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Thh design of a plug-holder unit for electrode implants is described. The plug-holder attaches to the stereotaxic and facilitates the insertion of the electrode contact pins into the plug by retaining the connector plug in a fixed rigid position. In addition, it prevents the accidental breakage of contact lead wires which can normally occur during the contact pin insertion procedure. The unit is inexpensive and simple to construct.

Administration of a single non-convulsive dose of insulin (1.0, I.U./kg., I.P.) which produced no observable gross behavioral changes in rats, reduced rapid eye movement (REM) sleep time 100% in the first 3 hrs. and 82% by the 4th hr., reaching control subject levels (saline-treated) by the 6th hr. In contrast, slow-wave sleep (NREM) time in insulin treated animals exceeded control subject levels by 49% by the end of the 2nd hr., returning to normal by the 5th hr. Although there was no difference between insulin and saline treated rats for the total 8 hr. post-injection recording period for total percentage of time awake, or slow-wave sleep time, a 44% reduction in REM sleep time was observed in insulin treated animals compared to that of a saline treated control. The significance of these findings are discussed in terms of known neurochemical changes i.e., an increase of both brain tryptophan and serotonin in rats, induced by a subconvulsive dose of exogenous insulin.

Administration of a high dose of glucose (2.5 g/kg, i.p.) that is known to produce severe hyperglycemia in euglycemic rats suppressed rapid eye movement (REM) sleep time significantly during the first three hours of 8 hr total electroencephalogram (EEG) recording period. Co-administration of glucose (2.5 g/kg, i.p.) and a non-convulsive dose of insulin (1.0 I.U./kg, i.p.) produced a significant reduction in REM sleep time during 1st through 5th hour and an increase in slow-wave sleep (NREM) time in the 3rd and 4th hour of 8 hr total EEG recording period. However, awake, NREM and REM sleep time in the 8 hr total EEG recording period were unaffected by either glucose alone or glucose plus insulin treatments. These results strongly suggest that the insulin's effects on the sleep-awake cycle i.e. reduction in REM and a slight increase in NREM sleep times of rats is not due to indirect effects of insulin on the central nervous system via hypoglycemia as reported by us previously, but could possibly be due to its direct effects on brain chemistry of neurotransmitters such as serotonin, catecholamines and acetylcholine which are believed to modulate the sleep-awake cycle pattern in rats.