Ventral tegmental area-mediated inhibition of neurons of the nucleus accumbens receiving input from the parafascicular nucleus of the thalamus is mediated by dopamine D1 receptors.
Microiontophoretic experiments were performed to determine whether inhibition mediated by the ventral tegmental area neurons of the nucleus accumbens, receiving input from the parafascicular nucleus of thalamus, is mediated by dopamine D1 or D2 receptors, using rats anesthetized with chloral hydrate. Spikes, elicited by test stimuli applied to the parafascicular nucleus were inhibited by conditioning stimuli to the ventral tegmental area, given 30 msec before the test stimuli. This inhibition was antagonized by iontophoretic application of SCH 23390, a D1 antagonist, in 18 of 25 neurons of the nucleus accumbens, but in only 3 of 22 neurons of the nucleus accumbens during application of domperidone, a D2 antagonist. The reduction by conditioning stimulation of the ventral tegmental area of the mean number of spikes of the 25 neurons upon stimulation of the parafascicular nucleus, was abolished by SCH 23390. In contrast, domperidone did not affect the mean number of spikes of the 22 neurons upon stimulation of the parafascicular nucleus in the presence of conditioning stimulation of the ventral tegmental area. In addition, spikes elicited by stimulation of the parafascicular nucleus were dose-dependently inhibited by iontophoretic application of both SKF 38393, a D1 agonist and bromocriptine, a D2 agonist. These results suggest that inhibition by dopamine, derived from the ventral tegmental area of neurons of the nucleus accumbens, receiving input from the parafascicular nucleus, is mediated mainly by dopamine D1 receptors, although both D1 and D2 receptors are expressed on the same neuron of the nucleus accumbens, which is also inhibited by exogenously applied D2 agonists.[1]References
- Ventral tegmental area-mediated inhibition of neurons of the nucleus accumbens receiving input from the parafascicular nucleus of the thalamus is mediated by dopamine D1 receptors. Hara, M., Sasa, M., Takaori, S. Neuropharmacology (1989) [Pubmed]
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