NEURAL MECHANISMS UNDERLYING THE ACTION OF PRIMER PHEROMONES IN MICE

Our electrophysiological experiments in female mice have provided evidence that electrical stimulation of the accessory olfactory bulb orthodromically excites a subpopulation of tuberoinfundibular arcuate neurons by way of the amygdala. The present study shows that half of such neurons are identified as dopaminergic by examining the effectiveness of infusing 6-hydroxydopamine and 5,7-dihydroxy-tryptamine locally into the median eminence in blocking their antidromic response. Further attention is focused on excitatory amino acid receptors within the amygdala and the amygdaloid pathway that mediate the accessory bulb-induced excitation of tuberoinfundibular arcuate neurons. The excitatory transmission was reversibly blocked by intra-amygdala infusion (3 nmol) of the excitatory amino acid antagonists kynurenic acid, d,l-2-amino-5-phosphonovalerate, γ-d-glutamylaminomethylsulphonate and d,l-2-amino-4-phosphonobutyrate. Intra-amygdala infusions (3 nmol) of N-methyl-d-aspartate and kainate markedly enhanced the firing activity of tuberoinfundibular arcuate neurons with excitatory inputs from the accessory bulb, whereas similar infusions of quisqualate were without effect. Intra-stria terminalis infusions of the local anaesthetic lignocaine completely abolished the excitatory transmission in all the cells tested. Furthermore, tuberoinfundibular arcuate neurons stimulated from the accessory bulb were also orthodromically stimulated from the stria terminalis with a shorter latency. These studies demonstrate that the projections of the accessory olfactory bulb activate excitatory amino acid receptors within the amygdala and subsequently the stria terminalis route, thereby causing excitation of tuberoinfundibular dopaminergic arcuate neurons. This functional pathway can account for the reproductive effects so far described as a consequence of vomeronasal chemoreception. © 1990.