Alterations in Brain Norepinephrine Metabolism Induced by Environmental Stimuli Previously Paired with Inescapable Shock

Cassens, Geraldine; Roffman, Mark; Kuruc, Alvin; Orsulak, Paul J.; Schildkraut, Joseph J.

doi:10.1126/science.7403874

Cited by 257 publications

(53 citation statements)

References 22 publications

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“…Along with the present findings, this suggests that cocaine-conditioned cues induce retrieval by activating dHipp-and PL-mPFC-projecting LC neurons, leading to b-AR activation in these regions. Indeed, NE is released upon conditioned cue exposure (Cassens et al, 1980), which activates dHipp and PL-mPFC b-ARs (Otis et al, 2013;Pedarzani and Storm, 1993). This activation enhances neural excitability and excitatory synaptic activity within dHipp (Hopkins and Johnston, 1984;Pedarzani and Storm, 1993) and PL-mPFC (Ji et al, 2008;Otis et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Otis

Fitzgerald

Mueller

2013

Neuropsychopharmacol

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Retrieval of drug-associated memories is critical for maintaining addictive behaviors, as presentation of drug-associated cues can elicit drug seeking and relapse. Recently, we and others have demonstrated that b-adrenergic receptor (b-AR) activation is necessary for retrieval using both rat and human memory models. Importantly, blocking retrieval with b-AR antagonists persistently impairs retrieval and provides protection against subsequent reinstatement. However, the neural locus at which b-ARs are required for maintaining retrieval and subsequent reinstatement is unclear. Here, we investigated the necessity of dorsal hippocampus (dHipp) b-ARs for drugassociated memory retrieval. Using a cocaine conditioned place preference (CPP) model, we demonstrate that local dHipp b-AR blockade before a CPP test prevents CPP expression shortly and long after treatment, indicating that dHipp b-AR blockade induces a memory retrieval disruption. Furthermore, this retrieval disruption provides long-lasting protection against cocaine-induced reinstatement. The effects of b-AR blockade were dependent on memory reactivation and were not attributable to reconsolidation disruption as blockade of b-ARs immediately after a CPP test had little effect on subsequent CPP expression. Thus, cocaine-associated memory retrieval is mediated by b-AR activity within the dHipp, and disruption of this activity could prevent cue-induced drug seeking and relapse long after treatment.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Otis

Fitzgerald

Mueller

2013

Neuropsychopharmacol

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“…The stimuli become associated with the reinforcement during pretraining and training, and thus are capable of eliciting a response-a truncated conditioned reflex, in Pavlovian terms (see Kupalov, 1961). This conditioned response, elicited during the reminder period, may include an increase in norepinephrine activity (such a conditioned NE response to environmental cues previously associated with footshock has recently been demonstrated by Cassens, Roffman, Kurac, Orsulak, & Schildkraut, 1980). Several lines of research have suggested that the noradrenergic forebrain projections are intimately involved in the regulation of attentional mechanisms (Robbins & Everitt, 1982;Segal & Bloom, 1976;Waterhouse & Woodward, 1980).…”

Section: Discussionmentioning

confidence: 99%

Background stimuli as a reminder after spontaneous forgetting: Role of duration of cuing and cuing-test interval

Deweer

Sara

1984

Animal Learning & Behavior

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With a relatively complex maze, reliable forgetting is seen clearly when the training-to-test interval is 25 days. This forgetting is demonstrated by longer time to run the maze and by an increase in the number of errors and retracings from the last training trials to the first test trial. In this case, forgetting is a lapse, not a loss, since performance attains the last training trial level at a subsequent test. Furthermore, a reminder-a 90-sec exposure to background stimuli in the experimental room just prior to the test trial-that does not in itself contain sufficient information to facilitate performance in naive animals, significantly improves maze performance in rats that have "forgotten," even on the first test trial. Two additional experiments were aimed at assessing the role of time and duration of pretest cuing. In the first experiment, the animals were presented the reminder (90 sec in duration) at different times before the test trial. The results show that this reminder significantly alleviates forgetting only when presented just prior to the test, and is less effective when given 1 or 24 h before the test. In the second experiment. contextual cues, which were presented just prior to testing in all experimental groups, varied in duration. The results showed that (1) animals given the reminder treatment for only 10 sec perform at the same level as controls; (2) cuing for 30 sec and especially for 90 sec alleviates forgetting; and (3) a longer exposure to background stimuli (300 sec) leads to intermediate levels of performance, probably due to a partial extinction of the cue value of these stimuli.

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“…[83][84][85][86] These amine alterations typically persist for only a few hours, depending on the stressor severity and several organismic variables (eg, age, species). 84,87,88 However, re-exposure to a mild stressor enhances the utilization of hypothalamic NE 89,90 and mesocortical DA (sensitization effect), [91][92][93] even if the re-exposure involves a different stressor. [94][95][96] Since humans typically encounter chronic, intermittent and unpredictable stressors, it may be more relevant to assess the effects of such regimens in animal studies.…”

Section: Biological Aspects Of Dysthymiamentioning

confidence: 99%

Dysthymia: a review of pharmacological and behavioral factors

et al. 2000

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Although dysthymia, a chronic, low-grade form of depression, has a morbidity rate as high as that of major depression, and increases the risk for major depressive disorder, limited information is available concerning the etiology of this illness. In the present report we review literature concerning the biological and characterological features of dysthymia, the effectiveness of antidepressant treatments, the influence of stressors in the precipitation and maintenance of the disorder, and both quality of life and psychosocial correlates of the illness. We also provisionally suggest that dysthymia may stem from disturbances of neuroendocrine and neurotransmitter functioning (eg, corticotropin releasing hormone and arginine vasopressin within the hypothalamus, or alternatively monoamine variations within several extrahypothalamic sites), and may also involve cytokine activation. The central disturbances may reflect phenotypic variations of neuroendocrine processes or sensitization of such mechanisms. It is suggested that chronic stressor experiences or stressors encountered early in life lead to the phenotypic neurochemical alterations, which then favor the development of the dysthymic state. Owing to the persistence of the neurochemical disturbances, vulnerability to double depression is increased, and in this instance treatment with antidepressants may attenuate the symptoms of major depression but not those of the basal dysthymic state. Moreover, the residual features of depression following treatment may be indicative of underlying neurochemical disturbances, and may also serve to increase the probability of illness recurrence or relapse. Molecular Psychiatry (2000) 5, 242-261.

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Alterations in Brain Norepinephrine Metabolism Induced by Environmental Stimuli Previously Paired with Inescapable Shock

Cited by 257 publications

References 22 publications

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Background stimuli as a reminder after spontaneous forgetting: Role of duration of cuing and cuing-test interval

Dysthymia: a review of pharmacological and behavioral factors

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