Repeated treatment with phencyclidine (PCP) over 14 days at 7.5 mg/kg per day significantly reduced the frequency of backpedalling, a serotonergic stereotyped behavior, indicating tolerance. This repeated treatment also decreased the equilibrium dissociation constant (Kd) of [3H]paroxetine binding to serotonin transporters in whole brain excluding the cerebellum, without changing the maximum number of binding sites (Bmax). A single PCP treatment did not alter binding parameters. The results suggest that repeated PCP treatment induces tolerance in serotonergic stereotyped behavior and increases the affinity of serotonin transporters, possibly as a compensatory response to chronic inhibition of serotonin uptake.
The binding properties and brain distribution of a radioactive form of the compound 3-OH-PCP, a derivative of phencyclidine (PCP), were examined in rat brain tissue using autoradiography. Binding occurred with fast and slow components, and the pattern of binding matched that of other PCP receptor labels, TCP and MK-801. Highest binding was in the hippocampus and outer cerebral cortex layers, while low binding was in the brain stem and cerebellum. The binding was strongly blocked by MK-801 and 3-OH-PCP, but less so by a related compound, (+)-SKF 10047, in certain brain regions. Antagonists of the NMDA receptor complex also displaced binding similarly to MK-801, indicating the binding site is essentially the same as the PCP site labeled by TCP and MK-801.
Floating in a sensory isolation tank increases randomness in orally generated number sequences, while lying on a bed in an isolation box decreases it. Seven student volunteers each completed one 40-minute session on a bed and two 40-minute sessions floating in a tank. Continuous polygraph recordings of EEG, EOG, ECG, and respiration showed that flotation induced more hypnagogic (drowsy) and light sleep states than the bed condition. The authors suggest that these states enhanced random generation.