Exposure to chronic mild stress alters thresholds for lateral hypothalamic stimulation reward and subsequent responsiveness to amphetamine

Lin, Don S.; Bruijnzeel, Adrie W.; Schmidt, P; Markou, Athina

doi:10.1016/s0306-4522(02)00366-4

Cited by 48 publications

(36 citation statements)

References 45 publications

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“…The hypersensitivity of brain reward systems that emerged during the post-nicotine phase of the experiment closely resembles the reward hypersensitivity that emerges in food-restricted rats undergoing a period of negative energy balance (Blundell and Herberg, 1968;Carr and Wolinsky, 1993;Carr, 1996;Lin et al, 2002). This reward hypersensitivity during food deprivation is hypothesized to increase the appetitive value of food and thereby drive food intake (Herberg and Blundell, 1967;Fulton et al, 2000).…”

Section: Discussionmentioning

confidence: 82%

Nicotine Self-Administration Acutely Activates Brain Reward Systems and Induces a Long-Lasting Increase in Reward Sensitivity

Kenny

Markou

2005

Neuropsychopharmacol

242

204

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Nicotine is a major component of tobacco smoke contributing to the initiation and persistence of the harmful tobacco habit in human smokers. The reinforcing effects of nicotine likely arise through its ability to stimulate brain circuitry mediating the detection and experiencing of natural rewards. Nevertheless, remarkably little is known concerning the acute or long-lasting actions of nicotine on brain reward systems in vivo. Here, we investigated the effects of intravenously self-administered nicotine (0.03 mg/kg/infusion, free base) on the sensitivity of brain reward systems, reflected in alterations of intracranial self-stimulation (ICSS) thresholds in rats. Rats selfadministered nicotine during 1 or 12 h daily sessions, with reward thresholds assessed 1 h before and 15 min after each self-administration session. Control rats remained nicotine naïve throughout. Nicotine self-administration increased the sensitivity of brain reward systems, detected by post-nicotine lowering of reward thresholds in 1 and 12 h rats. This nicotine-enhanced sensitivity of reward systems was reversed by the high-affinity nicotinic receptor antagonist dihydro-b-erythroidine (DHbE; 3 mg/kg). Surprisingly, nicotine-induced excitation of reward systems persisted for at least 36 days after nicotine self-administration had ceased. Overall, these data demonstrate that rats can voluntarily consume quantities of nicotine sufficient to increase the sensitivity of brain reward systems, an action likely crucial in establishing and maintaining the nicotine habit. Moreover, self-administered nicotine resets the sensitivity of reward systems to a new increased level, thereby imprinting an indelible 'memory' of its effects in reward systems, an action that so far appears unique to nicotine among drugs of abuse.

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Section: Discussionmentioning

confidence: 82%

Nicotine Self-Administration Acutely Activates Brain Reward Systems and Induces a Long-Lasting Increase in Reward Sensitivity

Kenny

Markou

2005

Neuropsychopharmacol

242

204

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“…Conversely, the NMDA antagonist ketamine, which primarily 902 depresses ICSS in the absence of explicit stress, also failed to reverse depression of ICSS induced by socialdefeat stress in mice (Donahue et al, 2014). Other research has shown that repeated stress can enhance amphetamine-induced facilitation of ICSS (Lin et al, 2002), whereas effects of cocaine and THC were not altered by olfactory bulbectomy or repeated stress, respectively (Slattery et al, 2007;Fokos and Panagis, 2010). Together, these results illustrate the potential for differential effects of stress as a modulator of abuserelated drug effects in ICSS procedures, but given the prominent role of stress as a risk factor in drug abuse (Neisewander et al, 2012;Volkow et al, 2012), this is a relatively undeveloped theme of research.…”

Section: A Statesmentioning

confidence: 91%

“…Food and water deprivation resulted in robust facilitation of ICSS. Multiple other studies soon replicated the general phenomenon of food deprivation-induced facilitation of ICSS (Olds, 1958a;Hodos and Valenstein, 1960;Katz et al, 1978), although relatively robust levels of food deprivation leading to more than 10% weight loss may be required to produce this effect (Lin et al, 2002).…”

Section: A Statesmentioning

confidence: 95%

“…Regimens of repeated stress, including chronic, intermittent exposure to stressors like restraint and soiled bedding (Moreau et al, 1992(Moreau et al, , 1994 or social defeat (Donahue et al, 2014), have been reported to depress basal ICSS, and ICSS was also depressed by an olfactory bulbectomy model of depression (Slattery et al, 2007). However, other regimens of chronic stress had no effect on ICSS (Fokos and Panagis, 2010) or produced effects that varied across time or across test subjects (Nielsen et al, 2000;Lin et al, 2002). A likely source of these discrepancies is variability in the stress regimens across studies.…”

Section: A Statesmentioning

confidence: 99%

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Intracranial Self-Stimulation to Evaluate Abuse Potential of Drugs

Negus

Miller

2014

Pharmacological Reviews

203

271

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“…Increased occurrence of substance abuse among depressed patients is largely thought to be to counteract the anhedonic aspects of depression 197 Rewarding effects of amphetamine correlate with severity of depression 198 Behavioral studies in mice Increased sensitivity to amphetamine following chronic stress and olfactory bulbectomy in rats 199,200 Murine models of depression JF Cryan and C Mombereau behavioral output) relevant to the disease state rather than an entire syndrome. 204,205 In parallel, similar urgings have been made for dissecting the DSM IV criteria of various psychiatric disorders into specific endophenotypes and use this modified classification as a basis for investigating novel treatments and underlying genes for specific endophenotypes.…”

Section: Does the Paradigm Meet Validity Criteria?mentioning

confidence: 99%

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice

2004

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The ability to modify mice genetically has been one of the major breakthroughs in modern medical science affecting every discipline including psychiatry. It is hoped that the application of such technologies will result in the identification of novel targets for the treatment of diseases such as depression and to gain a better understanding of the molecular pathophysiological mechanisms that are regulated by current clinically effective antidepressant medications. The advent of these tools has resulted in the need to adopt, refine and develop mouse-specific models for analyses of depression-like behavior or behavioral patterns modulated by antidepressants. In this review, we will focus on the utility of current models (eg forced swim test, tail suspension test, olfactory bulbectomy, learned helplessness, chronic mild stress, drug-withdrawal-induced anhedonia) and research strategies aimed at investigating novel targets relevant to depression in the mouse. We will focus on key questions that are considered relevant for examining the utility of such models. Further, we describe other avenues of research that may give clues as to whether indeed a genetically modified animal has alterations relevant to clinical depression. We suggest that it is prudent and most appropriate to use convergent tests that draw on different antidepressant-related endophenotypes, and complimentary physiological analyses in order to provide a program of information concerning whether a given phenotype is functionally relevant to depressionrelated pathology.

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Exposure to chronic mild stress alters thresholds for lateral hypothalamic stimulation reward and subsequent responsiveness to amphetamine

Cited by 48 publications

References 45 publications

Nicotine Self-Administration Acutely Activates Brain Reward Systems and Induces a Long-Lasting Increase in Reward Sensitivity

Nicotine Self-Administration Acutely Activates Brain Reward Systems and Induces a Long-Lasting Increase in Reward Sensitivity

Intracranial Self-Stimulation to Evaluate Abuse Potential of Drugs

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice

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