Increase in striatal acetylcholine by picrotoxin in the rat: Evidence for a gabergic-dopaminergic-cholinergic link

Ladinsky, H.; Consolo, S.; Bianchi, S.; Jori, A.

doi:10.1016/0006-8993(76)90191-8

Cited by 86 publications

(8 citation statements)

References 45 publications

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“…In a number of brain regions, low doses of GABA agonists increased acetylcholine levels (Scatton and Bartholini, 1982), probably via stimulation of GABA A receptors located on cholinergic cells. Earlier studies had suggested that the action of GABA was indirect, with dopamine suggested as an intermediary (Ladinsky et al, 1976; Javoy et al, 1977). However, lesions of the dopaminergic and serotonergic pathways did not affect GABA mediated responses (Scatton and Bartholini, 1982), indicating that they could play a minor role.…”

Section: Interactions With Intrinsic Neurotransmittersmentioning

confidence: 99%

Cholinergic connectivity: it's implications for psychiatric disorders

Scarr

Gibbons

Neo

et al. 2013

Front. Cell. Neurosci.

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Acetylcholine has been implicated in both the pathophysiology and treatment of a number of psychiatric disorders, with most of the data related to its role and therapeutic potential focusing on schizophrenia. However, there is little thought given to the consequences of the documented changes in the cholinergic system and how they may affect the functioning of the brain. This review looks at the cholinergic system and its interactions with the intrinsic neurotransmitters glutamate and gamma-amino butyric acid as well as those with the projection neurotransmitters most implicated in the pathophysiologies of psychiatric disorders; dopamine and serotonin. In addition, with the recent focus on the role of factors normally associated with inflammation in the pathophysiologies of psychiatric disorders, links between the cholinergic system and these factors will also be examined. These interfaces are put into context, primarily for schizophrenia, by looking at the changes in each of these systems in the disorder and exploring, theoretically, whether the changes are interconnected with those seen in the cholinergic system. Thus, this review will provide a comprehensive overview of the connectivity between the cholinergic system and some of the major areas of research into the pathophysiologies of psychiatric disorders, resulting in a critical appraisal of the potential outcomes of a dysregulated central cholinergic system.

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Section: Interactions With Intrinsic Neurotransmittersmentioning

confidence: 99%

Cholinergic connectivity: it's implications for psychiatric disorders

Scarr

Gibbons

Neo

et al. 2013

Front. Cell. Neurosci.

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show abstract

“…To test for GABA regulation either in the nigra (Ladinsky et al, 1976) or in the caudate (Scatton and Bartholini, 1980), picrotoxin was given prior to pargyline administration. This GABA antagonist facilitates an increase in dopamine-stimulated release induced by pargyline in the caudate nucleus without altering the effect of pargyline in the nucleus accumbens.…”

Section: Discussionmentioning

confidence: 99%

In vivo comparison of the regulation of releasable dopamine in the caudate nucleus and the nucleus accumbens of the rat brain

Kuhr¹,

Bigelow²,

Rm³

1986

J. Neurosci.

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In viva voltammetry has been used to measure the release of dopamine evoked by electrical stimulation of the medial forebrain bundle (MFB). Simultaneous measurements have been made with voltammetric-sensing electrodes ipsilateral to the stimulating electrode in the nucelus accumbens and the caudate nucleus of the anesthetized rat. During the stimulation, the species observed in both regions is voltammetrically identical to dopamine. Further evidence for the identity of dopamine is provided by anatomical, physiological, pharmacological, and postmortem data. Postmortem analysis of these brain regions after a single stimulation demonstrates that dopamine levels are unchanged, while dihydroxyphenylacetic acid (DOPAC) levels are increased in both regions. Systemic application of synthesis inhibitors results in a decrease in evoked release for each brain region. Amfonelic acid results in a restoration of stimulated release after synthesis inhibition. Evoked release is affected differently by pargyline in the two brain regions. The evoked release of dopamine is significantly elevated in the nucleus accumbens as a result of pargyline administration, but similar effects are not seen in the caudate nucleus. Tissue levels of dopamine are increased in both brain regions by pargyline, but the increase is significantly greater in the accumbens. Electrolytic lesions of the striatonigral pathway or systemic administration of picrotoxin eliminates the pargyline-induced difference in evoked release of dopamine. Amphetamine causes a reduction in stimulated release in the caudate nucleus with little effect on that observed in the nucleus accumbens. Administration of pargyline prior to amphetamine results in a diminution of release in both brain regions. Taken together, these data indicate that different factors affect regulation of the releasable pool of dopamine in the nucleus accumbens and caudate nucleus.Several major dopaminergic systems exist in the mammalian brain, including the nigrostriatal and mesolimbic systems. It is known that the mesolimbic system plays an important role in the regulation of normal brain function, and this role is distinct from that played by the nigrostriatal dopamine pathway (Mogenson and Yin, 1981;White and Wang, 1982). It has been shown by unit-recording techniques that these two regions respond in different manners to pharmacological stimuli thought to affect dopaminergic neurons (Rebec and Zimmerman, 1980; Reynolds et al., 1981). The behavioral responses elicited by electrical stimulation of these two pathways differ (van der Heyden, 1984). Lesions of the two regions also produce different behavioral responses (Kelly and Moore, 1976; Pycock and Marsden, 1978). Furthermore, anatomical differences have been shown at an ultrastructural level (Bouyer et al., 1984). A rec- Received June 10, 1985; revised Oct. 7, 1985; accepted Oct. 10, 1985. This work was supported by a grant from the National Science Foundation, Neurobiology Section.Correspondence should be addressed to R. M. Wigbtman, Department...

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“…Evidence has accumulated that GABA is involved in the regulation of other neuronal systems, such as dopaminergic (Dray, 1979;O'Neill, 1986) and cholinergic (Ferkany & Enna, 1980;Scatton & Bartholini, 1982;Miller & Richter, 1986) neurones. The major and extensive focus of studies of neurotransmitter interactions has been in the striatum (ST) and substantia nigra (SN) which are connected by the striatonigral GABAergic pathway and nigrostriatal dopaminergic pathway (Ladinsky et al, 1976;Dray, 1979;Ferkany & Enna, 1980). However, little is known concerning dopamine-GABA interactions within the cerebral cortex.…”

mentioning

confidence: 99%

“…The major and extensive focus of studies of neurotransmitter interactions has been in the striatum (ST) and substantia nigra (SN) which are connected by the striatonigral GABAergic pathway and nigrostriatal dopaminergic pathway (Ladinsky et al, 1976;Dray, 1979;Ferkany & Enna, 1980). However, little is known concerning dopamine-GABA interactions within the cerebral cortex.…”

mentioning

confidence: 99%

In vivo release of dopamine from rat striatum, substantia nigra and prefrontal cortex: differential modulation by baclofen

Santiago

Machado

Cano

1993

British J Pharmacology

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1 The effect of baclofen, a GABAB receptor agonist, on the release of dopamine from the striatum (ST), substantia nigra (SN) and prefrontal cortex (PFC) of the rat was examined by intracerebral microdialysis. 2 Perfusion of baclofen 50 LM did not affect the striatal release of dopamine. However, dopamine release was markedly reduced in the SN and PFC. 3 3,4-Dihydroxyphenylacetic acid and homovanillic acid output increased in the ST and decreased in the SN and PFC when baclofen was perfused through the microdialysis probe. 5-Hydroxyindoleacetic acid levels were not affected in any experimental condition by baclofen perfusion. 4 The results suggest that GABAB receptors modulate the release of dopamine in the SN and PFC, but do not affect the striatal release of dopamine, which indicates that the role of GABA receptor activation is different in the dopaminergic terminals of the ST and PFC.

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Increase in striatal acetylcholine by picrotoxin in the rat: Evidence for a gabergic-dopaminergic-cholinergic link

Cited by 86 publications

References 45 publications

Cholinergic connectivity: it's implications for psychiatric disorders

Cholinergic connectivity: it's implications for psychiatric disorders

In vivo comparison of the regulation of releasable dopamine in the caudate nucleus and the nucleus accumbens of the rat brain

In vivo release of dopamine from rat striatum, substantia nigra and prefrontal cortex: differential modulation by baclofen

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