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Pentylenetetrazol seizures increase pro‐nerve growth factor‐like immunoreactivity in the reticular thalamic nucleus and nerve growth factor mRNA in the dentate gyrus
Author(s) -
Humpel C.,
Ebendal T.,
Cao Y.,
Olson L.
Publication year - 1993
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490350409
Subject(s) - pentylenetetrazol , dentate gyrus , nerve growth factor , reticular connective tissue , kindling , thalamic reticular nucleus , chemistry , hippocampal formation , endocrinology , dentate nucleus , medicine , neuroscience , nucleus , biology , epilepsy , cerebellum , anatomy , anticonvulsant , receptor
Neurotrophins may have a neuroprotective role and are probably involved in the control of axonal sprouting and synaptic plasticity. An antibody raised against a pro‐sequence of nerve growth factor (NGF) was tested. In control undisturbed rats, a strong immunoreactivity was detected in scattered cells in and around the pyramidal and granule cell layer of the hippocampus and a moderate labeling was found in the reticular thalamic nucleus. In situ hybridization showed specific expression of NGF mRNA in a similar population of scattered cells in the hippocampal formation but not in the reticular thalamic nucleus. Acute epileptic seizures, induced by a convulsive dose of 50 mg/kg pentylenetetrazol (PTZ), strongly in creased NGF mRNA in neurons of the granular layer of the dentate gyrus 3 hr but not 6 hr after the injection. No change in pro‐NGF‐like immunoreactivity was observed in the hippocampus or reticular thalamic nucleus after acute seizures. Chemical kindling was induced by daily injections of subconvulsive doses (30 mg/kg) of PTZ for 4 weeks. This treatment significantly increased pro‐NGF‐like immunoreactivity in the reticular thalamic nucleus but did not affect NGF mRNA. These data strengthen a role for the reticular thalamic nucleus and NGF in PTZ kindling. © 1993 Wiley‐Liss, Inc.