PREFERENTIAL OCCUPATION OF MINERALOCORTICOID RECEPTORS BY CORTICOSTERONE ENHANCES GLUTAMATE-INDUCED BURST FIRING IN RAT MIDBRAIN DOPAMINERGIC-NEURONS

Sensitisation to the behavioural effects of amphetamine, a phenomenon which appears to involve the potentiation of excitatory amino acid (EA A)-mediated transmission at the level of dopaminergic (DA) neurons in the ventral tegmental area (the A10 cell group), is known to be affect ed by corticosteroid manipulations. Since there is evidence that corti costeroid manipulations can also influence unpotentiated EAA-mediated transmission elsewhere in the brain, the possibility was examined that the same may be true for midbrain DA neurons. The effect of iontophor etically administered glutamate on the activity of A10 DA neurons was investigated in adrenalectomised animals given a low dose of corticost erone intravenously (equivalent to 13.4 mu g/100 ml plasma - likely to preferentially occupy the mineralocorticoid subtype of corticosteroid receptor) at least 45 min (median 132.5) prior to recording. Cells fr om these animals were compared to those from adrenalectomised and sham operated animals administered saline. Adrenalectomy significantly red uced the firing rate of A10 cells, and this effect was reversed by cor ticosterone replacement. Adrenalectomy did not affect basal burst firi ng. However, in those cells which could be classified as 'bursting' un der basal conditions, cells from animals administered corticosterone s howed enhanced glutamate-induced bursting relative to the other two gr oups. The degree of enhancement was strictly determined by the basal b ursting level of the cell. Since the distinction between 'bursting' an d 'non-bursting' DA neurons is probably not related to differences at the level of the EAA receptor/effector mediating bursting, it is argue d that corticosterone's facilitation of glutamate-induced bursting is not produced at this level, but rather at the level of an intrinsic me mbrane property which modulates bursting.