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 (EAA)-mediated transmission at the level of dopaminergic (DA) neurons in the ventral tegmental area (the A10 cell group), is known to be affected by corticosteroid manipulations. Since there is evidence that corticosteroid 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 iontophoretically administered glutamate on the activity of A10 DA neurons was investigated in adrenalectomised animals given a low dose of corticosterone intravenously (equivalent to 13.4 micrograms/100 ml plasma - likely to preferentially occupy the mineralocorticoid subtype of corticosteroid receptor) at least 45 min (median 132.5) prior to recording. Cells from these animals were compared to those from adrenalectomised and sham operated animals administered saline. Adrenalectomy significantly reduced the firing rate of A10 cells, and this effect was reversed by corticosterone replacement. Adrenalectomy did not affect basal burst firing. However, in those cells which could be classified as "bursting' under basal conditions, cells from animals administered corticosterone showed enhanced glutamate-induced bursting relative to the other two groups. The degree of enhancement was strictly determined by the basal bursting level of the cell. Since the distinction between "bursting' and "non-bursting' DA neurons is probably not related to differences at the level of the EAA receptor/effector mediating bursting, it is argued that corticosterone's facilitation of glutamate-induced bursting is not produced at this level, but rather at the level of an intrinsic membrane property which modulates bursting.