Hyperkinesia and other physiologic effects of caudate deficit in the adult albino rat

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Abstract
A syndrome of caudate deficit can be produced in the adult albino rat. It is characterized by (1) transient consummatory failure with dissociation of acquisitive and ingestive phases, (2) relatively persistent ambulatory or cursive hyperkineasia, (3) increased histamine tolerance, and (4) somatomotor activity disorganization characterized by shift defect. These phenomena appear without motor weakness or biologically significant changes in fasting blood glucose, sodium and potassium, or hematocrit. A decrease in oxygen consumption associated with caudate deficit also was observed with cortical lesions. Whether the changes in histamine tolerance are secondary to the neural hyperkinesia or to endocrine or metabolic effects of the neural surgery per se remains to be determined.

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