Changes in brain dopamine and acetylcholine release during and following stress are independent of the pituitary-adrenocortical axis

Impérato, Assunta; Puglisi-Allegra, Stefano; Casolini, Paola; Angelucci, L.

doi:10.1016/0006-8993(91)90384-8

Cited by 308 publications

(142 citation statements)

References 30 publications

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“…However, this scenario is unlikely because existing data regarding the effects of various stressors on ACh outflow in NAc are mixed, and the increases in ACh outflow due to such stressors were usually short lived (Imperato et al, 1991;Mark et al, 1996;Thiel et al, 1998), unlike the chronic elevation in basal ACh seen in the current study.…”

Section: Discussionmentioning

confidence: 65%

Fluoxetine Alleviates Behavioral Depression while Decreasing Acetylcholine Release in the Nucleus Accumbens Shell

Chau

Rada

Kim

et al. 2011

Neuropsychopharmacol

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Selective serotonin reuptake inhibitors, such as fluoxetine, have demonstrated the ability to alleviate behavioral depression in the forced swim test; however, the sites and mechanisms of their actions remain to be further elucidated. Previous studies have suggested that behavioral depression in the swim test is mediated in part by acetylcholine (ACh) stimulating the cholinergic M1 receptors in the nucleus accumbens (NAc) shell. The current study tested whether acute, local, and chronic, subcutaneous fluoxetine treatments increase escape motivation during the swim test while simultaneously lowering extracellular ACh in the NAc shell. Experiment 1: Fluoxetine (1.0 mM) infused unilaterally in the NAc shell for 40 min reduced extracellular ACh while simultaneously increasing swimming time. Experiment 2: Fluoxetine (0.2, 0.5, and 0.75 mM) infused bilaterally in the NAc shell on day 3 dose-dependently decreased immobility and increased the total escape attempts (swimming and climbing) compared with Ringer given on day 2. Experiment 3: Fluoxetine (0.5 mM) infused bilaterally in the NAc for 40 min did not affect activities in an open field. Experiment 4: Chronic systemic fluoxetine treatment decreased immobility scores and increased total escape attempt scores compared with control saline treatment. In all, 14 days after the initial swim test, basal extracellular ACh in the shell was still elevated in the saline-treated group, but not in the fluoxetine-treated group. In summary, these data suggest that one of the potential mechanisms by which fluoxetine alleviates behavioral depression in the forced swim test may be to suppress cholinergic activities in the NAc shell.

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Section: Discussionmentioning

confidence: 65%

Fluoxetine Alleviates Behavioral Depression while Decreasing Acetylcholine Release in the Nucleus Accumbens Shell

Chau

Rada

Kim

et al. 2011

Neuropsychopharmacol

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“…The influential role of the NET in regulating DA overflow in the mPFC is further supported by a study resulting in significant DA increase after infusion of selective NET blocker desipramine (Gresch et al 1995). Interestingly, several studies suggest that changes in DA release during and following stress are not affected by andrenolectomy (Imperato et al 1991), or by 6-OH-DA lesions of the LC (Kawahara et al 1999).…”

Section: Brief Stress Attenuates the Da Response When Administered 2 mentioning

confidence: 89%

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Marsteller

Gerasimov

Schiffer

et al. 2002

Neuropsychopharmacology

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“…It is important to note that rat serum lacks the specific binding protein, α-1-acid glycoprotein, for RU-38486, thereby limiting its diffusion across the blood-brain barrier (23). Accordingly, the concentration of RU-38486 reaching the rat brain after systemic administration is only 28% of the serum levels (23), which may explain why Imperato et al (24) failed to observe any effect of RU-38486 when examining the role of GRs in stress-evoked DA efflux in the mPFC.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid receptors in the prefrontal cortex regulate stress-evoked dopamine efflux and aspects of executive function

Butts¹,

Weinberg

Young³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

158

123

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Enhanced dopamine efflux in the prefrontal cortex is a well-documented response to acute stress. However, the underlying mechanism(s) for this response is unknown. Using in vivo microdialysis, we demonstrate that blocking glucocorticoid receptors locally within the rat prefrontal cortex results in a reduction in stress-evoked dopamine efflux. In contrast, blocking glucocorticoid receptors in the ventral tegmental area did not affect stress-evoked dopamine efflux in the prefrontal cortex. Additionally, local administration of corticosterone into the prefrontal cortex increased prefrontal dopamine efflux. The functional impact of enhanced dopamine efflux evoked by acute stress was demonstrated using a cognitive task dependent on the prefrontal cortex and sensitive to impairment in working memory. Notably, stress-induced impairments in cognition were attenuated by blockade of glucocorticoid receptors in the prefrontal cortex. Taken together, these data demonstrate that glucocorticoids act locally within the prefrontal cortex to modulate mesocortical dopamine efflux leading to the cognitive impairments observed during acute stress.

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Changes in brain dopamine and acetylcholine release during and following stress are independent of the pituitary-adrenocortical axis

Cited by 308 publications

References 30 publications

Fluoxetine Alleviates Behavioral Depression while Decreasing Acetylcholine Release in the Nucleus Accumbens Shell

Fluoxetine Alleviates Behavioral Depression while Decreasing Acetylcholine Release in the Nucleus Accumbens Shell

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Glucocorticoid receptors in the prefrontal cortex regulate stress-evoked dopamine efflux and aspects of executive function

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