QUANTITATIVE AUTORADIOGRAPHIC STUDIES OF THE EFFECTS OF BILATERAL OLFACTORY BULBECTOMY IN THE RAT-BRAIN - CENTRAL-TYPE AND PERIPHERAL-TYPE BENZODIAZEPINE RECEPTORS

We investigated the discrete regional effects of bilateral olfactory bulbectomy on central- and peripheral-type benzodiazepine receptors in rat brains at weekly intervals until one month after bulb ablation. Persistent increases in [H-3]flunitrazepam binding to central benzodiazepine receptors were observed in the cingulum (27%) and in the frontal(15%) and parietal (14%) cortices. Progressive increases in central benzodiazepine receptors, reaching statistical significance four weeks after olfactory bulbectomy, were observed in the ventromedial thalamic nucleus (35%), the lateral hypothalamic region (22%), the basolateral amygdaloid nucleus (23%) and substantia nigra (25%). Persistent major increases (between four- and six-fold) in [H-3]PK-11195 [H-3]1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline carboxamide binding to peripheral-type benzodiazepine receptors were observed in all anterior olfactory nuclei. Similarly, throughout the time period studied, [H-3]PK-11195 binding densities were increased two- to three-fold in the piriform cortex and lateral olfactory tract. These observations confirm the usefulness of [H-3]PK-11195 binding as a marker of neuronal insult in the brain. Moreover, the persistent regional increases in [H-3]flunitrazepam binding to central-type benzodiazepine receptors suggest that GABAergic transmission is altered following olfactory bulb ablation.