Brain neurotransmitter systems mediating behavioral deficits produced by inescapable shock treatment in rats

Płaźnik, Adam; Tamborska, E; Hauptmann, M; Bidziński, Andrzej; Kostowski, Wojciech

doi:10.1016/0006-8993(88)90972-9

Cited by 61 publications

(20 citation statements)

References 52 publications

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“…Although the FST is most widely used as a behavioral screen for antidepressant efficacy, previous studies have also demonstrated that factors associated with human depression including chronic stress, inescapable stress, dysregulated monoamine function, and elevated glucocorticoids produce immobility in the FST (Hwang et al, 1999;Johnson et al, 2006;Plaznik et al, 1988;Prince and Anisman, 1984). The efficacy of desipramine validates the FST as a measure of depression in the present study.…”

Section: Discussionsupporting

confidence: 77%

“…Factors that reduce neurogenesis, such as stress and dysregulation of monoamines (Jacobs et al, 2000), have been shown to increase depression-like behavior (Hwang et al, 1999;Johnson et al, 2006;Plaznik et al, 1988;Prince and Anisman, 1984) as measured by the forced swim test (FST) in rodents (Porsolt et al, 1977). Major classes of antidepressants including tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors show efficacy in the FST (Cryan et al, 2005;Dalvi and Lucki, 1999;Lucki et al, 2001) and increase hippocampal neurogenesis .…”

Section: Introductionmentioning

confidence: 99%

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Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

Stevenson

Schroeder

Nixon

et al. 2008

Neuropsychopharmacol

133

102

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Alcoholism and depression show high degrees of comorbidity. Clinical evidence also indicates that depression that emerges during abstinence from chronic alcohol use has a greater negative impact on relapse than pre-existing depression. Although no single neurobiological mechanism can account for the behavioral pathologies associated with these devastating disorders, converging evidence suggests that aspects of both alcoholism and depression are linked to reductions in hippocampal neurogenesis. Here, we report results from a novel preclinical behavioral model showing that abstinence from voluntary alcohol drinking leads to the emergence of depressionlike behavior and reductions in neurogenesis. C57BL/6J mice were allowed to self-administer ethanol (10% v/v) vs H 2 O in the home cage for 28 days. Alcohol was then removed for 1 or 14 days, and mice were tested in the forced swim test to measure depression-like behavior. After 14 days, but not 1 day of abstinence from alcohol drinking, mice showed a significant increase in depression-like behavior. The significant increase in depression-like behavior during abstinence was associated with a reduction in proliferating cell nuclear antigen (PCNA) and doublecortin (DCX) immunoreactivity in the dentate gyrus of the hippocampus indicating that both the number of proliferating neural progenitor cells (NPC) and immature neurons were reduced, respectively. The number of NPCs that were labeled with bromo-deoxyuridine (BrdU) at the beginning of alcohol exposure was not altered indicating that survival of NPCs is not linked to abstinence-induced depression. Chronic treatment (14 days) with the antidepressant desipramine during abstinence prevented both the emergence of depression-like behavior and the reduction in hippocampal neurogenesis indicating that abstinence-induced depression is associated with structural plasticity in the hippocampus. Overall, the results of this study support the conclusion that profound functional (ie behavioral) and structural changes occur during abstinence from alcohol use and suggest that antidepressant treatment may alleviate some of these pathological neurobehavioral adaptations.

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

Stevenson

Schroeder

Nixon

et al. 2008

Neuropsychopharmacol

133

102

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“…80,81 Antidepressants, such as imipramine and desipramine, have been shown to improve the learned helplessness behavior in rats. 77,81,82 Interestingly, Plaznik et al 83 suggested that, besides decreased GABAergic activity, also noradrenergic, serotoninergic, and dopaminergic hypoactivity, and catecholaminergic hyperactivity contribute to the helplessness behavior. Also, adrenergic blockers, such as prazosin and penbutolol, diminished the reversal of depressive-like behavior by muscimol and imipramine-like drugs, 73 suggesting that noradrenergic receptors may play an important role in the antidepressant-like profile of GABA agonists.…”

Section: Gaba and The Pathophysiology Of Mood Disordersmentioning

confidence: 99%

GABAergic dysfunction in mood disorders

et al. 2003

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“…Further, it is well known that the recurrence phenomenon is also caused by stress. Several studies have shown that previous exposure to stress results in an increased passive behavioural response when the subject is subsequently confronted with a novel stressful situation (Anisman et al, 1978;Katz et al, 1981;Kennett et al, 1985;Cancela et al, 1991;Murua & Molina, 1991;Molina et al, 1994 test and reduced activity in response to a novel environment (Weiss et al, 1981;Plaznik et al, 1988;Van Dijken et al, 1992). The conditioned emotional response can be measured in terms of inhibition of locomotor activity and the inhibition of lever pressing behaviour for a food or water reward produced by stimuli previously paired with stress (Brady, 1956;Hunt, 1961).…”

Section: Effects Of Antipsychotics On the Pcp-induced Enhancement Of mentioning

confidence: 99%

Enhancement of immobility in a forced swimming test by subacute or repeated treatment with phencyclidine: a new model of schizophrenia

Noda

Yamada

Furukawa

et al. 1995

British J Pharmacology

210

124

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1 Immobility induced by forced swimming is well known as an animal model of depression. To develop an animal model for the negative symptoms of schizophrenia, in particular the depressive symptoms, the effect of phencyclidine (PCP) on immobility in the forced swimming test was investigated in mice, since PCP produces such negative symptoms in humans.2 Repeated treatment with PCP (10 mg kg-' day-', s.c., once a day for 14 days) prolonged the immobility time in the forced swimming test 24 h after the final injection compared with saline treatment; the effect was not obtained by single or 5 treatments with PCP (10 mg kg-', s.c.), or by repeated treatment with methamphetamine (0.5 and 1 mg kg-' day-', s.c., once a day for 14 days). 3 The enhancing effect of PCP (10 mg kg-' day-', s.c.) on the immobility persisted for at least 21 days after the withdrawal of the drug. 5 The enhancing effect of PCP on the immobility was attenuated by ritanserin (3 and 10 mg kg-', p.o.), risperidone (0.3 mg kg-', p.o.), and clozapine (3 and 10 mg kg-', p.o.), whereas haloperidol (0.3 and 1 mg kg-', p.o.) had no effect. 6 These results suggest that the enhancement of immobility in the forced swimming test brought about by repeated PCP treatment could be used as a model of the negative symptoms, particularly the depression, of schizophrenia. This effect of PCP appeared to be mediated, at least in part, via 5-HT2A receptors.

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Brain neurotransmitter systems mediating behavioral deficits produced by inescapable shock treatment in rats

Cited by 61 publications

References 52 publications

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

GABAergic dysfunction in mood disorders

Enhancement of immobility in a forced swimming test by subacute or repeated treatment with phencyclidine: a new model of schizophrenia

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