Rapid changes in ascorbate and dopamine release in rat nucleus accumbens after intracerebroventricular administration of NMDA

• Published in: Brain research Vol. 586; no. 2; p. 195
• Main Authors: Svensson, L, Wu, C, Hulthe, P, Johannessen, K, Engel, J A
• Format: Journal Article
• Language: English
• Published: Netherlands 24-07-1992
• Subjects: Animals; Anticonvulsants - pharmacology; Ascorbic Acid - metabolism; Atropine - pharmacology; Cerebral Ventricles - drug effects; Cerebral Ventricles - physiology; Dopamine - metabolism; Injections, Intraventricular; Male; Membrane Potentials - drug effects; N-Methylaspartate - administration & dosage; N-Methylaspartate - pharmacology; Neurons - drug effects; Neurons - physiology; Nucleus Accumbens - drug effects; Nucleus Accumbens - physiology; Pargyline - pharmacology; Picrotoxin - pharmacology; Piperazines - pharmacology; Rats; Rats, Inbred Strains; Time Factors
• ISSN: 0006-8993
• DOI: 10.1016/0006-8993(92)91627-Q

In vivo voltammetry at electrochemically pretreated carbon fibre electrodes was used to investigate the effect of intracerebroventricular (i.c.v.) administration of N-methyl-D-aspartic acid (NMDA) on neuronal activity in rat nucleus accumbens. Infusion of a low dose of NMDA (1 nmol) was followed a few minutes later by rapid changes in both Peak 1 and Peak 2 heights indicating large but short-lived increases in the extracellular concentrations of ascorbate and catecholamines, respectively. These responses did not seem to be dependent on the dose infused since infusion of NMDA for a longer time period neither changed the amplitude nor the time-course of these effects. The increase in Peak 2 height was resistant to pargyline pretreatment indicating that this response mainly reflected the release of dopamine. The administration of NMDA was followed by behavioural activation in the animals but not convulsions. Co-administration of the competitive NMDA receptor antagonist, CPP (1 nmol), completely blocked these effects while the acetylcholine receptor antagonist, atropine (1.5 nmol), and the GABA receptor antagonist, picrotoxin (1 nmol), failed in this respect. The phenomenon spreading depression is discussed as a possible explanation of these results.