GABAergic Modulation of Average Evoked Potentials in Rat Olfactory Bulb.

Abstract

The olfactory bulbar EEG alternation of inspiratory cyclic bursts and chaotic interburst activity as well as the damped sinusoidal oscillation seen in averaged evoked potentials (AEPs) and unit post-stimulus-time histograms (PSTHs) are best accounted for by modeling the bulb as a set of couple oscillators. Primary olfactory nerve (PON) induced AEPs are characterized by a damped oscillation riding a slow negative wave that is due to prolonged granule cell excitation. Antidromic stimulation via the lateral olfactory tract (LOT) also produces an oscillation in the AEP but lacks the slow negative component. The negative feedback relationship of the reciprocal synapses between mitral and granule cells in the external plexiform layer establishes these oscillators. Periglomerular (Pg) cells provide an excitatory bias which generates the slow component of the PON induced AEP. Temporal aspects of the mitral- granule oscillator network are subject to modulation from sources intrinsic and extrinsic to the bulb

The neurochemical basis of two intrinsic modulatory influences was investigated by applications of neuroactive substances acting on Gamma Amino Butyric Acid (GABA - an intrinsic glomerular layer neurotransmitter) and dopamine (an intrinsic neuromodulatory amine). Application of GABA increased the secondary component and transiently doubled the frequency of the PON-induced AEP. These effects indicated increased excitation within the glomerular layer (GI). Picrotoxin, a GABA, antagonist, or muscimol, a GABA, agonist, radically altered the frequency and amplitude of the AEP oscillation but not in a manner seen with GABA application. The GABA, agonist baclofen at low concentrations markedly increased the baseline shift and at high concentrations increased PON-induced AEP threshold High frequency signals were achieved with high concentrations of baclofen. Mitral cell firing rates tended to increase with low concentrations of baclofen but were suppressed under high concentrations. The eflects of baclofen and GABA were ascribed to glomerular excitation of mitral cells. Baclofen acted synergistically with dopamine to increase LOT-induced AEP oscillation. Histological evidence shows co-localization of GABA and dopamine in the glomerular layer. The functional significance of this action has yet to be determined