Dopaminergic regulation of cortical acetylcholine release

Day, Jamie C.; Fibiger, Hans C.

doi:10.1002/syn.890120405

Cited by 110 publications

(39 citation statements)

References 55 publications

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“…These results are consistent with previous work in which 5-HT4 agonists have been shown to increase ACh release in the PFC and 5-HT4 antagonists have been shown to attenuate the stimulatory effect of p-choloramphetamine and indeloxazine, a 5-HT releasing agent, on cortical ACh release (Yamaguchi et al, 1997a, Yamaguchi et al, 1997bConsolo et al, 1994). Moreover, activation of D1 receptors previously has been reported to increase ACh release in the PFC and antagonism of D1 receptors attenuates amphetamine-induced ACh release in the PFC (Damsma et al, 1990;Day and Fibiger, 1992;Imperato et al, 1993). To date, the localization of the D1 and 5-HT4 receptors mediating the stimulatory effect of MDMA on cortical ACh release is unknown.…”

Section: Cholinergic Neuronssupporting

confidence: 92%

“…Additionally, many psychostimulant drugs (e.g., amphetamine, cocaine, nicotine, methylphenidate) have been shown to increase ACh release in the cortex and hippocampus (Day and Fibiger, 1992;Imperato et al, 1993;Reid et al, 1993;Taguchi et al, 1998;Arnold et al, 2001). Inasumuch as cortical ACh may function in attentional processing (Sarter et al, 2003), it can be suggested that the stimulatory effect of these drugs of abuse on ACh release in the PFC contributes to the enhanced processing of drug associated environmental cues that accompany drug dependence.…”

Section: Cholinergic Neuronsmentioning

confidence: 99%

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Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons

Gudelsky

Yamamoto

2008

Pharmacology Biochemistry and Behavior

122

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Abstract3,4-Methylenedioxymethamphetamine (MDMA) is an amphetamine derivative and a popular drug of abuse that exhibits mild hallucinogenic and rewarding properties and engenders feelings of connectedness and openness. The unique psychopharmacological profile of this drug of abuse most likely is derived from the property of MDMA to promote the release of dopamine and serotonin (5-HT) in multiple brain regions. The present review highlights primarily data from studies employing in vivo microdialysis that detail the actions of MDMA on the release of these neurotransmitters. Data from in vivo microdialysis experiments indicate that MDMA, like most amphetamine derivatives, increases the release of dopamine in the striatum, n. accumbens and prefrontal cortex. However, the release of dopamine evoked by MDMA in each of these brain regions appears to be modulated by concomitantly released 5-HT and the subsequent activation of 5-HT2A/C or 5-HT2B/C receptors. In addition to its stimulatory effect on the release of monoamines, MDMA also enhances the release of acetylcholine in the striatum, hippocampus and prefrontal cortex, and this cholinergic response appears to be secondary to the activation of histaminergic, dopaminergic and/or serotonergic receptors. Beyond the acute stimulatory effect of MDMA on neurotransmitter release, MDMA also increases the extracellular concentration of energy substrates, e.g., glucose and lactate in the brain. In contrast to the acute stimulatory actions of MDMA on the release of monoamines and acetylcholine, the repeated administration of high doses of MDMA is thought to result in a selective neurotoxicity to 5-HT axon terminals in the rat. Additional studies are reviewed that focus on the alterations in neurotransmitter responses to pharmacological and physiological stimuli that accompany MDMA-induced 5-HT neurotoxicity.

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Section: Cholinergic Neuronssupporting

confidence: 92%

Section: Cholinergic Neuronsmentioning

confidence: 99%

Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons

Gudelsky

Yamamoto

2008

Pharmacology Biochemistry and Behavior

122

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“…Second, D1-mediated DA control of cortical ACh release involves distant but not local activation of D1 receptors. 19,20 Furthermore, in our hands blockade of a1-NE receptors by prazosin (1 mg/kg) effectively reversed cortical ACh, but not cortical DA efflux elicited by atomoxetine (data not shown). Alternatively, the atomoxetine-induced ACh release could involve an integrated mechanism operating only when parallel D1-DA and a1-NE signals temporally and spatially coincide.…”

Section: Discussionmentioning

confidence: 60%

Procholinergic and memory enhancing properties of the selective norepinephrine uptake inhibitor atomoxetine

et al. 2005

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Atomoxetine has been approved by the FDA as the first new drug in 30 years for the treatment of attention deficit/hyperactivity disorder (ADHD). As a selective norepinephrine uptake inhibitor and a nonstimulant, atomoxetine has a different mechanism of action from the stimulant drugs used up to now for the treatment of ADHD. Since brain acetylcholine (ACh) has been associated with memory, attention and motivation, processes dysregulated in ADHD, we investigated the effects of atomoxetine on cholinergic neurotransmission. We showed here that, in rats, atomoxetine (0.3-3 mg/kg, i.p.), -increases in vivo extracellular levels of ACh in cortical but not subcortical brain regions. The marked increase of cortical ACh induced by atomoxetine was dependent upon norepinephrine a-1 and/or dopamine D1 receptor activation. We observed similar increases in cortical and hippocampal ACh release with methylphenidate (1 and 3 mg/kg, i.p.) -currently the most commonly prescribed medication for the treatment of ADHD -and with the norepinephrine uptake inhibitor reboxetine (3-30 mg/kg, i.p.). Since drugs that increase cholinergic neurotransmission are used in the treatment of cognitive dysfunction and dementias, we also investigated the effects of atomoxetine on memory tasks. We showed that, consistent with its cortical procholinergic and catecholamine-enhancing profile, atomoxetine (1-3 mg/kg, p.o.) significantly ameliorated performance in the object recognition test and the radial arm-maze test.

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“…A relationship between ACh release from the cerebral cortex, hippocampus, and striatum and locomotor activity, considered a measure of behavioral arousal, was reported by Day et al (1991), and a similar correlation was also found by Mizuno et al (1991). However, Day and Fibiger (1992), Moore et al (1992), and Thiel et al (1998b) did not confirm this correlation. It is therefore important to define whether changes in ACh release from the cerebral cortex and hippocampus are always associated with, and in some way related to, motor activity or conditions exist in which increases in ACh release unrelated to motor activity take place.…”

Section: Ach Release and Motor Activitymentioning

confidence: 53%

Changes in Acetylcholine Extracellular Levels During Cognitive Processes: Table 1.

Pepeu

Giovannini²

2004

Learn. Mem.

180

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Measuring the changes in neurotransmitter extracellular levels in discrete brain areas is considered a tool for identifying the neuronal systems involved in specific behavioral responses or cognitive processes. Acetylcholine (ACh) is the first neurotransmitter whose diffusion from the central nervous system was investigated and whose extracellular levels variations were correlated to changes in neuronal activity. This was done initially by means of the cup technique and then by the microdialysis technique. The latter, notwithstanding some technical limitations, makes it possible to detect variations in extracellular levels of ACh in unrestrained, behaving animals. This review summarizes and discusses the results obtained investigating the changes in ACh release during performance of operant tasks, exposition to novel stimuli, locomotor activity, and the performance of spatial memory tasks, working memory, and place preference memory tasks. Activation of the forebrain cholinergic system has been demonstrated in many tasks and conditions in which the environment requires the animal to analyze novel stimuli that may represent a threat or offer a reward. The sustained cholinergic activation, demonstrated by high levels of extracellular ACh observed during the behavioral paradigms, indicates that many behaviors occur within or require the facilitation provided by the cholinergic system to the operation of pertinent neuronal pathways.Acetylcholine (ACh) is the first neurotransmitter whose diffusion from the central nervous system was investigated and whose extracellular levels variations were correlated to changes in neuronal activity. ACh outflow from the spinal cord was detected by Bulbring and Burn (1941) during nerve stimulation, and the first attempts to demonstrate ACh outflow from the intact cortex were made 50 years ago. The purpose was to demonstrate whether ACh had a role in the CNS, and the theoretical approach was the same used in the previous decade for demonstrating the neurotransmitter role of ACh in the peripheral nervous system (Burn 1968). Using the cup technique and the leech bioassay, MacIntosh and Oboring (1955) demonstrated in the dog that ACh release was related to the spontaneous electrical activity of the cortex. The cup was formed by a small cylinder exerting a slight pressure over the meninges, filled with Ringer solution containing a cholinesterase inhibitor. No ACh could be detected in the absence of the inhibitor. The method was perfected by Mitchell (1953), and a description of the procedure with an analysis of the early literature reporting the changes in ACh release induced by stimulation of peripheral nerves, specific brain areas, and drugs can be found in reviews by Pepeu (1973), and Moroni and Pepeu (1984).The first question asked was whether ACh diffusing from the brain into the cortical cup originated from cholinergic nerve endings and whether changes in its extracellular levels were expressions of changes in the activity of the cholinergic nerve endings under the cup. The answer ...

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Dopaminergic regulation of cortical acetylcholine release

Cited by 110 publications

References 55 publications

Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons

Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons

Procholinergic and memory enhancing properties of the selective norepinephrine uptake inhibitor atomoxetine

Changes in Acetylcholine Extracellular Levels During Cognitive Processes: Table 1.

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