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PMID:1469420

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Citation

Tomoda, H, Kato, M, Sakata, S and Shima, F (1992) Striatal dysfunction in Rolling mouse Nagoya: an electrophysiological study. J. Neurol. Sci. 112:106-12

Abstract

To elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling, genotype rol/rol), an experimental neurologic mutant mouse, we studied the physiological characteristics of neurons of the globus pallidus (GP) in rolling, comparing them with those of the behaviorally normal heterozygotes (+/rol) and normal controls (+/+). Forty-nine units in rolling, 41 in heterozygotes and 48 in controls were recorded under urethane anesthesia. The group mean of the interspike interval (ISI) of the spontaneous unit discharges was significantly shorter in rolling (42.2 +/- 2.6 msec, mean +/- SEM) than that of controls and of heterozygotes (55.4 +/- 2.4 msec, P < 0.001 and 50.4 +/- 2.6 msec, P < 0.05, respectively), indicating a significantly higher rate of spontaneous unit activity in the GP of rolling. In the controls and heterozygotes, about 60% of the GP neurons responded to striatal (ST) electrical stimulation with a predominantly inhibitory response, whereas a significantly smaller number of the GP neurons (22%, P < 0.001) exhibited inhibitory responses in rolling. The positive field potentials recorded in the GP evoked by ST stimulation were significantly smaller in amplitude in rolling (1.04 +/- 0.10 mV, mean +/- SEM) than that of the controls and heterozygotes (1.78 +/- 0.15 mV, P < 0.001 and 1.97 +/- 0.17 mV, P < 0.001, respectively). These results are in agreement with our previously reported findings of increased glucose metabolism and reduced concentration of GABA in the GP and substantia nigra pars reticula (SNr) in rolling.(ABSTRACT TRUNCATED AT 250 WORDS)

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Keywords

Animals; Corpus Striatum/physiopathology; Electric Stimulation; Electrophysiology; Evoked Potentials/drug effects; Female; Globus Pallidus/cytology; Globus Pallidus/physiology; Glucose/metabolism; Iontophoresis; Male; Mice; Mice, Inbred C3H; Mice, Neurologic Mutants; Nervous System Diseases/physiopathology; Neurons/drug effects; gamma-Aminobutyric Acid/metabolism

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