Corticotropin-releasing hormone is a rapid and potent convulsant in the infant rat

Baram, Tallie Z.; Schultz, Linda

doi:10.1016/0165-3806(91)90118-3

Cited by 154 publications

(165 citation statements)

References 32 publications

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“…Chronic infusion of synthetic CRH into the cerebral ventricles of the rat leads to desensitization of CRH receptors and to lower CSF ACTH [9]. Our findings are thus consistent with an increase of CRH in the central nervous system of patients with IS.…”

Section: Discussionsupporting

confidence: 86%

Cerebrospinal fluid corticotropin and cortisol are reduced in infantile spasms

Baram¹,

Mitchell²,

Hanson³

et al. 1995

Pediatric Neurology

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Infantile spasms respond to ACTH, and levels of the hormone in cerebrospinal fluid of untreated infants with this disorder were found to be lower than in age-matched controls. In this study we analyzed cerebrospinal fluid Cortisol and ACTH using improved immunoassays in a larger cohort of infants with infantile spasms. Analysis of 20 patients and 15 age-matched controls revealed significantly lower levels of both ACTH and Cortisol in the cerebrospinal fluid. These data, combined with the efficacy of ACTH and glucocorticoids for infantile spasms, support an involvement of the brain-adrenal-axis in this disorder.

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Section: Discussionsupporting

confidence: 86%

Cerebrospinal fluid corticotropin and cortisol are reduced in infantile spasms

Baram¹,

Mitchell²,

Hanson³

et al. 1995

Pediatric Neurology

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“…These observations suggest that ACTH acts to repress infantile spasms by suppressing the level of endogenous CRH [42,43]. EEG recordings during CRH seizures show rhythmic, sharp activity [41]. These EEG recordings are closer to those observed in limbic seizures than those observed in IS in humans.…”

Section: The Corticotropin-releasing Hormone Modelsupporting

confidence: 57%

“…CRH release is increased by stress. The model has been induced by intraperitoneal or intracerebroventricular administration of CRH [41]. CRH administration during the second week of life in rats caused severe seizures by inhibiting the hypothalamic-pituitary-adrenal axis.…”

Section: The Corticotropin-releasing Hormone Modelmentioning

confidence: 99%

Novel Animal Models of Pediatric Epilepsy

et al. 2012

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When mimicking epileptic processes in a laboratory setting, it is important to understand the differences between experimental models of seizures and epilepsy. Because human epilepsy is defined by the appearance of multiple spontaneous recurrent seizures, the induction of a single acute seizure without recurrence does not constitute an adequate epilepsy model. Animal models of epilepsy might be useful for various tasks. They allow for the investigation of pathophysiological mechanisms of the disease, the evaluation, or the development of new antiepileptic treatments, and the study of the consequences of recurrent seizures and neurological and psychiatric comorbidities. Although clinical relevance is always an issue, the development of models of pediatric epilepsies is particularly challenging due to the existence of several key differences in the dynamics of human and rodent brain maturation. Another important consideration in modeling pediatric epilepsy is that "children are not little adults," and therefore a mere application of models of adult epilepsies to the immature specimens is irrelevant. Herein, we review the models of pediatric epilepsy. First, we illustrate the differences between models of pediatric epilepsy and models of the adulthood consequences of a precipitating insult in early life. Next, we focus on new animal models of specific forms of epilepsies that occur in the developing brain. We conclude by emphasizing the deficiencies in the existing animal models and the need for several new models.

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“…Fetal rats were delivered by cesarian-section on fetal days 15, 16, 17, and 19, and decapitated heads were rapidly immersed in powdered dry ice. Postnatal rats aged 1,3,5,7,9,12,15,25,49, and 90 days were sacrificed within 45 s of disturbance. Brains were rapidly dissected onto powdered dry ice and stored at −80°C.…”

Section: Animals and Tissue Preparationmentioning

confidence: 99%

“…Unique developmental expression patterns of CRF 1 -mRNA were found in the amygdala, hippocampus, and cortex. CRF 1 has recently been demonstrated to mediate the proconvulsant actions of CRF [3], and the observed high levels of CRF 1 -mRNA in limbic structures may provide the mechanism for the dramatic excitatory effects of CRF in these regions during development [4,6,7]. Based on these facts, the current study focused on the developmental profile of CRF 2 -mRNA in hypothalamic, limbic and cortical regions of the rat brain to gain insight of the potential functions of this receptor in the developing brain.…”

Section: Introductionmentioning

confidence: 99%

The developmental profile of the corticotropin releasing factor receptor (CRF2) in rat brain predicts distinct age-specific functions

Eghbal-Ahmadi

Hatalski²,

Lovenberg³

et al. 1998

Developmental Brain Research

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Corticotropin releasing factor (CRF) activates two known receptor types, CRF 1 and CRF 2 . In the adult rat brain, CRF 2 has a distinct distribution pattern, suggesting that it may mediate functions exclusive of CRF 1 . The goal of this study was to determine the age-dependent distribution of CRF 2 -messenger RNA (CRF 2 -mRNA) in the rat brain. Brains from rats sacrificed under stressfree conditions on fetal days (F) 15, 16, 17 and 19, and postnatal days 1, 3, 5, 7, 9, 12, 15, 25, 49 and 90 (adult) were analyzed using semiquantitative in situ hybridization histochemistry. The onset and distribution of CRF 2 -mRNA in the developing rat brain revealed important differences from the adult expression pattern: earliest expression of CRF 2 -mRNA was observed in the ventromedial hypothalamus (VMH) on F16. High levels of CRF 2 -mRNA were present in the fronto-parietal cortex in the fetal and early postnatal brain but not later. Conversely, no CRF 2 -mRNA was detectable in the ventroposterior (lateral and medial) thalamic nuclei prior to postnatal day 7. Distinct developmental profiles of CRF 2 -mRNA were also observed in the lateral septum, medial, basal and cortical amygdala nuclei, and in several hippocampal fields. In conclusion, CRF 2 is expressed in the hypothalamus on F16, prior to the detection of CRF itself in the paraventricular nucleus. The differential levels and distributions of CRF 2 -mRNA in hypothalamic and limbic brain regions indicate a precise regulation of this receptor's expression during development, as shown for CRF 1 . Regulation of the levels of CRF 2 may modulate the effects of CRF (and related ligands) on target neurons, consistent with differential maturation of the functions mediated by this receptor.

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Corticotropin-releasing hormone is a rapid and potent convulsant in the infant rat

Cited by 154 publications

References 32 publications

Cerebrospinal fluid corticotropin and cortisol are reduced in infantile spasms

Cerebrospinal fluid corticotropin and cortisol are reduced in infantile spasms

Novel Animal Models of Pediatric Epilepsy

The developmental profile of the corticotropin releasing factor receptor (CRF2) in rat brain predicts distinct age-specific functions

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