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D E Moss

Publications and source records attributed to D E Moss.

At least 37 records · Page 2Linked to original sources
PubMed1986

Perioral behaviors induced by cholinesterase inhibitors: a controversial animal model.

Perioral behaviors induced by neuroleptic drugs have been interpreted as an animal model of tardive dyskinesia. However, these behaviors have also been induced or enhanced by physostigmine, a cholinesterase inhibitor. The latter result is contradictory to the clinical effect of physostigmine in human tardive dyskinesia. In view of this contradiction and other considerations, perioral behaviors have also been interpreted as a model of acute dystonia. The present experiments replicated an earlier failure to observe spontaneous perioral behaviors after long-term neuroleptic treatment in rats as well as the paradoxical effect of physostigmine. The effect of physostigmine was also compared to phenylmethanesulfonyl fluoride and methanesulfonyl fluoride, irreversible CNS active cholinesterase inhibitors. There were significant differences between the effects of the various cholinesterase inhibitors and their interactions with perioral behaviors and neuroleptic treatment. It is concluded that the effects of cholinesterase inhibitors on perioral behaviors in rodents may not be accounted for entirely by cholinesterase inhibition. Further experiments using additional agonists and antagonists will be required to clarify the behavioral effects of these cholinesterase inhibitors.

Animals↗
PubMed1985

Comparative behavioral effects of CNS cholinesterase inhibitors.

Phenylmethanesulfonyl fluoride, methanesulfonyl fluoride, and physostigmine were compared on the efficacy with which each could suppress methylphenidate-induced stereotyped gnawing, an extrapyramidal motor behavior. Whereas physostigmine produced powerful suppression of the stereotypy, the sulfonyl fluorides did not produce any clear behavioral effect. Biochemical experiments conducted with the behavioral tests demonstrated that the sulfonyl fluorides produced inhibition of whole brain, caudate, cortex, cerebellum, hippocampus and brain stem cholinesterate equal to that produced by physostigmine. The reason for the marked discrepancy between the behavioral effect of physostigmine and the sulfonyl fluorides is unknown. It is, however, clear that the effect of the various drugs on extrapyramidal motor behaviors is not a simple function of the degree to which each inhibited CNS cholinesterase.

Animals↗
PubMed1984

Comparative effects of tetrahydrocannabinol on psychostimulant-induced behaviors.

The behavioral effects of delta-9-tetrahydrocannabinol (THC), one of the major psychoactive cannabinoids in marijuana, were tested in two models of psychostimulant-induced behaviors in rats (locomotor behavior and stereotyped gnawing) induced by amphetamine (AMPH) and methylphenidate (MEPH). Pretreatment with THC (10 mg/kg gavage) almost doubled the amount of AMPH-induced gnawing but produced no effect on AMPH-induced locomotor behavior. In contrast to AMPH, THC produced no direct effect on MEPH-induced gnawing but caused a strong suppression of MEPH-induced locomotor activity. In addition, there was no additional interaction between THC and reserpine as measured by suppression of MEPH-induced gnawing. This result was unexpected in view of the powerful interaction between THC and reserpine reported previously. Because of the clear THC-induced dissociation of the behavioral effects of these two psychostimulants (AMPH and MEPH), our working hypothesis is that THC affects motor behaviors by some non-dopaminergic mechanism.

Amphetamine↗
PubMed1981

Tetrahydrocannabinol potentiates reserpine-induced hypokinesia.

Delta-9-tetrahydrocannabinol (THC), a substance in marihuana, was found to produce a profound potentiation of reserpine-induced hypokinesia in rats as measured with a bar test. In these experiments, THC had no hypokinetic effect by itself but produced a more than 20-fold increase in the hypokinesia produced by reserpine. Reserpine-induced hypokinesia has been viewed as animal model of Parkinson's Disease. THC potentiation of reserpine-induced hypokinesia was observed to be both time- and dose-dependent (1 to 10 mg/kg THC). When administered by gavage to reserpine-pretreated subjects (7.5 mg/kg IP, 24 hours before), THC produced a potentiation of hypokinesia that developed fully within 1 hour, lasted at least 5 hours, and was absent by 12 hours after THC administration. This THC effect was slightly increased by physostigmine, a cholinesterase inhibitor, relatively unaffected by scopolamine, a muscarinic antagonist, and almost completely blocked by ethopropazine, an anticholinergic antiparkinson drug. The effect was completely unaffected by naloxone. Insofar as reserpine has been used with some clinical efficacy in hyperkinetic movement disorders such as Huntington's disease and tardive dyskinesia, it may be that potentiation of reserpine's hypokinetic effect by a drug such as THC could greatly increase the clinical value of reserpine or related drugs in the treatment of these disorders.

Animals↗
PubMed1981

Time dependent changes in anterograde scopolamine-induced amnesia in rats.

These experiments studied the effect of scopolamine on memory formation and subsequent memory recall. Different groups of rats were trained on a Y-maze brightness discrimination task 20 min after IP injection of 2 mg/kg scopolamine HBr, an anticholinergic. Retention tests were then conducted 1 day or 2, 4, or 6 weeks after training. Deficits in retention performance were observed at 1 day and 2 weeks after training but not at the longer intervals. In addition, other rats were trained in the same manner and after the same dose of scopolamine but were then retention tested 20 min after 0.5 mg/kg physostigmine salicylate, a cholinesterase inhibitor. These subjects also showed deficits at 1 day and 2 weeks but were not different from controls at the longer intervals. Amnesia was not, however, produced after treatment with scopolamine methyl nitrate or by injections of scopolamine HBr administered immediately after training. These results suggest that scopolamine, present in the central nervous system during training or within the first few moments thereafter, modifies the formation of the memory trace in such a way that memory is not available for recall for a period of weeks.

Animals↗
PubMed1980

Tonic analgesic effects of delta 9-tetrahydrocannabinol as measured with the formalin test.

The analgesic effects of delta 9-tetrahydrocannabinol (THC), the psychoactive component of marihuana, were tested using the formalin test. Rats were treated with either THC (5 mg/kg or 10 mg/kg) or a placebo by gavage 4 h before the formalin test for analgesia was initiated. THC produced a highly significant analgesic effect against both phasic pain and tonic pain. THC is discussed as a model for the development of new analgesics or as a suitable analgesic if used with another potentiating drug.

Analgesics↗
PubMed1980

An automated method for studying stereotyped gnawing.

Stereotyped behavior in rats, consisting of compulsive, repetitive sniffing and gnawing, caused by high doses of amphetamine-like psychostimulants, may serve as an animal model for psychosis. Previous methods for measuring behavioral stereotypies of this kind have required continuous observation and rating of the behaviors or semiquantitative techniques that fail to produce a continuous record of the behaviors. The present paper describes a simple automated method that provides a continuous quantitative record of the specific gnawing behavior induced in rats by methylphenidate, an amphetamine-like psychostimulant. The apparatus described and the test procedures developed are compatible with a wide variety of common counters and recorders.

Animals↗
PubMed1978

Tetrahydrocannabinol and acetylcholinesterase.

Recent evidence suggests that the psychoactive effect of delta-9-tetrahydrocannabinol (delta9-THC), the major psychoactive constituent of marihuana, may be mediated through an alteration of cholinergic neurotransmission. One possible mechanism by which delta9-THC could have its effect is by affecting acetylcholinesterase (AChE) and there is evidence that has suggested that this may be an important mechanism. The results reported in the present study have shown that there is no physiologically important interaction between AChE and delta9-THC or its metabolites that could explain its psychoactive effects or the profound clinical depression observed when human marihuana users are administered the cholinesterase inhibitor physostigmine.

Animals↗
PubMedDate not supplied

Effect of cobra neurotoxin on retention of a brightness discrimination in rats.

In view of some recent evidence that blockade of nicotinic acetylcholine receptors might interfere with memory recall, the possibility that intracranial injections of purified corbra neurotoxin, an irreversible nicotinic receptor blocker, would produce long-lasting amnesia was explored with a brightness discrimination habit in rats. The results indicate that even the highest tolerable dose of neurotoxin had no detectable effect on memory recall.

Animals↗
PubMedDate not supplied

Methanesulfonyl fluoride enhances one-trial reward learning in mid-aged rats.

In previous studies, 18-month-old rats have shown no significant retention 24 hours after the single acquisition trial in a one-trial discriminative reward learning task. In the present study, ten 18-month-old rats pretreated with 0.5 mg/kg MSF IP showed significantly better retention in terms of speed and errors than eleven 18-month-old rats pretreated with injection vehicle alone. However, twelve two-three-month-old rats pretreated with the same dose of MSF failed to show better retention than eleven two-three-month-old rats pretreated with vehicle alone.

Aging↗