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Effects of phencyclidine (PCP) on eliciting afterdischarges (AD) by electrical stimulation of the hippocampus (HIPP), amygdala (AMY), thalamus (CM) and midbrain reticular formation (MRF) were studied in rhesus monkeys with permanently implanted encephalic electrodes. Prior to drug administration, the minimal amount of electrical stimulation for eliciting AD, i.e., minimal AD's stimulation (MADS), was determined for each stimulation site and employed as a parameter for evaluating the effects of PCP on AD. Following PCP administration (0.5 mg/kg IM), marked increases (130 to 240% above the control level) in MADS of the HIPP, AMY and MRF were demonstrated, while only slight increase (+40%) in MADS of the CM was found. These results suggest that PCP causes a marked decrement in the ability of electrical stimulation to elicit AD in the HIPP, AMY and MRF, along with only little similar stimulation effects in the CM. This selective increase in MADS in structures of the limbic system and the midbrain reticular formation tends to implicate these systems rather than the thalamocortical system in the modulation of PCP's effects on central nervous system activities.

Effects of acute and chronic administration of phencyclidine (PCP) on EEG activities and gross behavior were studied in monkeys with electrodes implanted in the brain. Administration of PCP (2.0 or 4.0 mg/kg i.v.) in monkeys produced a biphasic pattern of inhibition and excitation of behavior during 6-8 h observation period. The inhibitory phase appeared 1-3 min after PCP injection, and was uniquely characterized by high-voltage slow waves with delta waves (0.6-0.8 c/sec) in the parietal lobe and by those with theta waves (4-5 c/sec) in the occipital lobe and hippocampus during behavioral stupor. This inhibitory phase lasted 1-1.5 h, and subsequently, high-voltage fast wave with enhancement of theta waves and nystagmus appeared during behavioral arousal. Upon chronic PCP administration, the intensity and duration of the inhibitory phase progressively decreased, while the effects of the excitatory phase increased. The results suggest that PCP administration in monkeys produces a biphasic pattern of inhibitory and excitatory effects and upon chronic administration a tolerance develops to the inhibitory effect while an augmentation of the excitatory effect develops.

Effects of acute and chronic administration of phencyclidine (PCP) on both neocortical and subcortical visual potentials (VEPs) and on spontaneous EEGs were studied in the rhesus monkeys with permanently implanted brain electrodes. VEPs were evoked by brief single photo-stimulator flashes (0.8 pps. 10 microsec duration). Injection of PCP (0.5 to 4.0 mg/kg doses, IV) in monkeys produced a significant inhibition on the peak-amplitude of major VEP components predominantly in the occipital lobe and hippocampus. The PCP-induced VEP inhibition persisted in the presence of occipital and hippocampal theta-activities. Nystagmus persisted throughout the 6 to 8 hours course of PCP-induced behavior. A biphasic pattern of inhibitory and excitatory effects on EEGs and behavior was also observed during the 6 to 8 hours observation period. Chronic administration of PCP (2.0 and 4.0 mg/kg dose IV daily) produced a significant decrease in its inhibitory effects on VEPs, suggesting tolerance development to the inhibitory effect on VEPs. The results suggest that the hippocampus has important implications in the modulation of PCP effects on CNS activities related to the visual function of the rhesus monkey.

Effects of acute and chronic administration of phencyclidine (PCP) on heart rate (HR) and respiratory rate (RR) were studied in rhesus monkeys. Acute administration of PCP (2.0 and 4.0 mg/kg i.v.) produced decrements in both HR and RR within 15 to 30 min after drug administration. Simultaneously, with this cardiorespiratory slowing, EEG tracings evidenced High-Voltage Slow-Waves (HVSW) and delta-waves. As HR and RR began to recover, High-Voltage Fast-Waves (HVFW) along with theta-waves developed in EEG recordings and persisted for 2-6 h, while both HR and RR were gradually returning to their respective pre-drug control levels. The intensity and duration of these PCP-induced effects were directly related to dosage level. Following chronic administration of PCP (daily dose of 2.0 or 4.0 mg/kg i.v.), its ability to produce cardiorespiratory alterations was significantly diminished along with a decrease in PCP-induced depression of EEG and behavioral activities. These results suggest that chronic PCP administration produces a tolerance to its depressant effect on HR, RR, EEG and behavioral activities in rhesus monkeys.

Effects of acute and chronic administration of phencyclidine (PCP) on auditory evoked potentials (AEPs) were studied in rhesus monkeys with encephalic electrodes permanently implanted. AEPs were evoked by single clicks (1.0 pps in frequency) generated by an externally triggered audiomonitor. Single PCP injections (dose, 2.0 or 4.0 mg/kg IV) in monkeys produced a striking distortion in the amplitudes of major AEP components. This AEP distortion was manifested in superior temporal cortex (ST) by a complex pattern of amplitude reduction and enhancement, and was manifested in the medial geniculate body (MGB) by amplitude reduction. These effects persisted for 4 to 5 hours. Upon chronic administration (dose, 4.0 mg/kg IV daily), the effects of PCP on AEP components in ST were enhanced while little change was noted in its effect on AEP components in MGB. These results suggest that PCP administration in rhesus monkeys causes a significant disturbance of AEPs within central nervous system structures associated with auditory processing (i.e., ST and MGB), and that chronic PCP administration enhances its effects on AEPs predominantly in the primary auditory cortex while having little additional effects on AEPs from the subcortical auditory pathways.