Muscarinic receptors modulate N-, P-, and L-type Ca2+ currents in rat striatal neurons through parallel pathways

Howe, A; Surmeíer, D. James

doi:10.1523/jneurosci.15-01-00458.1995

Cited by 162 publications

(132 citation statements)

References 78 publications

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“…1j). Dopamine D2 receptor activation has been postulated to be upstream from mAChRs, which exert a strong control over calcium influx in rat striatal neurons (Howe & Surmeier 1995;Wang et al 2006). Pre-treatment with the unselective mAChR antagonist scopolamine (5 μM) also occluded nicotine-induced facilitation of eCB-LTD (F (1, 29) = 1.32, P > 0.05) (Fig.…”

Section: Nicotine Exposure Ex Vivo Facilitates Ecb-ltd In Slices Frommentioning

confidence: 87%

“…Inhibition of nAChRs on dopaminergic terminals has been postulated to reduce the activation of dopamine D2 receptors located on cholinergic interneurons, thereby increasing acetylcholine-release and mAChR activation, resulting in reduced postsynaptic calcium influx (Yan et al 1997;Partridge et al 2002). Elevated postsynaptic calcium is a prerequisite for eCB production (Adermark & Lovinger 2007a), and mAChRs exert a strong control over calcium influx in rat striatal neurons (Howe & Surmeier 1995;Wang et al 2006) (Fig. 1i).…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, the firing frequency of striatal cholinergic interneurons has been shown to be reduced following nicotine administration ex vivo (Storey et al 2016). Nicotine-induced suppression of cholinergic activity could thus reduce mAChR activation, thereby relieving the break on L-type calcium channels to allow postsynaptic calcium to reach the threshold required for eCB production (Howe & Surmeier 1995;Wang et al 2006;Adermark & Lovinger 2007a). It should be noted, however, that there is still some debate as to where the dopamine D2 receptors required for eCB-LTD are located and whether they exert a direct or indirect control over medium spiny neuron excitability (Lerner & Kreitzer 2012).…”

Section: Discussionmentioning

confidence: 99%

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Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

et al. 2018

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The endocannabinoid (eCB) system modulates several phenomena related to addictive behaviors, and drug-induced changes in eCB signaling have been postulated to be important mediators of physiological and pathological rewardrelated synaptic plasticity. Here, we studied eCB-mediated long-term depression (eCB-LTD) in the dorsolateral striatum, a brain region critical for acquisition of habitual and automatic behavior. We report that nicotine differentially affects ex vivo eCB signaling depending on previous exposure in vivo. In the nicotine-naïve brain, nicotine facilitates eCB-signaling and LTD, whereas tolerance develops to this facilitating effect after subchronic exposure in vivo. In the end, a progressive impairment of eCB-induced LTD is established after protracted withdrawal from nicotine. Endocannabinoid-LTD is reinstated 6 months after the last drug injection, but a brief period of nicotine re-exposure is sufficient to yet again impair eCB-signaling. LTD induced by the cannabinoid 1 receptor agonist WIN55,212-2 is not affected, suggesting that nicotine modulates eCB production or release. Nicotine-induced facilitation of eCB-LTD is occluded by the dopamine D2 receptor agonist quinpirole, and by the muscarinic acetylcholine receptor antagonist scopolamine. In addition, the same compounds restore eCB-LTD during protracted withdrawal. Nicotine may thus modulate eCB-signaling by affecting dopaminergic and cholinergic neurotransmission in a long-lasting manner. Overall, the data presented here suggest that nicotine facilitates eCB-LTD in the initial phase, which putatively could promote neurophysiological and behavioral adaptations to the drug. Protracted withdrawal, however, impairs eCB-LTD, which may influence or affect the ability to maintain cessation.

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Section: Nicotine Exposure Ex Vivo Facilitates Ecb-ltd In Slices Frommentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

et al. 2018

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“…The mouse MSN cultures were established with some modifications of the protocol used for rat MSN culture. Briefly, using landmarks described previously (43), striata were dissected from brains of D32 ϩ/ϩ and D32 Ϫ/Ϫ embryonic mice in ice-cold dissection solution (1ϫ divalent-free Hanks' balanced salt solution, 15 mM HEPES, 10 mM NaHCO 3 , and 100 units/ml penicillin/streptomycin (Invitrogen), pH 7.2). The striata from mice with identical genotypes were pooled and treated with 0.25% trypsin for 7 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Dopamine Receptor-mediated Ca2+ Signaling in Striatal Medium Spiny Neurons

Tang

Bezprozvanny

2004

Journal of Biological Chemistry

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Inositol 1,4,5-trisphosphate (InsP 3 ) and cAMP are the two second messengers that play an important role in neuronal signaling. Here, we investigated the interactions of InsP 3 -and cAMP-mediated signaling pathways activated by dopamine in striatal medium spiny neurons (MSN). We found that in ϳ40% of the MSN, application of dopamine elicited robust repetitive Ca 2؉ transients (oscillations). In pharmacological experiments with specific agonists and antagonists, we found that the observed Ca 2؉ oscillations were triggered by activation of D1 class dopamine receptors (DARs). We further demonstrated that activation of phospholipase C was required for induction of dopamine- Dopamine is an important transmitter and neuromodulator in the brain. The cellular mechanisms by which dopamine affects neuronal function are only beginning to be elucidated (1, 2). Striatal medium spiny neurons (MSN) 1 express multiple subtypes of dopamine receptors (DARs) (3-5). On the basis of their molecular structure and pharmacological properties, DARs are divided into the D1 class (D1R and D5R) and D2 class (D2R, D3R, and D4R) (6). D1 class DARs are coupled to G s/olf , activation of adenylyl cyclase, and cAMP production (3). Activation of D2 class DARs has dual effects of inhibiting cAMP production (3) and activating phospholipase C␤ (PLC␤) (7). A putative D1 class DAR subtype coupled to PLC activation and phosphatidylinositol 4,5-diphosphate hydrolysis, but not to cAMP production, has been postulated (8 -10), but has not yet been isolated or cloned. Recently, a specific agonist for this receptor (SKF83959) was identified (11). The D1R-binding protein calcyon has been isolated by yeast two-hybrid methods (12). Association of D1/D5 receptors with calcyon enables coupling of D1/D5 receptors with G q/11 , resulting in PLC activation and inositol 1,4,5-trisphosphate (InsP 3 ) generation (12, 13). Cross-talk between cAMP and Ca 2ϩ signaling pathways plays an important role in dopaminergic signaling in the neostriatum (1). Activation of D1 class DARs enhances L-type Ca 2ϩ channel activity (14 -16) and currents via the ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (17) and the N-methyl-D-aspartic acid (NMDA) receptor (18,19). In contrast, activation of D2 class DARs reduces L-type Ca 2ϩ currents (7) and NMDA receptor activity (20). D1/D5 receptormediated facilitation of L-type Ca 2ϩ channels and AMPA and NMDA receptors results from increased phosphorylation of these channels by protein kinase A (PKA) (16, 21) and decreased dephosphorylation of these channels by protein phosphatase-1 (PP1) (17,22,23). DARPP-32 (dopamine-and cAMPregulated phosphoprotein of M r 32,000) (24, 25) is partly responsible for inhibition of PP1 activity following activation of D1/D5 receptors (26). DARPP-32 phosphorylated by PKA at a single threonine residue (Thr-34) is transformed into a potent inhibitor of PP1, which in turn regulates the phosphorylation state of many neurotransmitter receptors and voltage-gated ion channels (1).The type 1 inos...

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“…Therefore, it is presumed that the tonic firing and the pauses of cholinergic interneurons influence striatal output by modifying the activity of spiny projection neurons that do innervate the output nuclei of the basal ganglia. The synapses formed by cholinergic neurons onto spiny neurons have not been shown to generate synaptic currents by way of ionotropic nicotinic receptors, but act primarily in a modulatory fashion (Uchimura and North, 1990;Howe and Surmeier, 1995;Galarraga et al, 1999;Gabel and Nisenbaum, 1999;Calabresi et al, 2000). It is possible, however, that a small excitatory synaptic response mediated by nAChRs has gone undetected and could contribute to the modulatory cholinergic action, as is the case in the hippocampus (Alkondon et al, 1998;Frazier et al, 1998;Hefft et al, 1999).…”

Section: Consequences Of the Activity Of Cholinergic Interneuronsmentioning

confidence: 99%

Cholinergic interneuron characteristics and nicotinic properties in the striatum

2002

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ABSTRACT:The neostriatum (dorsal striatum) is composed of the caudate and putamen. The ventral striatum is the ventral conjunction of the caudate and putamen that merges into and includes the nucleus accumbens and striatal portions of the olfactory tubercle. About 2% of the striatal neurons are cholinergic. Most cholinergic neurons in the central nervous system make diffuse projections that sparsely innervate relatively broad areas. In the striatum, however, the cholinergic neurons are interneurons that provide very dense local innervation. The cholinergic interneurons provide an ongoing acetylcholine (ACh) signal by firing action potentials tonically at about 5 Hz. A high concentration of acetylcholinesterase in the striatum rapidly terminates the ACh signal, and thereby minimizes desensitization of nicotinic acetylcholine receptors. Among the many muscarinic and nicotinic striatal mechanisms, the ongoing nicotinic activity potently enhances dopamine release. This process is among those in the striatum that link the two extensive and dense local arbors of the cholinergic interneurons and dopaminergic afferent fibers. During a conditioned motor task, cholinergic interneurons respond with a pause in their tonic firing. It is reasonable to hypothesize that this pause in the cholinergic activity alters action potential dependent dopamine release. The correlated response of these two broad and dense neurotransmitter systems helps to coordinate the output of the striatum, and is likely to be an important process in sensorimotor planning and learning.

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Muscarinic receptors modulate N-, P-, and L-type Ca2+ currents in rat striatal neurons through parallel pathways

Cited by 162 publications

References 78 publications

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

Dopamine Receptor-mediated Ca2+ Signaling in Striatal Medium Spiny Neurons

Cholinergic interneuron characteristics and nicotinic properties in the striatum

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