Apparent lack of a dopaminergic-cholinergic link in the rat nucleus accumbens septi-tuberculum olfactorium

Consolo, S.; Ladinsky, H.; Bianchi, S.; Ghezzi, D.

doi:10.1016/0006-8993(77)91029-0

Cited by 43 publications

(4 citation statements)

References 30 publications

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“…The present finding of almost identical types of associations between TH-and CAT-labeled neurons in the NAS and caudate-putamen nuclei supports physiological evidence indicating similarities (Mao et al. 1977) rather than differences between these two regions (Consolo et al, 1977;Stadler et al. 1975).…”

Section: Similarities In Caudate-putamen Nuclei and Nassupporting

confidence: 88%

Spiny neurons lacking choline acetyltransferase immunoreactivity are major targets of cholinergic and catecholaminergic terminals in rat striatum

Pickel

Chan

1990

J of Neuroscience Research

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The ultrastructural substrate for functional interactions between intrinsic cholinergic neurons and catecholaminergic afferents to the caudate-putamen nucleus and nucleus accumbens septi (NAS) was investigated immunocytochemically. Single sections of glutaraldehyde-fixed rat brain were processed 1) for the immunoperoxidase labeling of a rat monoclonal antibody against the acetylcholine-synthesizing enzyme choline acetyltransferase (CAT) and 2) for the immunoautoradiographic localization of a rabbit polyclonal antiserum against the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH). The ultrastructural morphology and cellular associations did not significantly differ in the caudate-putamen versus NAS. Immunoperoxidase reaction for CAT versus NAS. Immunoperoxidase reaction for CAT was seen in perikarya, dendrites, and terminals, whereas immunoautoradiography for TH was in terminals. The perikarya and dendrites immunolabeled for CAT were large, sparsely spiny, and postsynaptic mainly to unlabeled axon terminals. Only 2-3% of the CAT-labeled terminals (n = 136) and less than 1% of the TH-labeled terminals (n = 86) were apposed to, or formed synapses with, perikarya or dendrites immunoreactive for CAT. Most unlabeled and all labeled terminals formed symmetric synapses. In the same sample, 18% of the CAT and 16% of the TH-labeled terminals were directly apposed to each other. Unlabeled dendritic shafts received the major (40% for CAT versus 23% for TH) synaptic input from cholinergic terminals, while unlabeled spines received the major (47% for TH versus 23% for CAT) synaptic input from catecholaminergic terminals. Neither the unlabeled dendrites or spines received detectable convergent input from CAT and TH-labeled terminals. Thirteen percent of the CAT-labeled and 14% of TH-labeled terminals were in apposition to unlabeled terminals forming asymmetric, presumably excitatory, synapses with unlabeled dendritic spines. We conclude that in both the caudate-putamen and NAS cholinergic and catecholaminergic terminals 1) form symmetric, most likely inhibitory, synapses primarily with non-cholinergic neurons, 2) differentially synapse on shafts or spines of separate dendrites, and 3) have axonal appositions suggesting the possibility of presynaptic physiological interactions. These results support the hypothesis that the cholinergic-dopaminergic balance in striatal function may be mediated through inhibition of separate sets of spiny projection neurons with opposing excitatory and inhibitory functions.

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Section: Similarities In Caudate-putamen Nuclei and Nassupporting

confidence: 88%

Spiny neurons lacking choline acetyltransferase immunoreactivity are major targets of cholinergic and catecholaminergic terminals in rat striatum

Pickel

Chan

1990

J of Neuroscience Research

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“…This is borne out by the observation that after 6-hydroxydopamine treatment, degenerating dopaminergic nerve terminals which make contact with dendritic processes of interneurones that stain positively for choline acetyltransferase (acetyl-CoA: choline 0-acetyltransferase; EC 2.3.1.6) are seen (Hattori et al, 1976). The interaction between dopamine and acetylcholine appears to be specific for the striatum, as chlorpromazine and haloperidol have no effect on acetylcholine levels (Consolo et al, 1977) or output from the nucleus accumbens (Stadler et al, 1975).…”

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confidence: 96%

Dopamine Inhibition of the Release of Endogenous Acetylcholine from Corpus Striatum and Cerebral Cortex in Tissue Slices and Synaptosomes: A Presynaptic Response?

Belleroche

Coutinho‐Netto

Bradford

1982

Journal of Neurochemistry

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The effect of dopamine on the release of endogenous acetylcholine from striatal slices and synaptosomes and from cerebral cortex synaptosomes was studied. K+ (56 mM) and veratrine (75 microM) increased the release of acetylcholine from striatal slices by 3.7 and 3.3 times the resting release, respectively. The effect of veratrine was completely abolished by tetrodotoxin (1 microM). Dopamine (10(-6) to 10(-3) M) reduced the K+-evoked release of acetylcholine from striatal slices in a dose-dependent manner. The resting release of acetylcholine was also significantly reduced by dopamine. Apomorphine (20 microM) significantly reduced the K+-evoked release of acetylcholine, and both this effect and the inhibition due to dopamine (1 mM) were significantly antagonised by chlorpromazine (20 microM). Dopamine had a similar effect on the release of acetylcholine from striatal synaptosome beds; the resting release was depressed 32% by the presence of dopamine (1 mM). A greater effect of dopamine was seen on the release of acetylcholine from cerebral cortex synaptosome beds, the resting release being reduced by 54% and the K+-evoked release by 29%. These results are discussed in terms of the possible role of presynaptic dopamine receptors in controlling the release of acetylcholine and the magnitude of their contribution compared with that of the postsynaptic dopamine receptor.

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“…Various lines of evidence suggest that the nigro-striatal dopaminergic neurons inhibit the striatal cholinergic neurons (Trabucchi et al 1975;Choi and Roth 1978), while a dopaminergic-cholinergic link is lacking in the mesolimbic area such as the nucleus accumbens and olfactory tubercle (Consolo et al 1977(Consolo et al , 1978. There is also accumulated evidence that the mesoseptal dopaminergic neurons seem to play an inhibitory role in the control of the septal-hippocampal cholinergic neurons (Robinson et al 1979;Costa et al 1983).…”

Section: Discussionmentioning

confidence: 99%

Involvement of septal and striatal dopamine D-2 receptors in yawning behavior in rats

et al. 1986

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A behavioral study was performed in an attempt to understand the neuronal mechanisms involved in yawning behavior in rats. Subcutaneous injections of low doses of apomorphine (0.05-0.25 mg/kg) or piribedil (0.2-1.0 mg/kg), which preferentially activate presynaptic dopamine autoreceptors at those doses, evoked yawning. Marked yawning responses were also elicited by both 3-PPP (5-20 mg/kg, SC) and TL-99 (1-2 mg/kg, SC). SK & F 38393, a dopamine D-1 receptor agonist, at doses ranging from 0.1 to 8.0 mg/kg (SC) induced neither yawning nor stereotypy. However, bromocriptine (0.5-32.0 mg/kg, SC), a dopamine D-2 receptor agonist, induced yawning for which the dose-response curves showed a bell-shaped form. After a higher dose of 32 mg/kg (SC) bromocriptine, some rats occasionally showed sniffing and sawdust chewing. Yawning responses induced by systemic injection of apomorphine, piribedil, 3-PPP or bromocriptine were wholly suppressed after treatment with sulpiride (10 mg/kg SC), a dopamine D-2 receptor antagonist. Bilateral injections of apomorphine (20 micrograms/side X 2), piribedil (100 micrograms/side X 2) or 3-PPP (50, 100 micrograms/side X 2) into the striatum or septum also elicited marked yawning. The results indicate that low doses of apomorphine, piribedil, 3-PPP, TL-99 or bromocriptine elicit yawning by stimulating dopamine D-2 receptors and striatal and septal dopaminergic systems may be related to the occurrence of yawning behavior.

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Apparent lack of a dopaminergic-cholinergic link in the rat nucleus accumbens septi-tuberculum olfactorium

Cited by 43 publications

References 30 publications

Spiny neurons lacking choline acetyltransferase immunoreactivity are major targets of cholinergic and catecholaminergic terminals in rat striatum

Spiny neurons lacking choline acetyltransferase immunoreactivity are major targets of cholinergic and catecholaminergic terminals in rat striatum

Dopamine Inhibition of the Release of Endogenous Acetylcholine from Corpus Striatum and Cerebral Cortex in Tissue Slices and Synaptosomes: A Presynaptic Response?

Involvement of septal and striatal dopamine D-2 receptors in yawning behavior in rats

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