Spontaneous voltage oscillations in striatal projection neurons in a rat corticostriatal slice.

In a rat corticostriatal slice, brief, suprathreshold, repetitive cortical stimulation evoked longlasting plateau potentials in neostriatal neurons. Plateau potentials were often followed by spontaneous voltage transitions between two preferred membrane potentials. While the induction of plateau potentials was disrupted by non-NMDA and NMDA glutamate receptor antagonists, the maintenance of spontaneous voltage transitions was only blocked by NMDA receptor and L-type Ca&sup2+; channel antagonists. The frequency and duration of depolarized events, resembling up-states described in vivo, were increased by NMDA and L-type Ca&sup2+; channel agonists as well as by GABA[subA] receptor and K[sup+] channel antagonists. NMDA created a region of negative slope conductance and a positive slope crossing indicative of membrane bistability in the current-voltage relationship. NMDA-induced bistability was partially blocked by L-type Ca&sup2+; channel antagonists. Although evoked by synaptic stimulation, plateau potentials and voltage oscillations could not be evoked by somatic current injection - suggesting a dendritic origin. These data show that NMDA and L-type Ca&sup2+; conductances of spiny neurons are capable of rendering them bistable. This may help to support prolonged depolarizations and voltage oscillations under certain conditions. [ABSTRACT FROM AUTHOR]