The effects of the dopamine D1 antagonist (+)-SCH 23390 on the responses of ganglion cells in the superfused rabbit retinal preparation were studied by intracellular recording. At low micromolar concentrations, (+)-SCH 23390 hyperpolarized OFF-center brisk ganglion cells and reduced or abolished any spontaneous spike activity that was present. The light-evoked EPSPs at the onset of a spot or annulus were reduced or abolished, while the EPSPs at light offset were in most cases potentiated. (+)-SCH 23390 depolarized ON-center brisk ganglion cells and increased spontaneous spike activity. The light-evoked EPSPs to spots and annuli were either unaffected or reduced roughly to the same extent. The findings in this study are compared with findings in a recent study in which the effects of (+)-SCH 23390 on the extracellularly recorded responses of ganglion cells in the rabbit retina were examined.

Intracellular recordings from thalamocortical (TC) neurons in the ventrolateral (VL) nucleus as well as paired intracellular recordings from TC-VL neurons and area 4 cortical neurons under ketamine-xylazine anesthesia were performed to study changes in hyperpolarization-rebound sequences evoked by successive stimuli to the dorsal thalamus at different frequencies and the impact of these changes at the cortical level. The cellular mechanisms of such changes in synaptic networks connecting TC with cortical neurons are relevant for short-term plasticity during low-frequency oscillatory activities. The progressive decrease in hyperpolarization of TC cells in response to single thalamic stimulus above a certain frequency (generally >1 Hz) and to pulse-trains at 10 Hz was mainly due to synaptic factors and not to mechanisms intrinsic to TC cells, as revealed by comparing responses evoked by synaptic volleys to those elicited by hyperpolarizing current pulses mimicking the synaptically evoked hyperpolarization-rebound sequence. The decreased hyperpolarization to repetitive synaptic volleys, leading to a decreased number of action potentials in the post-inhibitory spike-burst, had an impact on cortical activities, being matched by a decreased rebound depolarization of cortical cell during repetitive augmenting responses. The alterations in hyperpolarization-rebound sequences upon repetitive stimulation, probably resulting from the decreased efficacy of connections between thalamic reticular (RE) neurons to TC connections, results in the dampening of activities sustaining normal, and possibly paroxysmal, oscillations in the TC network. Our results suggest that this phenomenon should be taken into account when analyzing complex activities, such as physiological and pathological oscillations.