Contribution of ventral tegmental area dopamine neurons to expression of conditional fear: Effects of electrical stimulation, excitotoxin lesions, and quinpirole infusion on potentiated startle in rats.

Borowski, Thomas; Kokkinidis, Larry

doi:10.1037/0735-7044.110.6.1349

Cited by 68 publications

(59 citation statements)

References 63 publications

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“…Furthermore, reduced dopaminergic signaling in the NAc is associated with emotional signs of nicotine withdrawal (Cryan et al, 2003;Paterson et al, 2007). Further confirmation that the mesolimbic dopaminergic system contributes to withdrawal from other addictive drugs would cohere with a growing body of literature demonstrating that it is also involved in a wide variety of aversive behaviors, including conditioned place aversion (Acquas et al, 1989;Calcagnetti and Schechter, 1991;Schechter and Meechan, 1994;Liu et al, 2008), fear conditioning (Borowski and Kokkinidis, 1996;Nader and LeDoux, 1999;Pezze and Feldon, 2004;Fadok et al, 2009;Muschamp et al, 2011), anxiety (Fride and Weinstock, 1988;Barrot et al, 2002;Barrot et al, 2005;Meloni et al, 2006;Rezayof et al, 2009;Richard and Berridge, 2011;Zweifel et al, 2011), intrinsic aversion to gustatory cues (Roitman et al, 2008), conditioned taste aversion Fenu et al, 2001), responses to stress (Geyer and Segal, 1974;Herman et al, 1982;Inglis and Moghaddam, 1999;Belda and Armario, 2009), and responses to nociceptive stimulation (Gear et al, 1999;Becerra et al, 2001;Barrot et al, 2002).…”

Section: Discussionmentioning

confidence: 86%

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Radke¹,

Gewirtz

2012

Neuropsychopharmacol

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A number of lines of evidence suggest that negative emotional symptoms of withdrawal involve reduced activity in the mesolimbic dopamine system. This study examined the contribution of dopaminergic signaling in structures downstream of the ventral tegmental area to withdrawal from acute morphine exposure, measured as potentiation of the acoustic startle reflex. Systemic administration of the general dopamine receptor agonist apomorphine or a cocktail of the D1-like receptor agonist SKF82958 and the D2-like receptor agonist quinpirole attenuated potentiated startle during morphine withdrawal. This effect was replicated by apomorphine infusion into the nucleus accumbens shell. Finally, apomorphine injection was shown to relieve startle potentiation during nicotine withdrawal and conditioned place aversion to morphine withdrawal. These results suggest that transient activation of the ventral tegmental area mesolimbic dopamine system triggers the expression of anxiety and aversion during withdrawal from multiple classes of abused drugs.

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Section: Discussionmentioning

confidence: 86%

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Radke¹,

Gewirtz

2012

Neuropsychopharmacol

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“…For example, lesions to the VTA were shown to inhibit fear-potentiated startle in rats [11]. Also, cocaine administered repeatedly over 5-7 days, but not acutely on a single day, facilitated LTP induction in VTA dopamine neurons [33].…”

Section: Discussionmentioning

confidence: 99%

Cocaine and Pavlovian fear conditioning: Dose–effect analysis

Wood

Fay

Sage

et al. 2007

Behavioural Brain Research

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Emerging evidence suggests that cocaine and other drugs of abuse can interfere with many aspects of cognitive functioning. The authors examined the effects of 0.1 -15 mg/kg of cocaine on Pavlovian contextual and cued fear conditioning in mice. As expected, pre-training cocaine dose-dependently produced hyperactivity and disrupted freezing. Surprisingly, when the mice were tested off-drug later, the group pre-treated with a moderate dose of cocaine (15 mg/kg) displayed significantly less contextual and cued memory, compared to saline control animals. Conversely, mice pre-treated with a very low dose of cocaine (0.1 mg/kg) showed significantly enhanced fear memory for both context and tone, compared to controls. These results were not due to cocaine's anesthetic effects, as shock reactivity was unaffected by cocaine. The data suggest that despite cocaine's reputation as a performance-enhancing and anxiogenic drug, this effect is seen only at very low doses, whereas a moderate dose disrupts hippocampus and amygdala-dependent fear conditioning. KeywordsHippocampus; Amygdala; Freezing; Memory A growing body of evidence supports the view that drugs of abuse interfere with many aspects of cognitive functioning. For example, cocaine use has been linked to deficits in such cognitive areas as attention, cognitive flexibility, and short-term and working memory [34,43]. However, these findings in humans are controversial as cocaine use is naturally confounded with many other variables [e.g. 23, 27, 31]. Some studies, in fact, provide evidence for enhancement of certain cognitive abilities in cocaine users [e.g. 27, 50]. Relatively few studies in animals have examined the effects of cocaine on learning outside of the realm of addiction (e.g. selfadministration, place preference, sensitization). Indeed, several studies have focused on the mechanisms underlying addiction, including structural plasticity [see 41 for review], but few have examined the acute, behavioral effects of cocaine in rodents on simple learning and memory paradigms. We believe that most researchers implicitly assume, as we once did, that cocaine, as a psychostimulant, would naturally enhance learning and memory. However, evidence now exists linking cocaine use with specific cognitive deficits [5,25,34,43] as well as with general problems such as unemployment [35]. Moreover, a view has emerged that addictive drugs such as cocaine may work by taking control of critical reinforcement-related learning and memory circuits in the brain [28]. If cocaine modulates such circuits, then it may 1 Address correspondence and reprint requests to: Suzanne C. Wood,

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“…While the impact of monoamine alterations on conditioned fear is far from clear, past studies investigating the influence of DA on cued conditioning suggest that decreases (Davis et al, 1993;Borowski and Kokkinidis, 1996;Munro and Kokkinidis, 1997), but not increases in DA mesolimbic activity may produce impairments. Concerning alterations in serotonergic activity, results obtained using the fear-potentiated startle paradigm have shown that systemic injections of buspirone, a partial 5-HT1A receptor agonist, block fear-potentiated startle Mansbach and Geyer, 1988;Risbrough et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Lesions of the habenula produce stress- and dopamine-dependent alterations in prepulse inhibition and locomotion

Heldt

Ressler

2006

Brain Research

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The habenula complex modulates the a ctivity of dopamine and serotonin systems in the brain. An important question remains whether there is a link between habenula dysfunction and monoaminerelated disorders, such as schizophrenia. In this study, we describe an interaction between habenula lesions and stress that produces long-lasting effects on behavior. Mice received control lesions or bilateral electrolytic lesions of the habenula and were tested for fear-potentiated startle and freezing measures of conditioned fear. They w ere also tested for prepulse inhibition (PPI) and locomotor activity in the presence or absence of a dopaminergic agonist (apomorphine) or an atypical antipsychotic with mixed dopamine/serotonin antagonist properties (clozapine). There were no detectable effects of habenula lesions on fear conditioning and no effects on PPI in the absence o f stress. However, following conditioned fear stress, habenula-lesioned animals showed decreased PPI which normalized with clozapine. Lesioned animals also showed diminished activity at baseline, with hyperlocomotion following apomorphine. These data support the hypothesis that the habenula may be normally involved in stress-dependent regulation of monoamine systems.

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Contribution of ventral tegmental area dopamine neurons to expression of conditional fear: Effects of electrical stimulation, excitotoxin lesions, and quinpirole infusion on potentiated startle in rats.

Cited by 68 publications

References 63 publications

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Cocaine and Pavlovian fear conditioning: Dose–effect analysis

Lesions of the habenula produce stress- and dopamine-dependent alterations in prepulse inhibition and locomotion

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