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Biomedical subjects

P M Adams

Publications and source records attributed to P M Adams.

At least 37 records · Page 2Linked to original sources
PubMed1984

Effects of paternal ethylene dibromide exposure on F1 generation behavior in the rat.

The effects of ethylene dibromide (EDB) exposure to the male rat were studied through behavioral assessments of their F1 progeny. Exposed males were bred with untreated female rats at 4 or 9 weeks after 5 daily EDB treatments. Behavioral assessment of motor reflexes and motor coordination were examined up to 21 days of age. Significant differences in the development of motor coordination and motor activity were observed in the F1 progeny of EDB-exposed males. These results support the evidence of EDB genotoxicity and further demonstrates the utility of behavioral end-points of the offspring as a sensitive means of assessing paternal reproductive risk.

Animals↗
PubMed1983

Post-meiotic cell mediation of behavior in progeny of male rats treated with cyclophosphamide.

Transmission of the effects of paternal pre-fertilization exposure to a genotoxic drug being manifested in the F1 progeny is well established using the traditional rodent dominant lethal protocol [7]. More recently, the induction of genotoxic effects in the F1 progeny following chronic paternal exposure prior to fertilization has been described in rats using behavioral testing as an endpoint [1]. In our initial study, male F344 adult rats were treated chronically with 10 mg/kg cyclophosphamide (CP) or saline for 5 weeks (5 days of daily treatment and 2 days of rest). The present study describes the behavior of progeny whose fathers were treated with a single intraperitoneal injection of 10 mg/kg CP and mated at different times post-injection. This design showed that post-meiotic germ cells are the most sensitive to the effects of CP as seen by behavioral testing of the F1 progeny.

Animals↗
PubMed1982

Effects of naloxone, metenkephalin, and morphine on phencyclidine-induced behavior in the rat.

The effects of naloxone, metenkephalin, and morphine were tested on phencyclidine(PCP)-induced stereotyped behaviors, ataxia, and hyperactivity in the rat. Naloxone (8 mg/kg) significantly decreased stereotypy, ataxia, and hyperactivity across all PCP doses tested (2.0, 4.0, and 6.0 mg/kg). Metenkephalin (40 micrograms/kg) and morphine (5 and 10 mg/kg) increased ataxia at the 4.0 and 6.0 mg/kg PCP doses. Stereotypy was altered by the opiates in a dose-dependent manner; enhanced by metenkephalin (40 micrograms/kg) at 2.0 mg/kg and inhibited by metenkephalin (40 micrograms/kg) and morphine (10 mg/kg) at 4.0 and 6.0 mg/kg PCP. Locomotor activity was increased by morphine (5 mg/kg) at 2 mg/kg PCP. These results suggest an involvement of central opiate receptor mechanisms in the mediation of PCP-induced behaviors in the rat.

Animals↗
PubMed1982

Physostigmine and haloperidol treatment of acute phencyclidine intoxication.

Twenty-four patients with phencyclidine intoxication were treated with either physostigmine (2 mg i.m.) or haloperidol (5 mg i.m.) based on the presence of delusions and/or hallucinations. Several symptoms subsequently improved. Schizophreniform symptoms showed substantial improvement with haloperidol.

Acute Disease↗
PubMed1982

Phencyclidine intoxication: assessment of possible antidotes.

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].

Antidotes↗
PubMed1981

Acute and chronic phencyclidine effects on locomotor activity, stereotypy and ataxia in rats.

Behavioral rating scales, developed to measure phencyclidine (PCP)-induced stereotypy and ataxia in rats, were tested using acute dose-response and chronic paradigms with concomitant assessment of locomotor activity by automated counters. Also, effects of chronic PCP on apomorphine-induced stereotypy were assessed as a test of dopamine supersensitivity. A linear dose-response effect was found for measures of all three behaviors through moderate dose levels (2-6 mg/kg), but only ataxia ratings continued to increase, showing a linear relationship through the higher (8 and 10 mg/kg) doses. Chronic daily PCP administration showed progressive augmentation of stereotypy, tolerance to ataxia at 10 min post-injection, and a biphasic increase followed by decrease to day 1 levels in locomotor activity over 14 days. No significant change was found in apomorphine stereotypy following chronic PCP treatment. The chronic behavioral changes demonstrated in this study may provide a model of PCP-induced psychological and cognitive changes seen following chronic usage in man.

Amphetamine↗
PubMed1981

Cyclophosphamide-induced spermatogenic effects detected in the F1 generation by behavioral testing.

Fischer 344 male rats were treated with cyclophosphamide (10 milligrams per kilogram of body weight) for 5 weeks and subsequently mated to females previously treated with saline or cyclophosphamide. The F1 progeny of the cyclophosphamide-treated males exhibited behavior deficits when compared to controls. These data could indicate a chemically induced genetic effect manifested by behavioral alterations.

Animals↗
PubMed1976

Effect of chronic pentobarbital treatment on the sleep patterns of squirrel monkeys.

Following a 30-day baseline, 60 days of sodium pentobarbital treatment (5 mg/kg) were given to squirrel monkeys 2 h prior to the start of a 12-h recording of EEG and EOG. Following the drug-treatment phase, an additional 30-day period was used to determine the rate of recovery. Repeated pentobarbital treatment significantly reduced awake time and slow wave sleep while it elevated the time spent in drowsy and light sleep. The recovery phase indicated a brief recovery of rapid eye movement sleep while the other stages failed to return to baseline levels. The cyclical nature of the changes observed with chronic pentobarbital suggest the importance of circadian fluctuations in the study of chronic drug treatment and the sleep-wakefulness process.

Animals↗
PubMed1976

Effects of rapid depletion of phenylalanine and tyrosine on sleep and behavior.

The effects of fluctuations of free amino acid concentrations in plasma on sleep patterns and operant behavior in the squirrel monkey were studied. Plasma phenylalanine (PHE) and tyrosine (TYR) were rapidly lowered to trace levels within 4 hr by intraperitoneal administration of phenylalanine ammonia-lyase (PAL), an enzyme which specifically deaminates both PHE and TYR to inactivate products. Significant alterations in sleep patterns and in performance on a chained operant task involving hold and reaction time components were found, but no significant effect on the performance of a simple operant task was observed. Adminstration of saline or trans-p-cinnamic acid and trans-p-coumaric acid, the products of PHE and TYR deamination, produced no changes in behavior or sleep patterns. The reduction of plasma PHE and TYR resulted in a significant decrease in PHE and TYR levels in whole rat brain. Brain serotonin levels were increased within 4 hr after PAL administration, whereas, dopamine and norepinephrine levels were decreased subsequently (within 8 hr). These studies suggest that circulating levels of PHE and TYR are involved directly or indirectly in the modulation of certain parameters of brain function.

Animals↗
PubMed1975

Role of biogenic amines in the effects of marijuana on EEG patterns in cats.

The results of pretreatment with drug having selective action on brain biogenic amine levels on the subsequent effects of acute marijuana treatment were assessed for behavior and EEG measures. Behavioral changes and alterations in the spontaneous EEG indicated that pretreatment with drugs affecting brain levels of 5-HT was most effective in altering the dual properties of acute marijuana treatment. The present findings support the interpretation that the availability of serotonin interacts with the effects of acute marijuana treatment but do not eliminate the possible involvement of other neurotransmitters in the action of marijuana.

5-Hydroxytryptophan↗