Nicotinic receptor subtypes differentially modulate glutamate release in the dorsal medial striatum

Howe, William M.; Young, Damon; Bekheet, George; Kozak, Rouba

doi:10.1016/j.neuint.2016.08.009

Cited by 23 publications

(25 citation statements)

References 28 publications

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“…The two major subtypes of CNS nicotinic receptors, α7 and α4β2 are expressed on cell bodies and synaptic terminals (Wonnacot, ; Parikh et al , ; Puddifoot et al ; Howe et al ) where they promote the influx of extracellular calcium leading to the release of neurotransmitters (Turner ; Zappettini et al , ). Nicotinic receptors can regulate the release of, at least, glutamate (McGehee et al, ; Gray et al, ; Albuquerque et al ; Gu et al, ; Puddifoot et al ; Pistillo et al , ; Howe et al ; Ryu et al ) and can modulate the release of GABA (Gray et al, ; Le Magueresse et al, ), dopamine (Schilstrom et al, ,b; Kaiser and Wonnacott ; Livingstone and Wonnacott, ; Livingstone et al ) and norepinephrine (Pittaluga and Raiteri ; Pittaluga et al ; Raiteri et al ; Li et al, ). It is reasonable to expect that the release of many other transmitters and modulators including serotonin, glycine, neuroactive peptides and perhaps kynurenines, proteases, cytokines and other factors may also be affected by nicotinic receptors on glia or synaptic terminals or cell bodies.…”

Section: Interpreting Resultsmentioning

confidence: 99%

Does kynurenic acid act on nicotinic receptors? An assessment of the evidence

Stone

2019

Journal of Neurochemistry

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As a major metabolite of kynurenine in the oxidative metabolism of tryptophan, kynurenic acid is of considerable biological and clinical importance as an endogenous antagonist of glutamate in the central nervous system. It is most active as an antagonist at receptors sensitive to N‐methyl‐D‐aspartate (NMDA) which regulate neuronal excitability and plasticity, brain development and behaviour. It is also thought to play a causative role in hypo‐glutamatergic conditions such as schizophrenia, and a protective role in several neurodegenerative disorders, notably Huntington’s disease. An additional hypothesis, that kynurenic acid could block nicotinic receptors for acetylcholine in the central nervous system has been proposed as an alternative mechanism of action of kynurenate. However, the evidence for this alternative mechanism is highly controversial, partly because at least eight earlier studies concluded that kynurenic acid blocked NMDA receptors but not nicotinic receptors and five subsequent, independent studies designed to repeat the results have failed to do so. Many studies considered to support the alternative ‘nicotinic’ hypothesis have been based on the use of analogs of kynurenate such as 7‐chloro‐kynurenic acid, or putatively nicotinic modulators such as galantamine, but a detailed analysis of the pharmacology of these compounds suggests that the results have often been misinterpreted, especially since the pharmacology of galantamine itself has been disputed. This review examines the evidence in detail, with the conclusion that there is no confirmed, reliable evidence for an antagonist activity of kynurenic acid at nicotinic receptors. Therefore, since there is overwhelming evidence for kynurenate acting at ionotropic glutamate receptors, especially NMDAR glutamate and glycine sites, with some activity at GPR35 sites and Aryl Hydrocarbon Receptors, results with kynurenic acid should be interpreted only in terms of these confirmed sites of action.

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Section: Interpreting Resultsmentioning

confidence: 99%

Does kynurenic acid act on nicotinic receptors? An assessment of the evidence

Stone

2019

Journal of Neurochemistry

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“…The prolonged debate about the interrelation between dopamine and ACh release has been slowly resolving, as more data are gathered. We now know that presynaptic nAChRs are highly expressed on striatal dopaminergic terminals (Jones et al, 2001;Zhou et al, 2001;Zoli et al, 2002;Salminen et al, 2004;Gotti et al, 2009;Livingstone & Wonnacott, 2009;Garcao et al, 2014;Wang et al, 2014;Gonzales & Smith, 2015;Howe et al, 2016), and that their activation facilitates dopamine release (Exley & Cragg, 2008).…”

Section: Dopaminergic Terminalsmentioning

confidence: 99%

Cholinergic modulation of striatal microcircuits

Abudukeyoumu

Hernández-Flores

García‐Muñoz

et al. 2018

Eur J of Neuroscience

107

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The purpose of this review is to bridge the gap between earlier literature on striatal cholinergic interneurons and mechanisms of microcircuit interaction demonstrated with the use of newly available tools. It is well known that the main source of the high level of acetylcholine in the striatum, compared to other brain regions, is the cholinergic interneurons. These interneurons provide an extensive local innervation that suggests they may be a key modulator of striatal microcircuits. Supporting this idea requires the consideration of functional properties of these interneurons, their influence on medium spiny neurons, other interneurons, and interactions with other synaptic regulators. Here, we underline the effects of intrastriatal and extrastriatal afferents onto cholinergic interneurons and discuss the activation of pre- and postsynaptic muscarinic and nicotinic receptors that participate in the modulation of intrastriatal neuronal interactions. We further address recent findings about corelease of other transmitters in cholinergic interneurons and actions of these interneurons in striosome and matrix compartments. In addition, we summarize recent evidence on acetylcholine-mediated striatal synaptic plasticity and propose roles for cholinergic interneurons in normal striatal physiology. A short examination of their role in neurological disorders such as Parkinson's, Huntington's, and Tourette's pathologies and dystonia is also included.

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“…Hence, mAChRs inhibition could exert opposite actions on basal corticostriatal transmission depending on their pre-or postsynaptic localization. Nicotinic a7 receptors have been described on cortical glutamatergic terminals but whether these receptors directly modulate corticostriatal transmission is still unclear (Howe et al, 2016).…”

Section: Consequences Of Cholinergic Interneuron Inhibition On Striatmentioning

confidence: 99%

Striatal Cholinergic Interneurons: How to Elucidate Their Function in Health and Disease

et al. 2019

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Striatal cholinergic interneurons (CINs) are the main source of acetylcholine in the striatum and are believed to play an important role in basal ganglia physiology and pathophysiology. The role of CINs in striatal function is known mostly from extracellular recordings of tonically active striatal neurons in monkeys, which are believed to correspond to CINs. Because these neurons transiently respond to motivationally cues with brief pauses, flanked by bursts of increased activity, they are classically viewed as key players in reward-related learning. However, CIN modulatory function within the striatal network has been mainly inferred from the action of acetylcholine agonists/antagonists or through CIN activation. These manipulations are far from recapitulating CIN activity in response to behaviorally-relevant stimuli. New technical tools such as optogenetics allow researchers to specifically manipulate this sparse neuronal population and to mimic their typical pause response. For example, it is now possible to investigate how short inhibition of CIN activity shapes striatal properties. Here, we review the most recent literature and show how these new techniques have brought considerable insights into the functional role of CINs in normal and pathological states, raising several interesting and novel questions. To continue moving forward, it is crucial to determine in detail CIN activity changes during behavior, particularly in rodents. We will also discuss how computational approaches combined with optogenetics will contribute to further our understanding of the CIN role in striatal circuits.

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Nicotinic receptor subtypes differentially modulate glutamate release in the dorsal medial striatum

Cited by 23 publications

References 28 publications

Does kynurenic acid act on nicotinic receptors? An assessment of the evidence

Does kynurenic acid act on nicotinic receptors? An assessment of the evidence

Cholinergic modulation of striatal microcircuits

Striatal Cholinergic Interneurons: How to Elucidate Their Function in Health and Disease

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