The neurotoxins colchicine and kainic acid block odor-induced fast waves and olfactory-evoked potentials in the dentate gyrus of the behaving rat.

It has previously been shown that the hilus of the dentate gyrus responds to odors (e.g. toluene) with a burst of fast waves and to electrical stimulation of the olfactory bulb with an evoked potential consisting of an early component immediately after the stimulus artifact, a second 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 colchicine or kainic acid were used in an attempt to destroy granule and pyramidal cells, respectively, while saline was injected on the opposite side as a control. Recordings from chronically implanted electrodes in the olfactory bulb and dentate gyrus demonstrated that saline had no effect while either neurotoxin abolished the odor-induced fast waves. In addition, the late 16-18-ms component of the dentate-evoked potentials after single-pulse stimulation of the olfactory bulb was abolished by either kainic acid or colchicine; the early dentate response, probably a volume-conducted olfactory response, was not abolished. Histological analysis indicated that kainic acid produced widespread non-specific damage in the hippocampal formation. Kainic acid-treated tissue exhibits a thinning of granule cell and molecular layers of the dentate gyrus as well as cell loss in CA3 and part of CA1.