Association of sleep parameters and memory in intact old rats and young rats with lesions in the nucleus basalis magnocellularis.

Relations between sleep and memory were examined as a function of aging in rats. Sleep (24 hr), passive avoidance retention, and choline acetyltransferase (CAT) activity were assessed in 3 age-groups (6, 15, and 24 months old). Age-related alterations were evident in sleep, memory, and cortical and striatal CAT activity. Retention deficits in old rats were significantly correlated with several measures of paradoxical sleep. Similar analyses in 6- and 15-month-old rats with ibotenic acid-induced lesions of the nucleus basalis magnocellularis (NBM) showed several alterations in sleep, memory, and cortical CAT activity comparable to those seen in the old rats. One measure of paradoxical sleep, bout duration, correlated significantly with retention scores in rats with lesions. Thus, fragmented paradoxical sleep accompanies memory impairments in old rats and in young rats with NBM lesions.

The differential effects of plasma from two groups of clinically similar schizophrenic patients on learning behavior in rats.

The effects of plasma from normal subjects and chronic schizophrenic patients were determined on the rate of learning a pole jump response in rats. The animals were trained to a buzzer CS and electroshock US. Mean trials to a 90 per cent avoidance criterion were determined using a 100 trial cut off. Plasma and other control solutions were given intraperitoneally in the morning and the procedure repeated in the afternoon with separate groups of rats. Test trials were initiated five minutes after injection. It was found that all plasma, in contrast to saline, produced an increase in the number of trials to learn the avoidance response. No difference in behavioral effects was noted comparing the plasma of all chronic schizophrenics to normals. However, within the chronic schizophrenic population there are subgroups whose plasma was differentially effective in reducing rate of learning. These results are preliminary and subject to continued experimentation. They are presented here to make others aware of the needto consider the existence of possible biologic subgroupings of schizophrenia in future investigations of the plasma-behavior interaction.

Effect of a chronic tryptophan dietary deficiency on the rat's sleep-wake cycle.

The sleep-wake cycle of 12 tryptophan dietary deficient rats and their non-deficient paired controls were observed for a 8:00 a.m. to 8:00 p.m. period. EEG, EMG and body activity were continuously monitored on polygraphic recordings throughout the 12 hr observation period. The results indicate no significant difference between the tryptophan deficient and sufficient animals in time spent awake, slow-wave or parodoxical sleep. There was a non-significant trend among the tryptophan deficient animals to be less active and spend more time in both slow-wave and paradoxical sleep, which is in contrast to an expected insomnia effect. The results do not support the suggested relationship between reduced serotonin levels and the occurrence of insomnia, questioning the serotonergic theory of sleep.

Reduction of rapid eye movement (REM) sleep by glucose alone or glucose and insulin in rats.

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.

Sleep: sequential reduction of paradoxical (REM) and elevation of slow-wave (NREM) sleep by a non-convulsive dose of insulin in rats.

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.

Plug-holder unit for implanting stimulating or recording electrodes.

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.