Withdrawal from IV cocaine "binges" in rats: ultrasonic distress calls and startle

Mutschler, Nicole H.; Miczek, Klaus A.

doi:10.1007/s002130050497

Cited by 75 publications

(60 citation statements)

References 28 publications

(47 reference statements)

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“…This is consistent with the effect of repeated amphetamine treatment which produces locomotor sensitization but not augmentation of PPI deficits (Druhan et al 1998). Repeated cocaine treatment also produced a nonsignificant rise (61%) in startle response to Pulse stimuli following challenge with either cocaine or saline (Table 1), an effect which might reflect withdrawal-induced anxiety (Sarnyai 1998;Mutschler and Miczek 1998). Since this effect was characterized by proportional changes in Pulse-and Prepulse-induced responses, it is unlikely that increased startle amplitude biased the magnitude of PPI observed.…”

Section: Resultsmentioning

confidence: 96%

The Disruptive Effect of Cocaine on Prepulse Inhibition Is Prevented by Repeated Administration in Rats

Byrnes

2000

Neuropsychopharmacology

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Section: Resultsmentioning

confidence: 96%

The Disruptive Effect of Cocaine on Prepulse Inhibition Is Prevented by Repeated Administration in Rats

Byrnes

2000

Neuropsychopharmacology

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“…In addition, rats in the previous study were subjected to restraint stress the day after their final injection of cocaine. This period probably reflects a time when the animals are experiencing the psychological effects of drug withdrawal, (Markou and Koob 1991;Mutschler and Miczek 1998) and compensatory homeostatic mechanisms are engaged to restore a post-binge equilibrium (Koob et al 1997). In contrast, animals in the present study were allowed to recover from the drug for two weeks, and thus tested at a time at when the effects of psychostimulant sensitization are most pronounced (Paulson et al 1991).…”

Section: Discussionmentioning

confidence: 99%

Exposure to Repeated, Intermittent d-amphetamine Induces Sensitization of HPA Axis to a Subsequent Stressor

Barr

Hofmann²,

Weinberg

et al. 2002

Neuropsychopharmacology

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Previous studies have demonstrated that exposure to psychostimulant drugs can produce a lasting crosssensitization to the behavioral effects of stress. The main purpose the present study was, therefore, to determine the effects of psychostimulant cross-sensitization on the stressinduced release of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Rats were given a series of injections of d -amphetamine or vehicle in a regimen (Goldstein 1990;Henry 1992;Folkow 1997;Sapolsky et al. 2000). Consequently, a complex set of homeostatic mechanisms, which include endocrine, metabolic, immune and neural defensive reactions, has evolved to ensure that the harmful effects of most stressors rarely exceed an organism's capacity to cope with them (Johnson et al. 1992;McEwen 1998). In certain instances, however, these homeostatic mechanisms become compromised, such as after chronic hypothalamicpituitary-adrenal (HPA) axis activation or prolonged stress, and the noxious effects of stressors then become exaggerated (McEwen 1998;Brown et al. 1999). The emerging concept of a physiological and psychological cost involved with chronically heightened neuroendocrine arousal to environmental stimuli, often referred to as "allostatic load", is seeing increased interest as an imporDepartment of Psychology (AMB, CEH, JW, AGP), Department of Anatomy (CEH, JW), Department of Psychiatry (AGP), University of British Columbia, Vancouver, Canada Address correspondence to: Anthony G. Phillips, Department of Psychology, 2136 West Mall, University of British Columbia, Vancouver, Canada, V6T1Z4, Tel.: 604-822-3245, Fax: 604-822-6923, E-mail: aphillips@cortex.psych.ubc.ca Received August 31, 2000; revised March 28, 2001; accepted June 5, 2001.Online publication: 6/6/01 at www.acnp.org/citations/Npp 060601130 N EUROPSYCHOPHARMACOLOGY 2002 -VOL . 26 , NO . 3 D -amphetamine Induces Sensitization of HPA Axis 287 tant factor in the development of many forms of human disease (McEwen 2000;Koob and Le Moal 2001). A wealth of evidence suggests that an increased reactivity to stressors and/or the inability to respond effectively and appropriately to stressors plays an important role in the development and expression of many forms of mental illness (Ehlert and Straub 1998;Kreek and Koob 1998;Dohrenwend 2000;Heim et al. 2000). Clearly, a better understanding of the underlying neurobiology of this sensitivity to stressors may help in the prophylaxis and treatment of these disorders.Animal and human studies have demonstrated that environmental manipulation, such as exposure to alcohol or stress during the pre-and early postnatal period (Liang and Boyce 1993;Weinberg et al. 1996;Day et al. 1998), can modify an organism's response to stressors. Such manipulations may lead to an increased reactivity to stressors ("sensitization"), which can be expressed both behaviourally and neurochemically (Pitman et al. 1990;Badiani et al. 1996;Pani et al. 2000). One form of sensitization involves the capacity of psychostimulant drugs, such as cocaine and d -amp...

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“…Rats exhibit transient cocaine withdrawal reactions for several days after its termination (Mutschler and Miczek, 1998). E xtinction training has been shown to accelerate recovery from cocaine withdrawal (Schmidt et al, 2001).…”

Section: Self-administration Trainingmentioning

confidence: 99%

Dissociable Effects of Lidocaine Inactivation of the Rostral and Caudal Basolateral Amygdala on the Maintenance and Reinstatement of Cocaine-Seeking Behavior in Rats

Kantak¹,

Black²,

Valencia³

et al. 2002

J. Neurosci.

184

155

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Cocaine addiction is a chronically relapsing brain disease, but its neural basis is not yet well understood. Clinical reports underscore the possible importance of associative processes for regulating at least some aspects of cocaine addiction. The present study reports the effects of reversible lidocaine-induced inactivation of rostral basolateral amygdala (rBLA) and caudal basolateral amygdala (cBLA) regions on the maintenance and reinstatement of drug-seeking behavior in rats trained to selfadminister 1 mg/kg cocaine under a second order schedule of drug delivery. Both regions of the basolateral amygdala were investigated because they have dissociable effects on cognitive task performance. Results demonstrated that after selfadministration training and a period of extinction and abstinence, lidocaine inactivation of the rBLA and cBLA attenuated the reinstatement of drug-seeking behavior induced by cocaine-associated cues examined in conjunction with a single priming injection of cocaine. In contrast, lidocaine inactivation of only the rBLA blocked reinstatement of drug-seeking behavior induced by cocaine-associated cues examined alone. Additional differences were shown during cocaine maintenance testing where inactivation of only the cBLA attenuated drugseeking behavior. Drug intake was not altered. Thus, the rBLA and cBLA appear to selectively and dissociably regulate drugseeking behavior under conditions of cocaine abstinence (cue-induced reinstatement) and repeated cocaine use (maintenance), respectively. These findings suggest that the basolateral amygdala may be more functionally heterogeneous than commonly thought for regulating drug-seeking behavior. The basis for this dissociation might be related to neuroanatomical connections of the rBLA and cBLA with segregated, but parallel, corticostriatalpallidothalamic circuits.Key words: caudal basolateral amygdala; cocaine; drug cues; drug prime; lidocaine; maintenance; reinstatement; rostral basolateral amygdala Cocaine addiction is a chronically relapsing brain disease. Clinical reports suggesting a link between limbic and cortical structures in mediating drug use and craving underscore the possible importance of associative processes for regulating some aspects of drug addiction. Imaging studies demonstrate that craving induced by cocaine-associated cues in abstinent addicts produces specific changes in patterns of activation in the amygdala, anterior cingulate, basal ganglia, dorsolateral prefrontal cortex, and cerebellum (Grant et al., 1996;Maas et al., 1998;Childress et al., 1999;Wang et al., 1999). Furthermore, Breiter et al. (1997) showed that craving and rush induced by a cocaine priming injection also modulate patterns of activation in memory circuits important for regulating cognitive functions. Animal studies examining cognitive aspects of addiction-related behavior are emerging, particularly in reference to the basolateral amygdala.An associative conditioning process involving mechanisms within the basolateral amygdala is thought to underlie the...

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Withdrawal from IV cocaine "binges" in rats: ultrasonic distress calls and startle

Cited by 75 publications

References 28 publications

The Disruptive Effect of Cocaine on Prepulse Inhibition Is Prevented by Repeated Administration in Rats

The Disruptive Effect of Cocaine on Prepulse Inhibition Is Prevented by Repeated Administration in Rats

Exposure to Repeated, Intermittent d-amphetamine Induces Sensitization of HPA Axis to a Subsequent Stressor

Dissociable Effects of Lidocaine Inactivation of the Rostral and Caudal Basolateral Amygdala on the Maintenance and Reinstatement of Cocaine-Seeking Behavior in Rats

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