Temporal components of cholinergic terminal to dopaminergic terminal transmission in dorsal striatum slices of mice

Wang, Li; Zhang, Xiaoyu; Xu, Hua‐Dong; Zhou, Li; Jiao, Ruiying; Liu, Wei; Zhu, Feipeng; Kang, Xinjiang; Liu, Bin; Teng, Susanto; Wu, Qihui; Li, Mingli; Dou, Hongwei; Zuo, Panli; Wang, Changhe; Wang, Shirong; Zhou, Zhuan

doi:10.1113/jphysiol.2014.271825

Cited by 42 publications

(50 citation statements)

References 65 publications

(122 reference statements)

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“…4D; see ref. 28). The nAChRs antagonist dihydro-β-erythroidine hydrobromide (DHβE) (1 μM) selectively abolished the second component of the eDA transient and had no effect on the first component, causing a reduction of 46 ± 4% in the total peak of eDA transient (n = 5/2; t 4 = 11.25; P < 0.001; Fig.…”

Section: B6mentioning

confidence: 99%

Muscarinic regulation of dopamine and glutamate transmission in the nucleus accumbens

Shin

Adrover

Wess

et al. 2015

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

107

100

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Cholinergic transmission in the striatum functions as a key modulator of dopamine (DA) transmission and synaptic plasticity, both of which are required for reward and motor learning. Acetylcholine (ACh) can elicit striatal DA release through activation of nicotinic ACh receptors (nAChRs) on DA axonal projections. However, it remains controversial how muscarinic ACh receptors (mAChRs) modulate striatal DA release, with studies reporting both potentiation and depression of striatal DA transmission by mAChR agonists. This study investigates the mAChR-mediated regulation of release from three types of midbrain neurons that project to striatum: DA, DA/glutamate, and glutamate neurons. We found that M5 mAChRs potentiate DA and glutamate release only from DA and DA/glutamate projections from the midbrain. We also show that M2/M4 mAChRs depress the nAChR-dependent mechanism of DA release in the striatum. These results suggest that M5 receptors on DA neuron terminals enhance DA release, whereas M2/M4 autoreceptors on cholinergic terminals inhibit ACh release and subsequent nAChR-dependent DA release. Our findings clarify the mechanisms of mAChR-dependent modulation of DA and glutamate transmission in the striatum.

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Section: B6mentioning

confidence: 99%

Muscarinic regulation of dopamine and glutamate transmission in the nucleus accumbens

Shin

Adrover

Wess

et al. 2015

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

107

100

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“…1b lower). As ChI-driven DA release, I amp (Lstim) was induced by the AP firing of the cholinergic somata/axons (through the ChI pathway) [14][15][16] .…”

Section: Resultsmentioning

confidence: 99%

“…It was discovered long ago that DA in the striatum is released from widespread axonal arbours whose somata are located in the distant midbrain (the ascending pathway). Recent studies discovered that, independent of the AP firing of dopaminergic somata/axons, the AP firing of striatal cholinergic interneurons (ChIs) also drives DA release [14][15][16] . This local axon-axon pathway is termed as the 'ChI pathway'.…”

mentioning

confidence: 99%

Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine

et al. 2014

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Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevant levels of nicotine modulate striatal DA release. The optogenetic stimulation of ChIs elicits DA release, which is potently inhibited by nicotine with an IC 50 of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by a6b2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP DA -dependent DA release (AP DA , AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine's effects on striatal DA release.

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“…Optogenetic activation of CINs drives dopamine release through nAChR-dependent depolarization of dopamine termi- nals (Cachope et al, 2012;Threlfell et al, 2012;Kress et al, 2014;Wang et al, 2014). The inhibition of dopamine release resulting from block of nAChRs following electrical stimulation was dependent on the frequency of stimulation.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic Interneurons Underlie Spontaneous Dopamine Release in Nucleus Accumbens

2017

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The release of dopamine from terminals in the NAc is regulated by a number of factors, including voltage-gated ion channels, D2-autoreceptors, and nAChRs. Cholinergic interneurons (CINs) drive dopamine release through activation of nAChRs on dopamine terminals. Using cyclic voltammetry in mouse brain slices, nAChR-dependent spontaneous dopamine transients and the mechanisms underlying the origin were examined in the NAc. Spontaneous events were infrequent (0.3 per minute), but the rate and amplitude were increased after blocking Kv channels with 4-aminopyridine. Although the firing frequency of CINs was increased by blocking glutamate reuptake with TBOA and the Sk blocker apamin, only 4-aminopyridine increased the frequency of dopamine transients. In contrast, inhibition of CIN firing with the /␦ selective opioid [Met 5 ]enkephalin (1 M) decreased spontaneous dopamine transients. Cocaine increased the rate and amplitude of dopamine transients, suggesting that the activity of the dopamine transporter limits the detection of these events. In the presence of cocaine, the rate of spontaneous dopamine transients was further increased after blocking D2-autoreceptors. Blockade of muscarinic receptors had no effect on evoked dopamine release, suggesting that feedback inhibition of acetylcholine release was not involved. Thus, although spontaneous dopamine transients are reliant on nAChRs, the frequency was not strictly governed by the activity of CINs. The increase in frequency of spontaneous dopamine transients induced by cocaine was not due to an increase in cholinergic tone and is likely a product of an increase in detection resulting from decreased dopamine reuptake.

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Temporal components of cholinergic terminal to dopaminergic terminal transmission in dorsal striatum slices of mice

Cited by 42 publications

References 65 publications

Muscarinic regulation of dopamine and glutamate transmission in the nucleus accumbens

Muscarinic regulation of dopamine and glutamate transmission in the nucleus accumbens

Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine

Cholinergic Interneurons Underlie Spontaneous Dopamine Release in Nucleus Accumbens

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