Exposure to chronic stress increases the locomotor response to cocaine and the basal levels of corticosterone in adolescent rats

Lepsch, Lucília Brochado; Gonzalo, L. A.; Magro, Fjb; DeLucia, Roberto; Scavone, Cristóforo; Planeta, Cleópatra da Silva

doi:10.1080/13556210500269366

Cited by 59 publications

(52 citation statements)

References 31 publications

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“…In addition, rats with increased HPA reactivity induced by prenatal stress or by the absence of neonatal handling show an early decline of cognitive functions associated with the hippocampus, as well as increased propensity to self-administer drugs such as amphetamine and cocaine (55). In addition, exposure to both chronic restraint and unpredictable stress increased cocaine-induced locomotion and basal corticosterone plasma levels and chronic unpredictable stress also displayed the largest locomotor response following a challenge dose with cocaine compared with control and chronic restraint stress groups (60). Drug abuse is associated with changes in brain function and neurodegenerative processes, which, for some drugs, have been shown to be associated with the induction of apoptotic/necrotic cell death (Lepsch LB, , , , , Munhoz CD, Kawamoto EM, Lima LS, Scavone C, unpublished results).…”

Section: Stress Aging and Neurodegenerative Diseasesmentioning

confidence: 99%

Stress-induced neuroinflammation: mechanisms and new pharmacological targets

Munhoz

García‐Bueno

Madrigal

et al. 2008

Braz J Med Biol Res

185

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Stress is triggered by numerous unexpected environmental, social or pathological stimuli occurring during the life of animals, including humans, which determine changes in all of their systems. Although acute stress is essential for survival, chronic, longlasting stress can be detrimental. In this review, we present data supporting the hypothesis that stress-related events are characterized by modifications of oxidative/nitrosative pathways in the brain in response to the activation of inflammatory mediators. Recent findings indicate a key role for nitric oxide (NO) and an excess of pro-oxidants in various brain areas as responsible for both neuronal functional impairment and structural damage. Similarly, cyclooxygenase-2 (COX-2), another known source of oxidants, may account for stress-induced brain damage. Interestingly, some of the COX-2-derived mediators, such as the prostaglandin 15d-PGJ 2 and its peroxisome proliferator-activated nuclear receptor PPARγ, are activated in the brain in response to stress, constituting a possible endogenous anti-inflammatory mechanism of defense against excessive inflammation. The stress-induced activation of both biochemical pathways depends on the activation of the N-methyl-Daspartate (NMDA) glutamate receptor and on the activation of the transcription factor nuclear factor kappa B (NFκB). In the case of inducible NO synthase (iNOS), release of the cytokine TNF-α also accounts for its expression. Different pharmacological strategies directed towards different sites in iNOS or COX-2 pathways have been shown to be neuroprotective in stress-induced brain damage: NMDA receptor blockers, inhibitors of TNF-α activation and release, inhibitors of NFκB, specific inhibitors of iNOS and COX-2 activities and PPARγ agonists. This article reviews recent contributions to this area addressing possible new pharmacological targets for the treatment of stress-induced neuropsychiatric disorders.

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Section: Stress Aging and Neurodegenerative Diseasesmentioning

confidence: 99%

Stress-induced neuroinflammation: mechanisms and new pharmacological targets

Munhoz

García‐Bueno

Madrigal

et al. 2008

Braz J Med Biol Res

185

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“…Following chronic cocaine selfadministration schedules, alterations to arousal-related dopaminergic and noradrenergic systems have been reported including increased densities of norepinephrine transporter binding in the hypothalamic nuclei and entorhinal cortex (Beveridge et al, 2005) as well as changes in the density of D1 and D2 receptors within striatal regions (Nader et al, 2002;Moore et al, 1998). Pre-exposure to cocaine in rats has also been associated with long-term sensitization of the corticotrophin-releasing factor (CRF) systems (Erb et al, 2003) and stress exposure has been shown to influence locomotor sensitization to cocaine (Lepsch et al, 2005;Haile et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Enhanced Sensitivity to Stress and Drug/Alcohol Craving in Abstinent Cocaine-Dependent Individuals Compared to Social Drinkers

Fox

Hong

Siedlarz

et al. 2007

Neuropsychopharmacol

165

164

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Chronic exposure to cocaine is associated with neuroadaptions in stress and reward circuits that may increase susceptibility to relapse. We examined whether there are alterations in stress response and craving in abstinent cocaine-dependent individuals compared with a demographically matched group of non-addicted socially drinking community controls. Forty treatment-engaged abstinent cocaine patients (17F/23M) and 40 controls (19F/21M) were exposed to a brief 5 min guided imagery of individually calibrated stressful situations, personal drug/alcohol-related situation and a neutral-relaxing situation, one imagery per session, presented in random order. Craving, anxiety, emotion rating scales, and physiological measures were assessed. Cocaine patients reported significantly higher and more persistent stress-and cue-induced drug/alcohol craving, negative emotions, and physiological responses compared with social drinkers. In cocaine patients, stress-and cue-induced drug craving was accompanied by increased anger, fear, sadness, heart rate, and SBP. Controls reported minimal stress-induced craving and only increases in anxiety and SBP during stress exposure. Cue-induced alcohol craving was accompanied only by an increase in relaxed state. Females reported increased stress-induced anxiety and sadness compared with males, while males were emotionally and physiologically more reactive in the cue condition. These findings are the first to document functional alterations in stress-and reward-related affect and physiology in recently abstinent cocaine patients that is marked by an enhanced sensitivity to stress-and drug-related cue exposure. These data suggest that recovery from chronic cocaine abuse could be hampered by a hyper-responsive stress-and drug-craving state that increases cocaine relapse susceptibility.

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“…Second, when exposed to a novel environment, LN and HN offspring exhibited more activity than NN offspring. High locomotor responsiveness in a novel environment results from a prior history of stress (31) and is associated with increased susceptibility for drug self-administration (39). Third, LN and HN offspring had exaggerated ACTH and Cort responses to restraint stress compared with NN offspring.…”

Section: Discussionmentioning

confidence: 99%

Dietary sodium manipulation during critical periods in development sensitize adult offspring to amphetamines

McBride

Culver²,

Flynn³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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McBride SM, Culver B, Flynn FW. Dietary sodium manipulation during critical periods in development sensitize adult offspring to amphetamines. Am J Physiol Regul Integr Comp Physiol 295: R899 -R905, 2008. First published July 9, 2008 doi:10.1152/ajpregu.00186.2008This study examined critical periods in development to determine when offspring were most susceptible to dietary sodium manipulation leading to amphetamine sensitization. Wistar dams (n ϭ 6 -8/group) were fed chow containing low (0.12% NaCl; LN), normal (1% NaCl; NN), or high sodium (4% NaCl; HN) during the prenatal or early postnatal period (birth to 5 wk). Offspring were fed normal chow thereafter until testing at 6 mo. Body weight (BW), blood pressure (BP), fluid intake, salt preference, response to amphetamine, open field behavior, plasma adrenocorticotropin hormone (ACTH), plasma corticosterone (Cort), and adrenal gland weight were measured. BW was similar for all offspring. Offspring from the prenatal and postnatal HN group had increased BP, NaCl intake, and salt preference and decreased water intake relative to NN offspring. Prenatal HN offspring had greater BP than postnatal HN offspring. In response to amphetamine, both prenatal and postnatal LN and HN offspring had increased locomotor behavior compared with NN offspring. In a novel open field environment, locomotion was also increased in prenatal and postnatal LN and HN offspring compared with NN offspring. ACTH and Cort levels 30 min after restraint stress and adrenal gland weight measurement were greater in LN and HN offspring compared with NN offspring. These results indicate that early life experience with low-and high-sodium diets, during the prenatal or early postnatal period, is a stress that produces long-term changes in responsiveness to amphetamines and to subsequent stressors. behavioral sensitization; psychomotor stimulant; salt appetite DRUGS OF ABUSE and natural motivators or stimuli, such as sodium deprivation or stress, activate similar neural circuits involved in mediating reward and drive-related responses (12,18,28). One of the main systems believed to be involved in triggering these behaviors is the mesocorticolimbic dopamine system, with dopaminergic projections traveling from the midbrain ventral tegmental area to the nucleus accumbens and other limbic and cortical areas (38, 44). With repeated exposure to both amphetamines and sodium deprivation, behavioral sensitization develops (38, 48). Sensitization can be described as an increased and enduring response to the same stimuli with repeated exposures (38). With amphetamines, sensitization manifests itself as increased locomotor behavior (21, 53). Repeated amphetamine treatment leading to sensitization is associated with morphological changes in nucleus accumbens neurons, including increased spine density, dendritic length, and dendritic branching (46). Repeated sodium deprivation can lead to an enduring daily increase in the ingestion of hypertonic NaCl in otherwise sodium-replete rats (48), and a history of sodium deple...

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Exposure to chronic stress increases the locomotor response to cocaine and the basal levels of corticosterone in adolescent rats

Cited by 59 publications

References 31 publications

Stress-induced neuroinflammation: mechanisms and new pharmacological targets

Stress-induced neuroinflammation: mechanisms and new pharmacological targets

Enhanced Sensitivity to Stress and Drug/Alcohol Craving in Abstinent Cocaine-Dependent Individuals Compared to Social Drinkers

Dietary sodium manipulation during critical periods in development sensitize adult offspring to amphetamines

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