The Japanese Journal of Pharmacology
Online ISSN : 1347-3506
Print ISSN : 0021-5198
ISSN-L : 0021-5198
Nigral-Induced Decrease in Striatal Blood Flow and the Influence on This Decrease of Several Drugs in Reserpinized and Non-Reserpinized Cats
Ryuya YANAGIHASHI
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1986 年 41 巻 4 号 p. 487-495

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The effect of nigral electrical stimulation on regional blood flow in the caudate nucleus and the cerebral cortex, and the influence of several drugs on these effects were examined in reserpinized or non-reserpinized cats. A doublethermistor element was inserted into the left caudate nucleus, and a plate-type thermocouple element was put on the left cerebral cortex. The left substantia nigra was electrically stimulated for 10 sec through a concentric bipolar electrode with a diameter of 0.3 mm (30 Hz, 1 msec, 10-30 V). In non-reserpinized cats, the nigral stimulation caused a decrease in striatal blood flow, increase in cortical blood flow and rise in mean blood pressure. Hexamethonium (3 mg/kg, i.v.) blocked completely the rise in mean blood pressure following nigral stimulation, but did not affect a decrease in striatal blood flow, indicating that a decrease in striatal blood flow following nigral stimulation was not due to the activation of the peripheral sympathetic nervous system.Nigral-induced decrease in striatal blood flow in non-reserpinized cats was blocked by haloperidol (0.1 mg/kg, i.v.), methysergide (1 mg/kg, i.v.) and reserpine (2 mg/kg, i.v.), but not by phentolamine (7 mg/kg, i.v.). In reserpinized cats, nigral stimulation caused an increase in striatal blood flow in contrast to a decrease in non-reserpinized cats. After administration of 5-HTP (50 mg/kg, i.v.) in reserpinized cats, nigral stimulation decreased the striatal blood flow. On the other hand, after administration of L-DOPA (30 mg/kg, i.v.) in reserpinized cats, nigral stimulation increased striatal blood flow. These results suggest that a decrease in striatal blood flow following nigral stimulation is due to the activation of a serotonergic mechanism mediated by dopaminergic neurons.

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