Stress and adenosine: II. Adenosine analogs mimic the effect of inescapable shock on shuttle-escape performance in rats.

Minor, Thomas R.; Winslow, Jeffrey L.; Chang, Wei‐Chao

doi:10.1037//0735-7044.108.2.265

Cited by 20 publications

References 4 publications

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Stressor controllability and learned helplessness research in the United States: Sensitization and fatigue processes

Minor¹,

Hunter²

2002

Integrative Physiological & Behavioral Science

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Recent work in the learned helplessness paradigm suggests that neuronal sensitization and fatigue processes are critical to producing the behavioral impairment that follows prolonged exposure to an unsignaled inescapable stressor such as a series of electric tail shocks. Here we discuss how an interaction between serotonin (5-HT) and corticosterone (CORT) sensitizes GABA neurons early in the pretreatment session with inescapable shock. We propose that this process eventually depletes GABA, thus removing an important form of inhibition on excitatory glutamate transmission in the amygdala, hippocampus, and frontal cortex. When rats are re-exposed to shock during shuttle-escape testing 24 hrs later, the loss of inhibition (as well as other excitatory effects) results in unregulated excitation of glutamate neurons. This state of neuronal over-excitation rapidly compromises metabolic homeostasis. Metabolic fatigue results in compensatory inhibition by the nucleoside adenosine, which regulates neuronal excitation with respect to energy availability. The exceptionally potent form of inhibition associated with adenosine receptor activation yields important neuroprotective benefits under conditions of metabolic failure, but also precludes the processing of information in fatigued neurons. The substrates of adaptive behavior are removed; performance deficits ensue.

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Stressor controllability and learned helplessness research in the United States: Sensitization and fatigue processes

Minor¹,

Hunter²

2002

Integrative Physiological & Behavioral Science

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Cytokine-purine interactions in behavioral depression in rats

Minor

Huang²,

Foley

2003

Integrative Physiological & Behavioral Science

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This paper reviews recent findings from our laboratories concerning metabolic and immune mediators of behavioral depression in rats. Specifically, a single injection of 6 mg/kg of reserpine substantially increases behavioral depression, as evidenced by an increase in the amount of time spent floating by independent groups of rats tested for swim performance at various times during the next week. The behavioral impairment consists of two components. An early component emerges one hour after reserpine treatment and persists for about 24 hours. The deficit is not reversed by intracranial ventricular infusion of the receptor antagonist for interleukin-1beta (IL-1beta). A second, late-component deficit appears approximately 48 hours after reserpine treatment and recovers within a week. Late-component depression is reversed by central infusion of the IL-1beta receptor antagonist, and is mimicked by central infusion of the proinflammatory cytokine. Importantly, both early and late components of reserpine-induced depression and IL-1beta induced depression are reversed by a systemic injection of the highly selective A2A adenosine receptor antagonist 8-(3-Chlorostyryl) caffeine. These data are discussed in terms of the overlap in the conservation-withdrawal reaction during sickness, traumatic stress, and major depression and the regional contribution of purines and cytokines to the organization of this reaction in the brain.

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DPCPX, a selective adenosine A1 receptor antagonist, enhances the antidepressant-like effects of imipramine, escitalopram, and reboxetine in mice behavioral tests

Szopa

Poleszak

Bogatko

et al. 2018

Naunyn-Schmiedeberg's Arch Pharmacol

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The main goal of the present study was to evaluate the influence of the adenosine A1 receptor (A1R) antagonist — DPCPX — on depressive-like behavior in mice, as well as the effect of DPCPX on the activity of imipramine, escitalopram, and reboxetine, each at non-effective doses. The influence of DPCPX on behavior and its influence on the activity of selected antidepressants was evaluated in the forced swim test (FST) and the tail suspension test (TST) in mice. Locomotor activity was measured to verify and exclude false-positive data obtained in the FST and TST. Moreover, serum and brain concentrations of tested antidepressants were determined using HPLC. DPCPX, at doses of 2 and 4 mg/kg, exhibited antidepressant activity in the FST and TST, which was not related to changes in the spontaneous locomotor activity. Co-administration of DPCPX with imipramine, escitalopram, or reboxetine, each at non-active doses, significantly reduced the immobilization period in the FST and TST in mice, which was not due to the increase in locomotor activity. Both antagonists of 5-HT receptors (WAY 100635 and ritanserin) completely antagonized the effect elicited by DPCPX in the behavioral tests. Results of assessment of the nature of the interaction between DPCPX and test drugs show that in the case of DPCPX and imipramine or reboxetine, there were pharmacodynamic interactions, whereas the DPCPX-escitalopram interaction is at least partially pharmacokinetic in nature. Presented outcomes indicate that an inhibition of A1Rs and an increase of monoaminergic transduction in the CNS may offer a novel strategy for the development of antidepressant drugs.

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Stress and adenosine: II. Adenosine analogs mimic the effect of inescapable shock on shuttle-escape performance in rats.

Cited by 20 publications

References 4 publications

Stressor controllability and learned helplessness research in the United States: Sensitization and fatigue processes

Stressor controllability and learned helplessness research in the United States: Sensitization and fatigue processes

Cytokine-purine interactions in behavioral depression in rats

DPCPX, a selective adenosine A1 receptor antagonist, enhances the antidepressant-like effects of imipramine, escitalopram, and reboxetine in mice behavioral tests

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