not been clearly linked to any human disease; however, an association between infection with the virus and selected neuropsychiatric disorders has been suggested. We reviewed recent advances in Borna disease virus research, focusing on evidence of infection in humans.
MeSH term(s)	Animals ; Antibodies, Viral/blood ; Borna Disease/complications ; Borna Disease/diagnosis ; Borna Disease/transmission ; Borna disease virus/genetics ; Humans ; Mental Disorders/etiology
Chemical Substances	Antibodies, Viral
Language	English
Publishing date	1997-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1380686-5
ISSN	1080-6040
ISSN	1080-6040
DOI	10.3201/eid0302.970205
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Article: Rapid phosphorylation of the CRE binding protein precedes stress-induced activation of the corticotropin releasing hormone gene in medial parvocellular hypothalamic neurons of the immature rat.

Chen, Y / Hatalski, C G / Brunson, K L / Baram, T Z

Brain research. Molecular brain research

2001 Volume 96, Issue 1-2, Page(s) 39–49

Abstract: The mechanisms of the molecular and neuroendocrine responses to stress in the immature rat have been a focus of intense investigation. A principal regulator of the these responses in both mature and developing rat is the neuropeptide corticotropin ... ...

Abstract	The mechanisms of the molecular and neuroendocrine responses to stress in the immature rat have been a focus of intense investigation. A principal regulator of the these responses in both mature and developing rat is the neuropeptide corticotropin releasing hormone (CRH), and levels of hypothalamic CRH mRNA are enhanced by stress. In vitro, transcription of the CRH gene is governed by binding of the phosphorylated form of cAMP responsive element binding protein (pCREB) to the promoter. Here we tested the hypothesis that rapid, stress-induced CRH transcription occurred during the first two postnatal weeks, and is associated with pCREB expression. The time-course of induction of unedited, heteronuclear CRH RNA (CRH hnRNA) was examined in hypothalamic paraventricular nucleus (PVN) of immature rats subjected to both modest and strong acute stressors using in situ hybridization; pCREB abundance was determined in individual neurons in specific PVN sub-nuclei using immunocytochemistry and unbiased quantitative analysis. CRH hnRNA signal was negligible in PVN of immature rats sacrificed under stress-free conditions, but was readily detectable within 2 min, and peaked at 15 min, in PVN of stressed animals. Enhanced pCREB immunoreactivity was evident within 2 min of stress onset, and was enhanced specifically in stress-responsive, CRH-expressing medial parvocellular neurons. These data support the notion that, already during early postnatal life, stress induces rapid CREB phosphorylation, interaction of pCREB-containing transcription complexes with the CRE element of the CRH gene promoter, and initiation of CRH hnRNA production in stress-responsive neurons of rat PVN.
MeSH term(s)	Acute Disease ; Age Factors ; Animals ; Cold Temperature ; Corticosterone/blood ; Corticotropin-Releasing Hormone/genetics ; Cyclic AMP Response Element-Binding Protein/metabolism ; Gene Expression Regulation, Developmental ; Handling (Psychology) ; Paraventricular Hypothalamic Nucleus/growth & development ; Paraventricular Hypothalamic Nucleus/metabolism ; Phosphorylation ; RNA, Messenger/analysis ; RNA, Nuclear/genetics ; Rats ; Stress, Physiological/metabolism ; Stress, Physiological/physiopathology ; Transcription, Genetic/physiology
Chemical Substances	Cyclic AMP Response Element-Binding Protein ; RNA, Messenger ; RNA, Nuclear ; Corticotropin-Releasing Hormone (9015-71-8) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2001-09-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	632883-0
ISSN	1872-6941 ; 0169-328X
ISSN (online)	1872-6941
ISSN	0169-328X
DOI	10.1016/s0169-328x(01)00265-0
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Zs.A 2181: Show issues

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Article: Effects of blocking GABA degradation on corticotropin-releasing hormone gene expression in selected brain regions.

Tran, V / Hatalski, C G / Yan, X X / Baram, T Z

Epilepsia

1999 Volume 40, Issue 9, Page(s) 1190–1197

Abstract: Purpose: The gamma-aminobutyric acid (GABA) degradation blocker gamma-vinyl-GABA (VGB) is used clinically to treat seizures in both adult and immature individuals. The mechanism by which VGB controls developmental seizures is not fully understood. ... ...

Abstract	Purpose: The gamma-aminobutyric acid (GABA) degradation blocker gamma-vinyl-GABA (VGB) is used clinically to treat seizures in both adult and immature individuals. The mechanism by which VGB controls developmental seizures is not fully understood. Specifically, whether the anticonvulsant properties of VGB arise only from its elevation of brain GABA levels and the resulting activation of GABA receptors, or also from associated mechanisms, remains unresolved. Corticotropin-releasing hormone (CRH), a neuropeptide present in many brain regions involved in developmental seizures, is a known convulsant in the immature brain and has been implicated in some developmental seizures. In certain brain regions, it has been suggested that CRH synthesis and release may be regulated by GABA. Therefore we tested the hypothesis that VGB decreases CRH gene expression in the immature rat brain, consistent with the notion that VGB may decrease seizures also by reducing the levels of the convulsant molecule, CRH. Methods: VGB was administered to immature, 9-day-old rats in clinically relevant doses, whereas littermate controls received vehicle. Results: In situ hybridization histochemistry demonstrated a downregulation of CRH mRNA levels in the hypothalamic paraventricular nucleus but not in other limbic regions of VGB-treated pups compared with controls. In addition, VGB-treated pups had increased CRH peptide levels in the anterior hypothalamus, as shown by radioimmunoassay. Conclusions: These findings are consistent with a reduction of both CRH gene expression and secretion in the hypothalamus, but do not support an indirect anticonvulsant mechanism of VGB via downregulation of CRH levels in limbic structures. However, the data support a region-specific regulation of CRH gene expression by GABA.
MeSH term(s)	4-Aminobutyrate Transaminase/antagonists & inhibitors ; Amygdala/drug effects ; Amygdala/metabolism ; Animals ; Brain/drug effects ; Brain/growth & development ; Brain/metabolism ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Corticotropin-Releasing Hormone/biosynthesis ; Corticotropin-Releasing Hormone/genetics ; Corticotropin-Releasing Hormone/physiology ; Gene Expression ; Hypothalamus/drug effects ; Hypothalamus/growth & development ; Hypothalamus/metabolism ; Immunohistochemistry ; In Situ Hybridization ; RNA, Messenger/analysis ; Rats ; Rats, Sprague-Dawley ; Vigabatrin ; gamma-Aminobutyric Acid/analogs & derivatives ; gamma-Aminobutyric Acid/metabolism ; gamma-Aminobutyric Acid/pharmacology
Chemical Substances	RNA, Messenger ; gamma-Aminobutyric Acid (56-12-2) ; Corticotropin-Releasing Hormone (9015-71-8) ; 4-Aminobutyrate Transaminase (EC 2.6.1.19) ; Vigabatrin (GR120KRT6K)
Language	English
Publishing date	1999-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/j.1528-1157.1999.tb00847.x
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Zs.A 517: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Corticotropin releasing hormone antagonist does not prevent adrenalectomy-induced apoptosis in the dentate gyrus of the rat hippocampus.

Gerth, A / Hatalski, C G / Avishai-Eliner, S / Baram, T Z

Stress (Amsterdam, Netherlands)

1998 Volume 2, Issue 3, Page(s) 159–169

Abstract: Adrenalectomy in the mature rat leads to death of granule cells in the dentate gyrus of the hippocampal formation. The mechanisms underlying this cell death have not been fully clarified: It has been considered that the granule cells require adrenal ... ...

Abstract	Adrenalectomy in the mature rat leads to death of granule cells in the dentate gyrus of the hippocampal formation. The mechanisms underlying this cell death have not been fully clarified: It has been considered that the granule cells require adrenal steroids for their survival, since corticosterone replacement prevents their death. However, adrenalectomy-induced loss of negative feedback also increases levels of corticotropin releasing hormone (CRH) in several limbic brain regions. CRH is known to induce neuronal death in hippocampal regions rich in CRH receptors. This study tested the hypothesis that adrenalectomy-induced granule cell death is mediated via the enhanced activation of CRH receptors. The extent of granule cell degeneration was compared among 4 groups of young adult male rats: Sham-adrenalectomy controls, adrenalectomized rats, adrenalectomized rats infused with a CRH antagonist from the onset of steroid deprivation to the time of sacrifice, and adrenalectomized rats infused with vehicle only. (9-41)-alpha-helical CRH was administered using an osmotic pump into the cerebral ventricles. Adrenalectomy led to robust granule cell degeneration, which was maximal in the suprapyramidal blade of the dentate gyrus. Infusion of the CRH antagonist in doses shown to block CRH actions on limbic neurons did not decrease the number of degenerating granule cells compared with the untreated or vehicle-infused adrenalectomized groups. Therefore, blocking the actions of CRH does not prevent adrenalectomy-induced granule cell death, consistent with a direct effect of corticoids on the survival of these neurons.
MeSH term(s)	Adrenalectomy ; Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Corticosterone/blood ; Corticotropin-Releasing Hormone/antagonists & inhibitors ; Corticotropin-Releasing Hormone/pharmacology ; Dentate Gyrus/cytology ; Dentate Gyrus/drug effects ; Dentate Gyrus/physiology ; Hormone Antagonists/pharmacology ; Male ; Models, Biological ; Neurons/cytology ; Neurons/drug effects ; Neurons/physiology ; Peptide Fragments/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone/drug effects ; Receptors, Corticotropin-Releasing Hormone/physiology
Chemical Substances	Hormone Antagonists ; Peptide Fragments ; Receptors, Corticotropin-Releasing Hormone ; Corticotropin-Releasing Hormone (9015-71-8) ; corticotropin releasing hormone (9-41) (96118-75-1) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	1998-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1387706-9
ISSN	1607-8888 ; 1025-3890
ISSN (online)	1607-8888
ISSN	1025-3890
DOI	10.3109/10253899809167280
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