Search PubMed⌕ Search

Biomedical subjects

J C Gillin

Publications and source records attributed to J C Gillin.

At least 325 records · Page 18Linked to original sources
PubMed1976

The inhibitory effect of intraventricular administration of serotonin on spontaneous motor activity of rats.

Spontaneous motor activity was studied following injection of 1, 10 and 50 mug of serotonin (5-HT) into the lateral ventricle of chronically cannulated rats. During the first 15 min, the rats receiving the higher doses of 5-HT showed significant decrements (P less than 0.01) in motor activity compared to saline controls. No activation was observed in either group. After 20 min, no significant differences for any treatment condition compared to saline controls were observed. It is concluded that a principal effect of directly increasing brain 5-HT concentration is to decrease activity. Possible mechanisms for this effect are discussed.

Animals↗
PubMed1976

Parachlorophenylalanine potentiates facilitatory effects of mescaline on shuttlebox escape/avoidance in rats.

Acute parachlorophenylalanine (pCPA) pretreatment (150 mg/kg, i.p., 24 h beforehand) potentiated facilitatory effects of mescaline (39.6 mg/kg i.p.) on shuttlebox escape/avoidance in hooded rats, tested in two different situations: 1. during aquisition of avoidance behavior (Experiment 1); and 2. in stable pretrained poor avoiders (Experiment 2). pCPA alone did not influence avoidance behavior in either situation. Mescaline, with pCPA pretreatment, may be associated with long-term behavioral effects; all rats treated with this combination were later found to be poor avoiders, unable to achieve a stable baseline of good avoidance. pCPA significantly depleted brain norepinephrine and dopamine, as well as serotonin, measured after testing in the second situation.

Animals↗
PubMed1976

REM sleep induction by physostigmine infusion during sleep.

Physostigmine (an anticholinesterase agent that increases acetylcholine at the synapse), in a dose of 0.5 milligram, was given intravenously to seven normal human volunteers. When injected during rapid eye movement (REM) sleep, physostigmine woke the subjects, and when injected during non-REM sleep, it induced REM sleep. This result suggests that cholinergic mechanisms play a role in the induction of REM sleep and in modulating cortical arousal mechanisms.

Acetylcholine↗
PubMed1976

The psychedelic model of schizophrenia: the case of N,N-dimethyltryptamine.

The authors review the research on N,N-dimethyltryptamine (DMT) as a possible "schizotoxin." DMT produces psychedelic effects when administered to normal subjects, the means are present to synthesize it in man, it has occasionally been found in man, and tolerance to its behavioral effects is incomplete. However, DMT concentrations have not been proven to differ significantly in schizophrenics and normal controls. Also, in vivo synthesis of DMT has not been convincingly demonstrated, and the psychological changes it produces do not closely mimic the symptoms of schizophrenia. The authors conclude that more data are necessary before the validity of this theory can be determined.

Chlorpromazine↗
PubMed1976

Dose-response effects of beta-phenylethylamine on stereotyped behavior in pargyline-pretreated rats.

We studied the dose-response and the time-course effect of beta-phenylethylamine (4.0-64.0 mg/kg, ip) on stereotyped behavior and motor activity in male Sprague-Dawley rats pretreated 2 hr eariler with pargyline (0.25-8.0 mg/kg, iv). Stereotyped behavior, defined as repetitive, nongoal-directed head movements and sniffing, and changes in motor activity were observed immediately after injection of beta-phenylethylamine for a 1 hr period. With increasing doses of pargyline pretreatment, beta-phenylethylamine produced, in a dose-response relationship, progressively more stereotyped behavior accompanied by increased motor activity. Without pargyline pretreatment, only 64.0 mg/kg beta-phenylethylamine induced behavioral changes. Stereotyped behavior and increased motor activity had an onset at 4-6 min after the injection of beta-phenylethylamine, peak at 10-30 min, and gradual decline in the next 10-20 min. These results are discussed in terms of a possible relationship with the degree of inhibition of Type a and Type B monoamine oxidase acused by the different doses of pargyline.

Animals↗
PubMed1976

The effect of probenecid on the free and conjugaed 3-methoxy-4-hydroxyphenylglycol (MHPG) in lumbar cerebrospinal fluid.

Free and conjugated lumbar cerebrospinal fluid 3-methoxy-4-hydroxyphenylglycol (MHPG) was measured before and after probenecid treatment in 12 schizophrenic patients by a gas liquid chromatography-mass fragmentographic procedure. Neither the free nor conjugated MHPG was appreciably altered by probenecid. Total MHPG was statistically increased by probenecid but not to the point that the probenecid test would be clinically useful for estimating norepinephrine turnover from probenecid-induced changes in MHPG concentrations.

3-Methoxy-4-hydroxyphenylethanol↗
PubMed1975

Dopamine-sensitive adenylyl cyclase in human caudate nucleus. A study in control subjects and schizophrenic patients.

Striatal adenylyl cyclase activity from autopsied human brain is selectively stimulated by low concentrations of dopamine. Under the experimental conditions used, norepinephrine was about three times less potent than dopamine. Histamine and serotonin were ineffective. The stimulation by dopamine was competitively inhibited by haloperidol. There was no difference between the basal adenylyl cyclase activity or its level after dopamine stimulation between nine control subjects without a psychiatric history and seven patients with chronic schizophrenia.

Adenosine Triphosphate↗
PubMed1975

L-Histidine: failure to affect the sleep-waking cycle in man.

L-Histidine was administered to three patients with intractable narcolepsy (20 g/day for 2 weeks), to 4 normal volunteers (32.4 g/day for 5 days), and to a patient with progressive systemic sclerosis (48.6 g/day for 16 days). No effect was observed on noctural EEG sleep patterns in any of the subjects or on the symptoms of the patients with narcolepsy. These results fail to support the hypothesis that histamine is a waking factor.

Adult↗