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J S Craig

Publications and source records attributed to J S Craig.

5 recordsLinked to original sources
PubMed1992

Effect of amygdala kindling on the in vivo release of GABA and 5-HT in the dorsal raphe nucleus in freely moving rats.

Our laboratory has previously reported a significant subsensitivity to iontophoretically applied GABA (gamma-aminobutyric acid) in dorsal raphe neurons of amygdala-kindled rats. This subsensitivity was selective for GABA and persisted at least 3 months after the last kindled seizure. In the present series of experiments, we explored mechanisms by which kindling could result in persistent GABA sensitivity changes, using in vivo microdialysis to quantitate neurotransmitter [including GABA and 5-hydroxytryptamine (5-HT)] release in the dorsal raphe nucleus of awake, unrestrained amygdala-kindled rats. Depolarization-induced release of GABA is markedly increased in the dorsal raphe nucleus in amygdala-kindled animals. This change in depolarization-induced GABA release appeared to be graded, dependent upon the stage to which the animal is kindled. Thus GABA release is increased in animals kindled to Stage 2 and even greater in animals kindled to Stage 5 seizures. The change in GABA release is also selective, since no consistent change in the release of other putative amino acid neurotransmitters or 5-HT was observed in these same animals. We hypothesize that this increase in depolarization-induced release of GABA in the amygdala-kindled animal underlies the development of subsensitivity to GABA in dorsal raphe neurons.

Amino Acids↗
PubMed1992

Amygdala kindling potentiates seizure-stimulated immediate-early gene expression in rat cerebral cortex.

Kindling induces long-term adaptations in neuronal function that lead to a decreased threshold for induction of seizures. In the present study, the influence of amygdala kindling on levels of mRNA for the immediate-early genes (IEGs) c-fos, c-jun, and NGF1-A were examined both before and after an acute electroconvulsive seizure (ECS). Although amygdala kindling did not significantly influence resting levels of c-fos mRNA in cerebral cortex, ECS-stimulated levels of c-fos mRNA (examined 45 min after ECS) were approximately twofold greater in the cerebral cortex of kindled rats relative to sham-treated controls. The influence of kindling on IEG expression was dependent on the time course of kindling, as ECS-stimulated levels of c-fos mRNA were not significantly increased in stage 2 kindled animals. ECS-stimulated levels of c-jun and NGF1-A mRNA were also significantly increased in cerebral cortex of kindled rats relative to sham-treated controls. The influence of kindling on IEG expression was long-lasting because an acute ECS stimulus significantly elevated levels of c-fos and c-jun mRNA in the cerebral cortex of animals that were kindled 5 months previously. In contrast to these effects in cerebral cortex, kindling did not influence ECS-stimulated levels of c-fos mRNA in hippocampus. Finally, immunohistochemical studies revealed lamina-specific changes in the cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1984

The Ia-1 gene effects T-B cell collaboration for the in vitro antibody response.

The I-A subregion mutant B6.C-H-2bm12 (bm12) and the C57BL/6 parent were used to examine the role of the Ia-1 gene product as a restriction element in the antibody response to sheep red blood cells (SRBC). Using an in vitro culture system, it was shown that cooperation between histocompatible T cells, B cells and macrophages was required to generate a secondary IgM response to SRBC. The alteration in the Ia-1 gene in bm12 altered the ability of bm12 T cells to collaborate with C57BL/6 B cells, but not with C57BL/6 macrophages. Similarly, C57BL/6 T cells could not collaborate with bm12 B cells. The mutation in bm 12 did not affect the ability of T cells to interact with C57Bl/6 macrophages, either in vitro or in vivo, or of bm12 macrophages to interact with C57BL/6T cells. Thus in this system, the Ia-1 gene product restricts T-B cell interaction but not T cell-macrophage interaction.

Animals↗