Biomedical subjects

H Anisman

Publications and source records attributed to H Anisman.

At least 19 recordsLinked to original sources

PubMed1992

Strain-specific alterations in consumption of a palatable diet following repeated stressor exposure.

Exposure to acute inescapable shock caused reductions in the consumption of a highly palatable diet. The magnitude and duration of the reduction varied across strains of mice. With repeated exposure to footshock, consumption of the diet returned to baseline levels, although alterations of weight appeared to be more persistent. The course of the adaptation varied across strains of mice; however, the rate of adaptation was unrelated to the extent of the alterations of consumption induced by the acute stressor. When mice were exposed to a series of different stressors, the adaptation progressed less readily, and reductions of diet consumption were apparent in strains that had not shown such an effect following acute stressor application or when repeatedly exposed to a single type of stressor. Data were discussed with respect to the mechanisms that might be operative in subserving stressor-induced anhedonia.

Animals↗

PubMed1992

Depression as a consequence of inadequate neurochemical adaptation in response to stressors.

Stressors induce behavioural disturbances and neurochemical changes in animals, some of which are reminiscent of the symptoms and presumed neurochemical concomitants of depression in humans. Just as in humans, where considerable inter-individual variability is evident in the symptom profile of depression, there is marked inter-individual and inter-strain variability in the behavioural effects of stressors in animals. It is proposed that stressors induce adaptive neurochemical changes, failure of which may engender behavioural disturbances. Variability in the symptoms of depression and in the efficacy of its pharmacological treatment may reflect the biochemical heterogeneity of the illness. Inter-individual differences in vulnerability to stressor-provoked neurochemical changes may contribute to the behavioural profiles observed.

Adjustment Disorders↗

PubMed1991

Time-dependent variations of central norepinephrine and dopamine following antigen administration.

Administration of sheep red blood cells (10(6) cells, i.p.) resulted in central norepinephrine (NE) and dopamine (DA) changes which corresponded with the time of the peak immune response. These amine variations, however, appeared to be specific to certain brain regions. The increased accumulation of the NE metabolite, 3-methoxy-4-hydroxyphenylethylene glycol, was evident in hypothalamus, locus coeruleus and hippocampus and a moderate reduction of NE was evident in the hypothalamus. Alterations of DA levels or utilization appeared in mesocorticolimbic structures (i.e. nucleus accumbens and prefrontal cortex) but not in striatum. This profile of transmitter changes was reminiscent of that previously shown to be induced by uncontrollable stressors and the possibility was offered that antigenic challenge is interpreted as a stressor by the central nervous system.

Animals↗

PubMed1991

Stressor-induced alterations of natural killer cell activity and central catecholamines in mice.

Natural killer (NK) cell cytotoxicity was determined at various intervals (0.5, 24 or 48 h) following exposure to uncontrollable footshock in 3 strains of mice. Stressor application provoked reductions of NK activity, but the time course of the NK changes varied across strains. Whereas NK cytotoxicity was markedly reduced in C57BL/6J mice 0.5-48 h following stressor exposure, this effect was delayed in C3H/HeJ mice, being evident 24-48 h following stressor application. In BALB/cByJ mice, NK activity was significantly reduced 24 h after footshock, but in contrast to the other strains returned to control levels within 48 h of stressor exposure. Central NE and DA concentrations and activity were influenced by the stressor treatment in a strain-dependent fashion. However, the relationship between the central amine variations and the alterations of NK cytotoxicity associated with the stressor was limited.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1991

Alterations of central norepinephrine, dopamine and serotonin in several strains of mice following acute stressor exposure.

Exposure to inescapable footshock provoked region-specific alterations of norepinephrine (NE), dopamine (DA) and serotonin (5-HT) activity across six strains of mice (A/J, BALB/cByJ, C3H/HeJ, C57BL/6J, DBA/2J and CD-1). The stressor provoked reductions of hypothalamic NE and increased MHPG accumulation in all strains. In contrast, the effects of the stressor on NE activity in the hippocampus and locus coeruleus varied appreciably across strains. In the mesocortex and nucleus accumbens shock induced an increase of DOPAC accumulation and pronounced reductions of DA in some strains, while in others these variations were less pronounced or entirely absent. Stressor-provoked alterations of 5-HT and 5-HIAA were most evident in the mesocortex. Strain-specific neurochemical alterations following footshock are discussed relative to stressor-induced behavioral disturbances and animal models of depression.

Animals↗

PubMed1991

Immunosuppression elicited by stressors and stressor-related odors.

Exposure of footshock 72 h after administration of sheep red blood cells (SRBC) provoked a reduction of the splenic plaque-forming cell (PFC) response and plasma antibody titers in CD-1 mice. At this time following SRBC inoculation the antibody titers and PFC response were also modifiable by nonpainful stressors, such as the presentation of a weak light or odor cues of conspecifics that had been exposed to a stressor (light). Data are discussed in terms of the sensitivity of the immune response to environmental and psychological stressors, and the implications of this particular sensitivity to further analyses of stressor effects on immune activity.

Animals↗

PubMed1991

Stressor-induced anhedonia in the mesocorticolimbic system.

It has been suggested that uncontrollable stressors induce motivational changes in animals which are reminiscent of reward alteration in human depression. Although there is considerable support for this position, most animal models of depression do not adequately address this issue. The present review suggests that stressor-induced reductions in the rewarding value of electrical brain stimulation (ICSS) from the mesocorticolimbic system may simulate the anhedonia of human depression. The magnitude, severity and the site of these stressor-induced reward alterations within the mesocorticolimbic system vary with the strain of animal employed. The anhedonic effects of stressors are attenuated by treatments which influence mesocorticolimbic DA turnover, including systemic antidepressant and intraventricular neuropeptide administration. Although the diverse symptom profile of depression should be addressed by consideration of the constellation of behavioral disturbances induced by stressors, considerable emphasis should be devoted to an assessment of reward loss in depression. The implications of these data to the stressor depression topography and the potential role of mesocorticolimbic DA in depression and anhedonia are discussed.

Animals↗

PubMed1991

Age-related enhancement and suppression of a T-cell-dependent antibody response following stressor exposure.

The effects of uncontrollable footshock on the peak splenic plaque-forming cell (PFC) response and serum antibody titers to sheep red blood cells (10(6) cells ip) were assessed in 3-month-old and 9-month-old male CD-1 mice. Exposure to uncontrollable footshock provoked an immunosuppression in mice of both age groups. The critical period for the induction of the suppression (i.e., 72 hr after inoculation) did not differ between the 3-month-old and 9-month-old mice; however, the suppression could be provoked more readily in the older animals. In the 9-month-old mice, the variations of immune activity were dependent on the severity of the stressor and the time of stressor application. Specifically, in contrast to the suppression induced by footshock, a relatively mild stressor such as exposure to a novel environment effectively increased the PFC response. A marked enhancement of the PFC response and antibody titers was evident in older animals that were shocked immediately or 24 hr after inoculation. The possibility exists that stressor application in older mice may influence regulatory processes that are associated with an immune response and that the nature of these regulatory mechanisms may vary with the time after antigenic challenge.

Aging↗

PubMed1990

Stressor induced variations of intracranial self-stimulation from the mesocortex in several strains of mice.

Intracranial self-stimulation (ICSS) from the mesocortex was assessed in BALB/cByJ, C57BL/6J and DBA/2J mice immediately, 24 h and again 168 h following stressor application. Stressor exposure failed to influence ICSS performance in C57BL/6J mice, while self-stimulation performance was reduced among BALB/cByJ mice only in the immediate post-stressor interval. In contrast, DBA/2J mice exhibited reduced rates of responding for brain stimulation at each of the post-stressor intervals. The potential contribution of DA alterations to the strain-dependent variations of ICSS performance induced by uncontrollable footshock are discussed.

Animals↗

PubMed1990

Behavioral characterization of intracranial self-stimulation from mesolimbic, mesocortical, nigrostriatal, hypothalamic and extra-hypothalamic sites in the non-inbred CD-1 mouse strain.

A behavioral analysis of intracranial self-stimulation (ICSS) was provided for mesolimbic/mesocortical, nigrostriatal, hypothalamic and extrahypothalamic sites in the CD-1 mouse. Robust responding and rapid acquisition of mesocortical ICSS appeared dorsally along notably fluorescent sites in rostral and caudal planes. ICSS was diminished demonstrably in medial and ventral positions in posterior planes. Mesolimbic ICSS from the medial and ventral nucleus accumbens (Nas), was accompanied by significant elevations in locomotor activity, corresponding to regions of dopamine (DA) and cholecystokinin co-localization. Stimulation-induced seizures appeared from both the Nas as well as the mesocortex. ICSS from the ventral tegmental field (VTA) was evident along its medial, lateral and dorsal borders with longer pulse durations more likely to elicit responding. Seizure activity was absent from the VTA. Striatal ICSS was conspicuously poor in dorsal and medial locations; regions presumably devoid of tegmental innervation. ICSS emerged from both the ventrocaudal and anteromedial striatum; regions linked to innervation by the dorsolateral and ventromedial VTA. The red nucleus, a previously neglected self-stimulation site supported marked responding for ICSS. Regions supporting rubral ICSS were correlated with thalamic innervation sites; notably the ventrolateral thalamic nucleus and the parafascicular nucleus, regions found to support ICSS. The substantia nigra supported high rates of responding for ICSS when electrode placement was restricted to the dorsomedial portion of the pars compacta. Electrode deviations lateral and dorsal to the substantia nigra pars medialis induced a progressive decline in responding. Hypothalamic sites were found to support significant responding for ICSS, although such performance was frequently associated with seizure induction. Taken together these data (1) provide the first behavioral analysis of ICSS in mice responding from previously unexamined DA sites in the mesolimbic (e.g. VTA, Nas) and nigrostriatal systems (e.g. caudate, red nucleus) (2) suggest an anatomical reconsideration of the assumptions underlying the elicitation of ICSS from the frontal cortex (3) suggest that the neural circuitry underlying thalamic, caudate, rubral and frontal cortical ICSS are interrelated and (4) suggest that the Nas and the frontal cortex, like the hypothalamus, in the mouse appear to be particularly sensitive to stimulation-induced seizures.

Animals↗

PubMed1990

Mouse strain differences in plasma corticosterone following uncontrollable footshock.

Exposure to acute inescapable footshock provoked marked increases of plasma corticosterone concentrations in six strains of mice (A/J, Balb/cByJ, C57BL/6J, C3H/HeJ, DBA/2J and CD-1). However, the magnitude of the increase, as well as the time required for corticosterone to return to control values, varied appreciably across strains. Moreover, it appeared that the strain-specific corticoid increases ordinarily observed after acute shock were also evidence following a chronic stressor regimen. The data were related to previously observed strain differences in stressor-induced alterations of brain norepinephrine, dopamine and serotonin, as well as variations in performance in several behavioral paradigms.

Animals↗

PubMed1990

Situation specific effects of stressor controllability on plasma corticosterone changes in mice.

The immediate and proactive effects of controllable and uncontrollable stressors on plasma corticosterone were assessed in CD-1 mice. A progressive increase of plasma corticosterone concentrations was associated with graded increases in stressor severity. When a footshock stressor was employed, however, the magnitude of the glucocorticoid response, as well as the decay of plasma corticosterone concentrations, was independent of stressor controllability. This was the case regardless of the number of escapable vs. yoked inescapable shock trials mice received, the spacing of shock trials (i.e., applied within a single session or spaced over days), or the degree to which the escape response had been established. In contrast, in a swim task stressor controllability influenced plasma corticosterone concentrations provided that the escape response required of the animal was a highly prepared one (i.e., swim to an illuminated region). When mice were required to emit a contraprepared response (swim to dark) corticosterone concentrations did not differ between escapable and inescapable swim. It is suggested that glucocorticoid secretion is a fundamental response to stressors, and the differential effects of controllable and uncontrollable stressors will be most apparent when the response required of the animal is a highly prepared one.

Animals↗

PubMed1990

Multiple neurochemical and behavioral consequences of stressors: implications for depression.

Animal models of clinical depression have frequently focused on the contribution of stressors to the induction of behavioral impairments and pharmacological intervention in the amelioration of these disturbances. Stressors provoke various behavioral disturbances and influence the activity of central neurotransmitters implicated in depression. It is our contention that those variables which favor the provocation of amine depletions or prevent the development of a neurochemical adaptation will increase vulnerability to behavioral disturbances. It is essential to consider, however, that marked interindividual and interstrain differences exist in the behavioral and neurochemical response to stressors, and in the effectiveness of antidepressant treatments.

Animals↗

PubMed1990

Stressor-induced behavioral alterations in intracranial self-stimulation from the ventral tegmental area: evidence for regional variations.

Exposure to uncontrollable footshock reduced responding for electrical brain stimulation (ICSS) from the ventral tegmental area (VTA) of the CD-1 mouse. Such an effect, however, varied with electrode position in the tegmental field. In both a rate-dependent and a current intensity paradigm, ICSS from the dorsal VTA was reduced immediately, 24 hr and 168 hr following exposure to acute uncontrollable footshock. In contrast, ICSS from the ventral VTA was unaffected by the stressor regimen. These data are consistent with the suggestion that a stressor may reduce the rewarding value ordinarily derived from ICSS. Inasmuch as the stressor differentially affected ICSS from the dorsal and ventral tegmentum, these data provide evidence for a functional differentiation within the midbrain tegmental area.

Animals↗

PubMed1989

Strain-specific effects of antidepressants on escape deficits induced by inescapable shock.

The effects of several antidepressants (desmethylimipramine, amitriptyline and bupropion) on escape deficits induced by inescapable shock were assessed in four strains of mice. The extent of the escape interference engendered by inescapable shock varied across strains of mice. These deficits of escape performance were differentially affected by the drug treatments across strains. Repeated administration of desmethylimipramine eliminated the escape interference in A/J, but did not affect the performance in Balb/cByJ, C57BL/6J or CD-1 mice. Bupropion, in contrast, had a modest effect only in CD-1 mice. Unlike these compounds, the 5-HT reuptake blocker, amitriptyline, was found to influence escape performance irrespective of whether the drug was acutely or chronically applied. It is suggested that (a) the relative contributions of various mechanisms subserving the escape interference may vary across strains of mice, hence accounting for the strain-specific effects of the drug treatments, and (b) various antidepressants influence performance by affecting different components of the behavioral output, some of which may be apparent after acute treatment while others are expressed only after repeated treatment with the compound.

Amitriptyline↗

PubMed1989

Alterations of immune functioning following exposure to stressor-related cues.

A critical period exists (approximately 72 h) following administration of sheep red blood cells (SRBC) during which inescapable footshock suppressed the peak splenic plaque forming cell (PFC) response and serum antibody titers in CD-1 mice. The immunosuppression was likewise provoked in mice that were exposed to the stressor 2 weeks prior to immunization and reexposed to stressor-related cues 72 h after inoculation. In contrast, when the stressor was initially applied immediately after immunization, reexposure to the stressor-related cues was found to provoke an immunoenhancement. Moreover, stressor exposure immediately following inoculation had the effect of counteracting the immunosuppression otherwise induced by a stressor applied at the 72-h interval. Evidently, environmental cues associated with a stressor provoke profound alterations of immunoresponsiveness, but the direction of the effect is dependent upon the time at which the stressor was initially applied.

Animals↗

PubMed1988

Critical periods associated with stressor effects on antibody titers and on the plaque-forming cell response to sheep red blood cells.

A series of experiments assessed the effects of stressors on the antibody response in mice. A critical period existed (72 h following antigen administration; sheep red blood cells 10(6) cells, ip) at which footshock reduced the plaque-forming cell (PFC) response in CD-1 mice. When shock was applied at other intervals following immunization (0, 24, 48, or 95 h) the PFC response was unaffected. The immunosuppression was unrelated to the time between stressor application and sacrifice, in that the reduced PFC response was evident both 24 and 48 h after stressor application, and reduced serum antibody titers (IgG) were evident 1 week after stressor exposure. The reduction of the PFC response was dependent on the severity of the stressor, but was not related to stressor controllability, being evident after both escapable and inescapable shock. It appears that stressful events may profoundly influence the immune response but the time between antigen administration and subsequent exposure to a stressor is critical in determining whether such an effect will be evident.

Animals↗

PubMed1988

Stressor-provoked behavioral changes in six strains of mice.

Behavioral changes induced by inescapable shock were examined in six strains of mice. Exposure to shock provoked time-dependent disturbances of shuttle escape performance. In some strains the shock treatment did not affect escape performance, whereas in others profound performance deficits were evident. The inescapable shock treatment likewise induced strain-dependent alterations of performance in a forced-swim task. In most instances the shock treatment initially provoked invigorated responding, but in other strains the shock had no effect or depressed active responding. Finally, Y-maze spontaneous alteration performance was not affected by the shock treatment, although a strain-dependent increase of perseverative responses was evident. The occurrence of a stressor-induced deficit in one task in a particular strain of mouse was not predictive of behavioral alterations in a second task. These data are discussed with respect to animal models of depression and genetic differences associated with the response to stressors.

Animals↗