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      Burst firing of mesencephalic dopamine neurons is inhibited by somatodendritic application of kynurenate.

      Acta physiologica Scandinavica

      Action Potentials, drug effects, Amino Acids, antagonists & inhibitors, physiology, Animals, Kynurenic Acid, administration & dosage, pharmacology, Male, Mesencephalon, Rats, Rats, Inbred Strains, Receptors, Dopamine

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          Abstract

          Midbrain dopamine neurons of the zona compacta substantia nigra (SN) and ventral tegmental area (VTA), giving rise to the nigrostriatal and mesolimbocortical midbrain dopamine pathways, respectively, typically display a spontaneous activity consisting of single spikes and bursts. Previously, intracerebroventricular administration of the excitatory amino acid (EAA) antagonist kynurenate has been shown to inhibit burst firing and induce a regular, pacemaker-like firing of ventral tegmental area midbrain dopamine neurons. In the present experiments, zona compacta substantia nigra and ventral tegmental area midbrain dopamine neurons were recorded in the chloral hydrate anaesthetized male rat. Kynurenate was administered locally, either by micro-iontophoresis or by pneumatic (micropressure) ejection. Both forms of local kynurenate application produced an immediate inhibition of burst firing and a slightly increased regularity of firing in both zona compacta substantia nigra and ventral tegmental area midbrain dopamine neurons. The present results indicate that excitatory amino acid nerves tonically modulate midbrain dopamine neuronal burst firing directly on the midbrain dopamine cell bodies, further stressing the importance of excitatory amino acid innervation in the physiological function of midbrain dopamine neurons, particularly in the dynamic aspects involved in the behavioural modulation and pharmacological responses of these psychopharmacologically important neurons.

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          Journal
          1877358
          10.1111/j.1748-1716.1991.tb09134.x

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