Relation of glomerular neuronal activity to glomerular transmission attenuation

Abstract

Paired shock electrical stimulation of the primary olfactory nerve (PON) has revealed long-lasting attenuation of subsequent input through the PON by an afferent volley. Input through the LOT does not induce the process and is unaffected by it. The attenuation rises to a peak at paired shock intervals of 25–50 msec and decays exponentially at a rate ranging from less than 3/sec to over 20/se. The magnitude and decay rate increase with increasing stimulus intensity and are extrapolated to zero at threshold. The spatial distribution of the process approximates that of unit activity induced in the glomerular layer by PON axon terminals. Evoked unit activity in the glomerular layer is maximal during the rising phase of the attenuation process, but the decay rate of induced firing probability of glomerular units as shown in PST histograms in an order of magnitude faster than that for the attenuation process. The attenuation process resembles a running time-integral of the intensity of glomerular unit activity. The clearest electrical correlate of the process is localized, long-lasting intraglomerular depolarization (reported by others). It is concluded that glomerular neurons probably participate in the process but not by direct synaptic action. The attenuation appears to occur as a side-effect of synaptic transmission, which is accentuated by the structure of the glomeruli, particularly the glial capsules. Its main function is inferred to be generalized automatic input control similar to the process subserving light adaptation in the retina, but with faster recovery.