Direct and GABA‐mediated indirect effects of nicotinic ACh receptor agonists on striatal neurones

Luo, Ruixi; Janssen, Megan J.; Partridge, John G.; Vicini, Stefano

doi:10.1113/jphysiol.2012.241786

Cited by 61 publications

(99 citation statements)

References 50 publications

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“…This nicotinic receptor profile differs from that striatal FSIs and NPY-NGF GABAergic interneurons (Koós and Tepper, 2002, English et al, 2012) but is consistent with a recent report by Luo and colleagues (2013) that found the same antagonist sensitivities for striatal Type I THINs as we report here, and additionally demonstrated that striatal Type I THINs respond to cytisine, a selective α3β4 agonist nicotinic agonist. Here we show additionally that although all THINs tested exhibited a nicotinic excitation with a similar or identical pharmacology, there appeared to be subtype-specific differences in the strength of the excitation.…”

Section: Discussionsupporting

confidence: 93%

Dopaminergic and cholinergic modulation of striatal tyrosine hydroxylase interneurons

et al. 2015

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The recent electrophysiological characterization of TH-expressing GABAergic interneurons (THINs) in the neostriatum revealed an unexpected degree of diversity of interneurons in this brain area (Ibáñez-Sandoval et al., 2010, Unal et al., 2011, 2013). Despite being relatively few in number, THINs may play a significant role in transmitting and distributing extra- and intrastriatal neuromodulatory signals in the striatal circuitry. Here we investigated the dopaminergic and cholinergic regulation of THINs in vitro. We found that the dominant effect of dopamine was a dramatic enhancement of the ability of THINs to generate long-lasting depolarizing plateau potentials (PPs). Interestingly, the same effect could also be elicited by amphetamine-induced release of endogenous dopamine suggesting that THINs may exhibit similar responses to changes in extracellular dopamine concentration in vivo. The enhancement of PPs in THINs is perhaps the most pronounced effect of dopamine on the intrinsic excitability of neostriatal neurons described to date. Further, we demonstrate that all subtypes of THINSs tested also express nicotinic cholinergic receptors. All THIS responded, albeit differentially, with depolarization, PPs and spiking to brief application of nicotinic agonists. Powerful modulation of the nonlinear integrative properties of THINs by dopamine and the direct depolarization of these neurons by acetylcholine may play important roles in mediating the effects of these neuromodulators in the neostriatum with potentially important implications for understanding the mechanisms of neuropsychiatric disorders affecting the basal ganglia.

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Section: Discussionsupporting

confidence: 93%

Dopaminergic and cholinergic modulation of striatal tyrosine hydroxylase interneurons

et al. 2015

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“…3 and 7). Although NPY-NGF interneurons are sparsely distributed in the striatum, considering the reported high-connectivity to SPNs (∼60-87%) (26,55), single NPY-NGF interneurons might possess more powerful inhibition to the striatal network than we expected.…”

Section: Discussioncontrasting

confidence: 39%

“…Therefore, dendritic plateau potentials could be sustained despite FS-mediated inhibition. Another interesting finding is the very effective inhibition mediated by GABAergic IPSCs with slow kinetics, presumably mediated by NPY-NGF interneurons (26,55). Dendritic slow GABAergic IPSCs showed the strongest efficacy in dendritic inhibition (Figs.…”

Section: Discussionmentioning

confidence: 98%

Cell-type–specific inhibition of the dendritic plateau potential in striatal spiny projection neurons

Lindroos

et al. 2017

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

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Striatal spiny projection neurons (SPNs) receive convergent excitatory synaptic inputs from the cortex and thalamus. Activation of spatially clustered and temporally synchronized excitatory inputs at the distal dendrites could trigger plateau potentials in SPNs. Such supralinear synaptic integration is crucial for dendritic computation. However, how plateau potentials interact with subsequent excitatory and inhibitory synaptic inputs remains unknown. By combining computational simulation, two-photon imaging, optogenetics, and dualcolor uncaging of glutamate and GABA, we demonstrate that plateau potentials can broaden the spatiotemporal window for integrating excitatory inputs and promote spiking. The temporal window of spiking can be delicately controlled by GABAergic inhibition in a celltype-specific manner. This subtle inhibitory control of plateau potential depends on the location and kinetics of the GABAergic inputs and is achieved by the balance between relief and reestablishment of NMDA receptor Mg 2+ block. These findings represent a mechanism for controlling spatiotemporal synaptic integration in SPNs.O ne of the principal functions of neurons is to integrate excitatory and inhibitory synaptic inputs and transform subthreshold membrane potential fluctuations into suprathreshold spiking activities. Both theoretical and experimental works have proposed that a single neuron can process inputs as a multilayer computational device in which individual dendritic branches function as a computational unit and can generate dendritic spikes or plateau potentials (1-4). In vivo studies have demonstrated that dendritic plateau potentials evoked by coincident inputs can amplify excitatory signals and enhance the capacity of learning and information storage at a specific branch (5-7). However, a majority of the understanding of dendritic computation is based on studies focusing on pyramidal cells of hippocampal and cortical areas. It is relatively less known whether these conclusions apply to the striatal neurons (8).The striatum, the main input nucleus of the basal ganglia, receives convergent glutamatergic inputs from the cortex and thalamus (9-11). The integration of these functionally distinct inputs is critical for fine movement control and action selection (12, 13). The principal neurons in the striatum-spiny projection neurons (SPNs)-display hyperpolarized membrane potentials (∼−80 mV) at rest, often referred to as the "down-state" (14, 15). It is generally believed that coherent cortical inputs can effectively depolarize SPNs and promote membrane potential transitions from a hyperpolarized down-state to a depolarized "up-state" (∼−55 mV), at which point action potentials can be generated (14-16). To achieve this ∼20-to 30-mV state transition, it has been estimated that a large number (hundreds to thousands) of active inputs would be required (14-17). Interestingly, striatal SPNs are capable of producing long-lasting plateau potentials following activation of spatially clustered and temporally synchronized excit...

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“…Vicini's (Ade et al 2008;Janssen et al 2009;Janssen et al 2011;Luo et al 2013) and other groups (Kirmse et al 2008;Janssen et al 2009;Santhakumar et al 2010) have provided solid evidence for the presence and the developmental profile of a tonic GABA A current in MSNs. (Note, however, that one study did not find any evidence for a tonic GABA A current in D2 + or D1 + MSNs; Gertler et al 2008.)…”

Section: Striatummentioning

confidence: 98%

GPCR Modulation of Extrasynapitic GABAA Receptors

Connelly

Errington

Yagüe

et al. 2014

Extrasynaptic GABAA Receptors

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γ-Aminobutyric acid type A (GABA A ) receptors (GABA A Rs), the main inhibitory neurotransmitter-gated ion channels in the central nervous system, are finely tuned by other neurotransmitters and endogenous ligands. The regulation of synaptic GABA A Rs (sGABA A Rs) by G protein-coupled receptors (GPCRs) has been well characterized and is known to occur either through the conventional activation of second-messenger signalling cascades by G proteins or directly by protein-protein coupling. In contrast, research on the modulation of extrasynaptic GABA A R (eGABA A Rs) is still in its infancy and it remains to be determined whether both of the above mechanisms are capable of controlling eGABA A R function. In this chapter, we summarize the available literature on eGABA A R modulation by GPCRs, including GABA B , serotonin (5-HT), dopamine (DA), noradrenaline (NA) and metabotropic glutamate (mGlu) receptors. Although at present these GPCRs-eGABA A Rs cross-talks have been investigated in a limited number of brain areas (i.e., thalamus, cerebellum, hippocampus, striatum), it is already evident that eGABA A Rs show a nucleus-and neuronal type-selective regulation by GPCRs that differs from that of sGABA A Rs. This distinct regulation of eGABA A Rs versus sGABA A Rs by GPCRs provides mechanisms for receptor adaptation in response

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Direct and GABA‐mediated indirect effects of nicotinic ACh receptor agonists on striatal neurones

Cited by 61 publications

References 50 publications

Dopaminergic and cholinergic modulation of striatal tyrosine hydroxylase interneurons

Dopaminergic and cholinergic modulation of striatal tyrosine hydroxylase interneurons

Cell-type–specific inhibition of the dendritic plateau potential in striatal spiny projection neurons

GPCR Modulation of Extrasynapitic GABAA Receptors

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