OPPOSITE MEMBRANE-POTENTIAL CHANGES INDUCED BY GLUCOSE DEPRIVATION INSTRIATAL SPINY NEURONS AND IN LARGE ASPINY INTERNEURONS

We have studied the electrophysiological effects of glucose deprivatio n on morphologically identified striatal neurons recorded from a corti costriatal slice preparation. The large ma jority of the recorded cell s were spiny neurons and responded to aglycemia with a slow membrane d epolarization coupled with a reduction of the input resistance. In vol tage-clamp experiments aglycemia caused an inward current. This curren t was associated with a conductance increase and reversed at -40 mV. T he aglycemia-induced membrane depolarization was not affected by tetro dotoxin (TTX) or 6-cyano-7-nitroquinoxaline-2,3-dione plus aminophosph onovalerate, antagonists acting respectively on AMPA and NMDA glutamat e receptors. Also, the intracellular injection of bis(2-aminophenoxy)e thane-N,N,N',N'-tetra-acetic acid, a calcium (Ca2+) chelator, and low Ca2+/high Mg2+-containing solutions failed to reduce-this phenomenon. Conversely, it was reduced by lowering external sodium (Na+) concentra tion. A minority of the recorded cells had the morphological character istics of large aspiny interneurons and the electrophysiological prope rties of ''long-lasting afterhyperpolarization (LA) cells.'' These cel ls responded to aglycemia with a membrane hyperpolarization/outward cu rrent that was coupled with an increased conductance. This current was not altered by mt, blockers of ATP-dependent potassium (K+) channels, and adenosine Al receptor antagonists, whereas it was reduced by solu tions containing low Ca2+/high Mg2+. This current reversed at -105 mV and was blocked by barium, suggesting the involvement of a K+ conducta nce. We suggest that the opposite membrane responses of striatal neuro nal subtypes to glucose deprivation might account for their differenti al neuronal vulnerability to aglycemia and ischemia.