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Biomedical subjects

H Anisman

Publications and source records attributed to H Anisman.

At least 145 records · Page 8Linked to original sources
PubMed1981

Noradrenergic and dopaminergic interactions in escape behavior: analysis of uncontrollable stress effects.

The effects of norepinephrine receptor blockade on the deficits of escape behavior induced by haloperidol and by inescapable shock were evaluated. Phenoxybenzamine, the alpha-norepinephrine receptor blocker, was found to enhance escape behavior and to eliminate the disruptive effects of both inescapable shock and haloperidol. In contrast, the beta-norepinephrine receptor antagonist, propranolol, was without effect on behavior under any of these conditions, while the dopamine-beta-hydroxylase inhibitor, FLA-63, disrupted performance. Like phenoxybenzamine, the norepinephrine receptor stimulant, clonidine, was found to eliminate the behavioral disruption produced by haloperidol. These somewhat paradoxical findings were discussed in terms of the contribution of DA-NE interactions in determining behavioral change in aversive paradigms.

Animals↗
PubMed1981

Cholinergic influences on escape deficits produced by uncontrollable stress.

A series of experiments assessed the potential role of acetylcholine (ACh) in the escape interference produced by inescapable shock. Treatment with the anticholinesterase, physostigmine, successfully mimicked the effects of inescapable shock. That is, the drug disrupted performance when escape was prevented for 6 s on any given trial, thereby necessitating sustained active responding. When escape was possible upon shock onset, the drug treatment did not influence performance. The centrally acting anticholinergic scopolamine hydrobromide antagonized the effects of physostigmine, and when administered prior to escape testing antagonized the disruptive effects of previously administered inescapable shock. In contrast, the peripherally acting agent scopolamine methylbromide did not influence the effects of these treatments, suggesting that the effects of physostigmine and inescapable shock involved central ACh changes. Scopolamine hydrobromide administered prior to inescapable shock did not prevent the escape interference from subsequently appearing, but this effect could not be attributed to state dependence. It was argued that the interference of escape following uncontrollable stress was due to non-associative motor deficits. Alterations of the escape deficits by scopolamine were due to elimination of the motor disruption.

Acetylcholine↗
PubMed1981

Amphetamine psychosis and schizophrenia: a dual model.

Several of the behavioral consequences of acute and chronic amphetamine treatment were evaluated and related to the underlying neurochemical correlates of drug treatment. It was suggested that decreased noradrenergic activity after long-term amphetamine treatment influences stimulus sampling, whereas enhanced dopaminergic activity was responsible for the progressive augmentation of stereotypy and self-stimulation behavior observed after long-term exposure to amphetamine. It was hypothesized that amphetamine-induced psychosis and the symptomatology associated with schizophrenia are related to alterations in both norepinephrine and dopamine activity.

Amphetamine↗
PubMed1981

Adaptation to the tumor-enhancing effects of stress.

Growth of P815 mastocytoma in syngeneic DBA/2J male mice was evaluated following several stress regimens. Although escapable shock did not enhance tumor growth, an equivalent amount of inescapable shock applied in a yoked paradigm markedly augmented tumor development. If mice received repeated stress sessions on 5-10 consecutive following tumor cell transplantation, the tumor-enhancing effects of an acute session were abrogated. This effect was not due to an antitumor effect exerted by a shock session applied several days after cell transplantation. It seems that the tumorigenic effects of stress are subject to adaptation since stress exposure prior to cell transplantation also inhibited the effects of an acute stress session. The data were discussed in relation to stress-induced neurochemical alterations.

Adaptation, Physiological↗
PubMed1980

Extinction and dopamine receptor blockade after intermittent reinforcement training: failure to observe functional equivalence.

Response decrements in an operant task produced by either extinction or by the dopamine receptor blocker pimozide were examined in three experiments which employed intermittent reinforcement schedules. In contrast to the congruency between these treatments previously observed following continuous reinforcement training, treatment with pimozide was markedly more effective than extinction in decreasing performance after training with variable interval, fixed interval, and fixed ratio reinforcement. The two treatments also produced substantially different patterns of responding. A shift from extinction to pimozide did not alter the progressive decline in response rate over days, but a shift from pimozide to extinction caused a pronounced increase of performance. These results indicate that the pimozide and extinction treatment did not produce functionally equivalent effects, and that the role of dopamine on reward processes should not be inferred from comparisons between pimozide and extinction.

Animals↗
PubMed1980

Dissociation of antinociception and escape deficits induced by stress in mice.

Several experiments with mice were conducted to assess the conditions under which stress would induce antinociception in a subsequent hot-plate test. Both footshock and tail shock produced the antinociception. This effect was apparent with as little as a single shock trial. The magnitude of the antinociception was maximal following 15 shock presentations and was largely reduced after 60 shocks. In contrast to the results of Jackson, Maier, and Coon, whether stress was escapable was not a necessary feature needed to produce the antinociception. Moreover, the magnitude of the antinociception induced by stress was not enhanced in mice that had previously been exposed to stress. Finally, morphine (10.0, 20.0, and 30.0 mg/kg) produced a pronounced antinociception but did not appreciably influence escape performance in a shuttle task in which performance is disrupted by inescapable shock. It is suggested that the antinociception and shuttle-escape deficits induced by uncontrollable shock are independent of one another.

Animals↗
PubMed1980

Social stress influences tumor growth.

Growth of syngeneic P815 mastocytoma in DBA/2J male mice was evaluated following social and physical stress exposure. Although social isolation following tumor cell transplantation enhanced tumor growth, it appeared that it was the abrupt change in social conditions, rather than the isolation per se which was responsible for the exacerbation of tumorigenicity. Moreover, it was found that the animals' behavior after social change could modify this effect. If mice engaged in persistent fighting, the tumorigenic consequences of social change were not apparent. In addition, it was observed that social conditions interacted with physical stress. Footshock enhanced tumor growth among group housed mice, but retarded tumor development among socially isolated mice.

Adaptation, Psychological↗
PubMed1980

Differential effects of inescapable shock on escape performance and discrimination learning in a water escape task.

The effects of inescapable shock on subsequent T-maze water escape and position discrimination performance were evaluated in seven experiments. Escapable shock did not disrupt water escape performance; however, escape performance was retarded 24 hr after inescapable shock. These deficits were not apparent if escape was possible upon stress inception; however, pronounced deficits were noted if sustained active responding was necessitated by briefly (3-5 sec) preventing escape. When water escape testing was conducted in relatively warm water (20 degrees C), the disruptive effects of preshock were not apparent. In colder water (15 degrees C), which increases the motor difficulty of the task, the disruptive effects of preshock were noted. When the motor difficulty of the task was increased further, by testing mice in 10 degrees C water, or when the associative difficulty was increased by using a vigorous reversal learning task, the differences between the preshocked and nonpreshocked groups were obviated. Exposure to inescapable shock did not disrupt position discrimination performance regardless of the motor difficulties of the task. Similarly, deficits of discrimination performance were not apparant in mice exposed to inescapable shock even when the associative difficulty of the task was increased by removing intramaze cues or by testing animals in a position discrimination reversal task. It is concluded that inescapable shock results in deficits of response maintenance but probably has a minor, if any, influence on cognitive/associative processes.

Animals↗
PubMed1979

Deficits of escape performance following catecholamine depletion: implications for behavioral deficits induced by uncontrollable stress.

Following exposure to inescapable shock, mice exhibit deficits of escape performance, which are progressively more pronounced as training continues. Comparable effects were produced by DA and NE depletion by alpha-MpT and reserpine, NE depletion by FLA-63, and DA receptor blockade through haloperidol. Treatment with PCPA or 5-HTP did not influence performance. The disruptive effects of reserpine and alpha-MpT, as well as haloperidol and FLA-63, were additive. Unexpectedly, mice that received both reserpine and FLA-63 exhibited escape latencies that were significantly lower than those of mice that received either treatment alone. Consistent with the view that increased DA synthesis in the reserpine plus FLA-63 condition prevented the escape interference, L-DOPA antagonized the effects of both alpha-MpT and FLA-63. The results suggest that DA and NE act in a serial fashion to produce the escape deficits. Moreover, although both newly synthesized and previously stored amines contribute to the interference, the short latency responses seen during initial test trials could not be ascribed to previously stored amines.

Animals↗
PubMed1979

Stress and coping factors influence tumor growth.

Growth of syngeneic P815 mastocytoma in DBA/2J male mice was evaluated as a result of various stress regimens. A single session of inescapable shock resulted in earlier tumor appearance, exaggeration of tumor size, and decreased survival time in recipient animals. Escapable shock had no such effects. The effects of the inescapable shock were mitigated if mice received long-term shock treatment.

Animals↗
PubMed1979

Circling behavior following systemic d-amphetamine administration: potential noradrenergic and dopaminergic involvement.

Systemic treatment with d-amphetamine produced a dose-dependent increase in the circling behavior of normal mice. Treatment with both alpha-methyl-p-tyrosine (alpha-MpT) and FLA-63 antagonized the amphetamine-induced circling behavior. Similarly, blockade of B-adrenergic receptors by propranolol and dopamine receptors by haloperidol reversed the circling response elicited by amphetamine. In contrast to alpha-MpT and haloperidol, however, neither FLA-63 nor propranolol attenuated the locomotor excitation engendered by amphetamine. Following repeated d-amphetamine injections the circling ordinarily induced by a single injection was abolished, whereas the locomotor effects of amphetamine remained unaltered. These findings are consistent with earlier work suggesting that tolerance may occur in those behaviors that involve a noradrenergic component.

Animals↗
PubMed1979

Effect of an inhibitor of dopamin-beta-hydroxylase on the acquistion and retention of four different avoidance tasks in mice.

The effect of [bis-(4-methyl-1-homopiperazinylthiocarbonyl)-disulfide] (FLA-63) (40 mg/kg, i.p.) on acquisition and retention in four different avoidance tasks was evaluated in mice. In all tasks animals were submitted to a training session on one day and to a retest session 24 h later. The drug or its vehicle were given either 2 h prior to training and/or retest (pretrial treatments) or immediately after the end of the training session (posttrial treatments). Two hours after injection, FLA-63 was found to lower brain norepinephrine (NE) levels by 51% without affecting those of dopamine (DA). Pretrial administration of the drug resulted in poorer performance of step-through and step-down passive avoidance as well as of step-up active avoidance in retest sessions. There was no apparent posttrial effect of the drug nor any effect on acquisition in these tasks. The drug was without influence on either acquisition or retention in an any-way passive avoidance task in which the response required from the animals was immobility. No evidence for state-dependent learning was detected in any of the tasks. The data are consistent with the hypothesis of an involvement of NE either in memory processes or in events parallel and related to memory processes. The present results rule out, however, several such possible parallel events (effects on acquisition, motor disturbances, and effects on reactivity to shocks).

Animals↗