Biomedical subjects

H Anisman

Publications and source records attributed to H Anisman.

At least 91 records · Page 5Linked to original sources

PubMed1994

Central catecholamine alterations induced by stressor exposure: analyses in recombinant inbred strains of mice.

Stressors increase plasma corticosterone concentrations and the turnover of norepinephrine (NE) and dopamine (DA) in some brain regions. However, appreciable interindividual and interstrain differences exist in this respect. The present investigation assessed the NE and DA changes induced by uncontrollable footshock in the BALB/cByJ and C57BL/6ByJ mice and seven recombinant inbred strains. Stressor exposure indeed provoked strain dependent alterations of plasma corticosterone, hypothalamic and mesocortical NE, as well as mesocortcolimbic DA. The profile of stressor effects in the recombinant strains with respect to the NE alterations, the mesocortical DA changes, as well as plasma corticosterone was commensurate with a polygenic mode of inheritance. The data were related to behavioral changes induced by stressors in these strains of mice, as well as to the contribution of the brain amines to stressor-induced behavioral changes.

Animals↗

PubMed1994

Cytokine-specific central monoamine alterations induced by interleukin-1, -2 and -6.

Cytokine-specific alterations of monoamine activity were evident in the hypothalamus, hippocampus and prefrontal cortex 2 h following peripheral administration of recombinant interleukin (IL)-1 beta, IL-2 and IL-6 (200 ng, i.p.) in male, BALB/c mice. IL-1 induced the broadest range of neurochemical changes, affecting central norepinephrine (NE), serotonin (5-HT) and dopamine (DA) activity. In particular, IL-1 enhanced NE turnover in the hypothalamus and hippocampus, 5-HT turnover in the hippocampus and prefrontal cortex (owing to increased utilization and reduced content of the transmitters in these brain regions), and enhanced DA utilization in the prefrontal cortex. IL-6 increased 5-HT and DA activity in the hippocampus and prefrontal cortex in a manner similar to IL-1, but failed to affect central NE activity. Moreover, IL-2 increased hypothalamic NE turnover (reflecting a profound increase in NE utilization) and enhanced DA turnover in the prefrontal cortex, but did not influence central 5-HT activity. Hence, these cytokines differentially altered neurochemical activity in brain regions that mediate neuroimmune interactions and that are influenced by physical and psychological stressors. In addition to the neurochemical changes, plasma corticosterone concentrations were profoundly enhanced in IL-1-treated animals, but not significantly altered by IL-2 or IL-6 treatment. The IL-1-induced corticosterone elevations did not significantly correlate with alterations of hypothalamic NE activity.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Influence of change from grouped to individual housing on a T-cell-dependent immune response in mice: antagonism by diazepam.

Transferring CD-1 mice from grouped to individual housing and then maintaining them individually resulted in a decline in the peak IgM plaque-forming cell (PFC) response to sheep red blood cells (SRBCs). However, the immunosuppression was dependent on the amount of time mice were maintained individually. In particular, individual housing for 5-10 days prior to SRBC inoculation and for 4 days following inoculation resulted in a suppression of the splenic PFC response and serum antibody titers. Shorter periods of individual housing (4 days following inoculation) did not provoke the immunosuppression. Likewise, following more protracted individual housing (15-30 days prior to inoculation) the immunosuppression was not evident. Inasmuch as daily treatment with an anxiolytic, diazepam (1.0 mg/kg), antagonized the suppression induced by 5 days of individual housing, it was suggested that the change from group to individual housing and then maintenance of animals individually acted much like a stressor to induce the immunosuppression.

Animals↗

PubMed1994

Norepinephrine and serotonin alterations following chronic stressor exposure: mouse strain differences.

Exposure to acute uncontrollable foot shock influenced the levels and utilization of norepinephrine (NE) and serotonin (5-HT) in several brain regions. These effects varied between the BALB/cByJ and C57BL/6J mouse strains, with the former displaying more pronounced amine variations. Following repeated exposure to foot shock over 15 days, the decline of NE associated with an acute stressor was abrogated. In the hypothalamus, this was accompanied by high MHPG accumulation, suggesting that the increased NE stemmed from a compensatory increase in synthesis. In the locus coeruleus and prefrontal cortex the accumulation of MHPG declined with repeated exposure, possibly suggesting moderation in utilization. In animals exposed to a chronic unpredictable stressor regimen, the NE decline in the hypothalamus was precluded, but pronounced NE reductions were still evident in the locus coeruleus and prefrontal cortex. The data are related to behavioral impairments associated with stressor application, as well as to the particular vulnerability of BALB/cByJ mice to stressor-induced behavioral impairments.

Animals↗

PubMed1993

Acute and chronic stressor effects on the antibody response to sheep red blood cells.

Exposure to inescapable foot-shock 72 h following immunization with sheep red blood cells resulted in a marked suppression of the peak splenic immunoglobulin (Ig)M plaque-forming cell response and plasma antibody titers in CD-1 mice. However, the nature of this effect was influenced by the animal's stressor history. In particular, if mice were initially exposed to a single stressor session immediately or 24 h following antigen treatment subsequent reexposure to the stressor (72 h following inoculation) did not provoke the immunosuppression. Moreover, reexposure to the stressor-related cues elicited a marked immunoenhancement. In contrast, if animals were exposed to a single stressor session 48 h prior to inoculation then later reexposure to the stressor-related cues provoked an immunosuppression. Among mice that had been exposed to a repeated stressor regimen on successive days prior to inoculation, the immunosuppression ordinarily elicited by an acute stressor was absent. Indeed, chronic stressor exposure typically favored potentiation of the immune response. However, the immunofacilitation elicited by the chronic stressor treatment likely was unrelated to the immunoenhancing effects of pairing a stressor with antigenic challenge.

Acute Disease↗

PubMed1993

Escape deficits induced by uncontrollable foot-shock in recombinant inbred strains of mice.

Although uncontrollable stressors reliably induce numerous behavioral disturbances, considerable interindividual variability exists in this respect. Inasmuch as genetic factors may be fundamental in determining vulnerability to stressor effects, the present investigation assessed alterations in escape performance following exposure to uncontrollable foot-shock in the BALB/cByJ and C57BL/6ByJ mice and seven recombinant inbred strains. Exposure to uncontrollable foot-shock disrupted shuttle escape performance in a strain-specific manner; however, any differences due to gender were not particularly remarkable. The profile of stressor effects in the recombinant strains (i.e., performance deficits greater, lesser or intermediate to the progenitor strains) suggest that the stressor effects on escape performance may be subserved by two or more genetic determinants. The findings are related to central mechanisms that may potentially account for strain differences.

Animals↗

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↗