L-DOPA inhibits excitatory synaptic transmission in the rat nucleus tractus solitarius through release of dopamine. (30th September 2017)

• Record Type: Journal Article
• Authors: Ohi, Y.; Kodama, D.; Haji, A.
• Is Part Of: Neuroscience. Volume 360(2017)
• Page Start: 18
• Page End: 27
• Publication Date: 2017-09-30
• Subjects: ADN aortic depressor nerve -- DNQX 6, 7-dinitroquinoxaline-2, 3-dione -- eEPSCs evoked EPSCs -- EGTA ethylene glycol-bis(β-aminoethyl ether)-N, N, N′, N′-tetraacetic acid -- EPSC excitatory postsynaptic current -- HEPES 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid -- IEI inter-event interval -- L-DOPA ME L-DOPA methyl ester -- mEPSCs miniature EPSCs -- NTS nucleus tractus solitarius -- OA1 receptor ocular albinism 1 receptor -- PPR paired-pulse ratio; excitatory synaptic transmission -- dopamine -- L-DOPA -- nucleus tractus solitarius -- second-order neuron; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2017.07.043
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: Exogenous L-DOPA presynaptically inhibited the excitatory transmission in second-order NTS neurons similarly to dopamine. The effect of L-DOPA was blocked by a competitive L-DOPA antagonist and also by a D2 receptor antagonist. Depletion of endogenous dopamine by reserpine abolished the action of exogenous L-DOPA but not that of exogenous dopamine. L-DOPA may release dopamine in the NTS and released dopamine inhibits excitatory transmission via presynaptic D2 receptors. Abstract: The mode of action of L-DOPA on excitatory synaptic transmission in second-order neurons of the nucleus tractus solitarius (NTS) was studied using the rat brainstem slices. Superfusion of L-DOPA (10 μM) reduced the frequency of miniature excitatory postsynaptic currents (mEPSCs) without any effect on the amplitude. A low concentration (1 μM) was ineffective on the mEPSCs, and the highest concentration (100 μM) exerted a stronger inhibitory effect. L-DOPA (10 μM) decreased the amplitude of EPSCs (eEPSCs) evoked by electrical stimulation of the tractus solitarius and increased the paired-pulse ratio. The inhibitory effects of L-DOPA on mEPSCs and eEPSCs were similar to those of dopamine (100 μM). The effects of L-DOPA were blocked by a competitive antagonist, L-DOPA methyl ester (100 μM) and also by a D2 receptor antagonist, sulpiride (10 μM), while those of dopamine were blocked by the latter but not by the former. In reserpine (5 mg/kg, s.c.)-treated rats, the effects of L-DOPA on both mEPSCs and eEPSCs were completely abolished, but those of dopamine remained unchanged. The present results suggest a possibility that L-DOPA may induce the release of dopamine from the axon terminals in the NTS and the released dopamine suppresses the glutamatergic transmission through activation of the presynaptic D2 receptors.