Amygdala kindling rate is altered in rats with a deficit in the responsiveness of the hypothalamo-pituitary-adrenal axis

Weiss, Gerald K.; Castillo, Natalie; Fernandez, Michael

doi:10.1016/0304-3940(93)90650-a

Cited by 17 publications

(15 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Consistent with this hypothesis, Lewis rats, which have inherently reduced CRF expression, take longer to kindle (i.e., more electrical stimulations are required), supporting the proconvulsive role of CRF (Weiss et al, 1993).…”

Section: Effects Of Corticotropin-releasing Factor On Seizuressupporting

confidence: 51%

Stress and Epilepsy: Multiple Models, Multiple Outcomes

Sawyer

Escayg

2010

Journal of Clinical Neurophysiology

View full text Add to dashboard Cite

Human studies show a link between stress and epilepsy, with stress causing an increase in seizure frequency and severity in patients with epilepsy. Many different animal model systems have been used to better understand this connection and the possible mechanisms involved. This review highlights the results of such studies relating stress and seizure susceptibility, with a focus on the hypothalamic-pituitary-adrenal axis and its relationship to seizure generation. The effects of hypothalamic-pituitary-adrenal axis mediators, acute stress, chronic stress, and early life stress on the seizure phenotype are summarized. Results suggest that stress has both anticonvulsive and proconvulsive properties, depending on the animal strain and the stress/seizure induction paradigm used. Attempts to interpret the stress-epilepsy literature must take these variables into account. The growing availability of genetically modified mice that carry either human epilepsy mutations or mutations in stress pathway genes now provide the opportunity to examine the relationship between stress and epilepsy more directly.

show abstract

Section: Effects Of Corticotropin-releasing Factor On Seizuressupporting

confidence: 51%

Stress and Epilepsy: Multiple Models, Multiple Outcomes

Sawyer

Escayg

2010

Journal of Clinical Neurophysiology

View full text Add to dashboard Cite

show abstract

“…In the adult rat, Ehlers [15] described the long latency (hours) to the onset of seizures induced by CRH. Additionally, a single administration of CRH produced a sequence of behaviors similar to the behavioral stages of kindling [15,46]. Therefore, it was hypothesized that CRH could be a kindling stimulus for the development of limbic seizures [46,47].…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, a single administration of CRH produced a sequence of behaviors similar to the behavioral stages of kindling [15,46]. Therefore, it was hypothesized that CRH could be a kindling stimulus for the development of limbic seizures [46,47]. Weiss et al [47], using mature male SpragueDawley rats, studied the effect of CRH on the development of kindling.…”

Section: Discussionmentioning

confidence: 99%

The in vivo proconvulsant effects of corticotropin releasing hormone in the developing rat are independent of ionotropic glutamate receptor activation

Brunson¹,

Schultz²,

Baram³

1998

Developmental Brain Research

View full text Add to dashboard Cite

Corticotropin releasing hormone (CRH) produces age-dependent limbic seizures in the infant rat. Both the phenotype and the neuroanatomic matrix of CRH-induced seizures resemble the seizures induced by the rigid glutamate analogue, kainic acid (KA), and by rapid amygdala kindling. The experiments described in this study tested the hypothesis that the in vivo proconvulsant effects of CRH require activation of ionotropic glutamate receptors. Non-competitive (+MK-801) or competitive (CGP-39551) antagonists of N-methyl-D-aspartate (NMDA) receptors decreased or eliminated the motor effects of CRH, but electrographic CRH-induced seizures were unaffected. Administration of CRH antagonists did not affect the acquisition or the maintenance of rapid kindling, which are mediated by NMDA and α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA) receptor activation, respectively. CRH receptor blockers failed to alter the latency or duration of seizures induced by activation of KA receptors, and threshold doses of CRH and KA had additive effects. CRH given repeatedly decreased the convulsant threshold dose of KA, probably via injury to hippocampal neurons. These results suggest that CRH and glutamate increase neuronal excitability via independent mechanisms. Because the proconvulsant effects of CRH are highly specific to the developmental period, glutamate-receptor-independent, CRHreceptor mediated excitation may account for some of the enhanced susceptibility to seizures during this period.

show abstract

“…In general, CRH is an excitatory neurotransmitter (Young, 1992;Curtis et al, 1995), and CRH-induced excitation has been demonstrated in the mature rat amygdala (Ehlers et al, 1983;Rainnie et al, 1992;Weiss et al, 1993). In the adult rat, in vivo administration of CRH into the cerebral ventricles results in epileptiform discharges in the amygdala and the hippocampus, which progress to seizures 3-7 hours later (Ehlers et al, 1983).…”

Section: Introductionmentioning

confidence: 96%