Effects of bulbar reticular tetanic stimulation on the responses of dorsal spinocerebellar tract (DSCT) units were studied in the decerebrate cat. The conditioning stimulation of lateral or paramedian reticular nucleus was found to reduce polysynaptic activation of DSCT cells (type 3 response) selectively without affecting either the spontaneous background discharge or the monosynaptic activation (type 1 response) or inhibition (type 2 response) by afferent inputs from the peripheral nerves of hindleg. These results show that the descending inhibition to the polysynaptic activation of DSCT cells occurs presynaptically by reticulospinal pathways from brain-stem reticular formation.

Responses of dorsal spinocerebellar tract (DSCT) neurons to random electrical stimulation of peripheral nerves of the hindleg in decerebrate cats were studied using cross-correlation analysis of the output spike train. The spontaneous background discharge in barbiturate's cats had longer mean interspike interval than that in decerebrate cats, but there was no difference of the coefficient of variation in the two groups. This suggests that barbiturate has no effect on raising of the electrical threshold of the axon, but prolonging effect on interspike interval. Comparison of the conduction velocity showed to be slower in barbiturate's cats, so barbiturate reduces the conduction rate of the axon. The DSCT responses to the electrical stimulation of peripheral nerve in decerebrate cats were recorded in 60%, while 85% in barbiturate's cats. The reasons for this difference are that the DSCT cells in decerebrate cats are tonically inhibited from the pontine and bulbar reticular formation and the function of brain-stem reticular formation is suppressed by the barbiturate. Type 2 response in decerebrate cats, which represents reduced excitability of the DSCT cells, had inhibition with shorter initial peak latency and duration as compared to that in barbiturate's cats. This confirms the result of Eccles et al. that barbiturate in moderate dosage increases and prolongs the presynaptic inhibition.

The relation between copper content and histologic changes in the brain under disturbed copper metabolism was studied. In this experiment, three groups of mongrel dogs were used, i.e. (1) Copper administration only, (2) Copper administration with Eck's fistula, (3) Normal control. The copper content in each brain tissue was measured by the atomic absorption spectrophotometry and routine histologic preparations with some special stains were examined. Following results were obtained. (1) In the group of longstanding copper administration, there were no remarkable histologic changes in the brain, and the significant increase of copper content was not demonstrated in the cortex, medulla and basal ganglia. (2) The group of copper administration with Eck's fistula was divided into two subgroups by the presence or absence of icterus. (a) Without Icterus: Diffuse gliosis and type II Alzheimer's neuroglia were observed and copper content in the brain increased up to 1.8 fold of that of normal control. (b) With Icterus: The histologic changes which were observed in the non-icteric group were more severe especially in the brain stem containing vacuolar degeneration, shrinkage and ghost appearance of the nerve cells, hemorrhages and demyelination, but there were no marked histologic changes in cortex and medulla. The copper content of the brian increased up to 2 fold or more of that of normal control. Copper was not demonstrated histochemically in all groups. The copper content in the cortex and basal ganglia was almost the same but that of medulla was half as much as that of the formers in every group of this experiment. The difference of the copper content between cortex which had no remarkable histologic changes, and basal ganglia which had aforementioned severe changes, was not proved, and also the difference between the groups with icterus and without icterus was not demonstrated. The copper content did not always correlate with the severity of the histologic changes. From these results, it can be suggested that copper does not play a significant role in pathogenesis of specific histologic changes of the brain.