THE NEUROTOXINS COLCHICINE AND KAINIC ACID BLOCK ODOR-INDUCED FAST WAVES AND OLFACTORY-EVOKED POTENTIALS IN THE DENTATE GYRUS OF THE BEHAVING RAT

Citation
Vr. Heale et al., THE NEUROTOXINS COLCHICINE AND KAINIC ACID BLOCK ODOR-INDUCED FAST WAVES AND OLFACTORY-EVOKED POTENTIALS IN THE DENTATE GYRUS OF THE BEHAVING RAT, Brain research, 690(2), 1995, pp. 157-166
Citations number
40
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
690
Issue
2
Year of publication
1995
Pages
157 - 166
Database
ISI
SICI code
0006-8993(1995)690:2<157:TNCAKA>2.0.ZU;2-C
Abstract
It has previously been shown that the hilus of the dentate gyrus respo nds to odors (e.g. toluene) with a burst of fast waves and to electric al stimulation of the olfactory bulb with an evoked potential consisti ng of an early component immediately after the stimulus artifact, a se cond component with a 16-18-ms latency and additional late components. Spectral analysis revealed that odor-induced fast-wave bursts in the olfactory bulb and dentate gyrus both had a peak frequency of 15-20 Hz and were highly coherent. Unilateral intrahippocampal injections of c olchicine or kainic acid were used in an attempt to destroy granule an d pyramidal cells, respectively, while saline was injected on the oppo site side as a control. Recordings from chronically implanted electrod es in the olfactory bulb and dentate gyrus demonstrated that saline ha d no effect while either neurotoxin abolished the odor-induced fast wa ves. In addition, the late 16-18-ms component of the dentate-evoked po tentials after single-pulse stimulation of the olfactory bulb was abol ished by either kainic acid or colchicine; the early dentate response, probably a volume-conducted olfactory response, was not abolished. Hi stological analysis indicated that kainic acid produced widespread non -specific damage in the hippocampal formation. Kainic acid-treated tis sue exhibits a thinning of granule cell and molecular layers of the de ntate gyrus as well as cell loss in CA3 and part of CA1.