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T McCabe

Publications and source records attributed to T McCabe.

8 recordsLinked to original sources
PubMed2000

Selective antagonism of nigral neuropeptide responses to methamphetamine by conantokin G, a naturally occurring conopeptide.

Some conopeptides derived from cone snails act on specific subunits of the NMDA receptor and thus, exert an influence on the dopamine system. In this study, one such conopeptide, conantokin G, was administered i.c.v. in conjunction with methamphetamine, a potent central nervous system stimulant known to cause dopamine release and changes in tissue levels of neurotensin and dynorphin A in some brain structures. Both single and multiple administrations of the conantokin G preferentially attenuated the methamphetamine-induced increases in tissue levels of these neuropeptides in the substantia nigra. Conantokin G also enhanced the behavioral effects of the methamphetamine.

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PubMed1993

Hyperthermia induces 72kDa heat shock protein expression in rat brain in non-neuronal cells.

The distribution of the nonconstitutive 72 kDa heat shock protein (HSP) in the brains of rats 24 h following graded periods of hyperthermia was studied immunocytochemically. Hyperthermia induced HSP-72 diffusely in cells throughout the cortex, hippocampus and basal ganglia in a dose dependent manner. The cell morphology and location in white matter appeared non-neuronal. Following ischemia, neuronal HSP expression was prominent. These data raise questions regarding prior reports of hyperthermic induction of neuronal HSP expression and the potential pathogenesis of prior hyperthermia in protection against subsequent neuronal injury from ischemia.

Animals↗
PubMed1991

Up regulation of calbindin-D28K mRNA in the rat hippocampus following focal stimulation of the perforant path.

Calbindin-D28K is a constitutive Ca2(+)-binding protein expressed in hippocampal neurons that are resistant to various forms of excitotoxic injury. However, the local factors controlling calbindin-D28K expression within the central nervous system are unknown. We report that neuronal excitation via the perforant path leads to an increased expression of calbindin-D28K mRNA within dentate granule cells. This response is related specifically to stimulation that induces prolonged periods of bursting afterdischarges and precedes cellular injury. The up regulation of calbindin-D28K mRNA occurs during the type of neuronal activation associated with elevated cytosolic Ca2+ and suggests that the maintenance of Ca2+ homeostasis includes a system of feedback control at the level of gene expression.

Animals↗