Ultrastructural Immunolocalization of the α7 nAChR Subunit in Guinea Pig Medial Prefrontal Cortex

Lubin, Mona; Erişir, Alev; Aoki, Chiye

doi:10.1111/j.1749-6632.1999.tb11337.x

Cited by 34 publications

(25 citation statements)

References 10 publications

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“…Different subsets of cholinergic neurons have been found to discharge intermittent bursts of action potentials (Khateb et al, 1992;Alonso et al, 1996;Manns et al, 2000), and ACh released from cholinergic nerve endings is rapidly degraded by acetylcholinesterase. Morphological evidence consistent with a presynaptic or perisynaptic release of ACh has been provided in cortical and limbic areas of the brain (Woolf, 1991;Lubin et al, 1999). Pulsatile delivery of ACh producing persistent facilitation of glutamatergic transmission likely occurs at sites of MHN-IPN contact in vivo, because the IPN receives the most abundant cholinergic innervation in the brain, arising from cholinergic nuclei located within the basal forebrain, the brainstem, and from cholinergic neurons within the MHN per se (Woolf, 1991).…”

Section: Nicotinic Ach Receptor-mediated Facilitationmentioning

confidence: 99%

Long-Lasting Enhancement of Glutamatergic Synaptic Transmission by Acetylcholine Contrasts with Response Adaptation after Exposure to Low-Level Nicotine

Girod

Role

2001

J. Neurosci.

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Attempts to mimic synaptic delivery of acetylcholine (ACh) with brief, repetitive pulses of high concentration ACh at synapses of medial habenula (MHN) and interpeduncular nucleus (IPN) neurons in vitro elicited temporally distinct facilitation and inhibition of glutamate secretion via nicotinic and muscarinic ACh receptor-mediated pathways, respectively. ACh-induced nicotinic facilitation was sustained for up to 2 hr, whereas muscarinic inhibition was transient. Prolonged exposure to nicotine inactivated nicotinic receptors selectively, thus decreasing the relative contribution of the facilitatory versus inhibitory influences of ACh. The net effect of ACh in modulating glutamatergic transmission at MHN-IPN synapses may be determined by pre-exposure to nicotine, because the drug appears to switch the balance between the facilitatory and inhibitory actions of ACh.Key words: neuromodulation; glutamate; acetylcholine; nicotine; presynaptic; nicotinic acetylcholine receptors; medial habenula; interpeduncular nucleusThe cholinergic system in the brain has been implicated in a variety of behavioral and cognitive functions, such as working memory, aspects of learning, attention, and arousal. These actions underlie the interaction of the endogenous neurotransmitter ACh with a variety of receptors that modulate neuronal excitability in networks that receive cholinergic afferents (Wainer et al., 1993;Sarter and Bruno, 1997). However, the cellular mechanisms underlying this neuromodulation are poorly understood. Although muscarinic acetylcholine receptors (mAChRs) are renowned for their effects in cortical regions affected in Alzheimer's disease, nicotinic acetylcholine receptors (nAChRs) may also contribute to cholinergic signaling in the normal and aging brain. Nicotine alters a variety of cognitive and behavioral functions through its specific interaction with nAChRs found within the diffuse terminal fields of central cholinergic projections (Woolf, 1991;Levin, 1992). Activation of nAChRs in circuits related to behavioral reinforcement may underlie the renowned effects of nicotine as an addictive drug (Stolerman and Shoaib, 1991;Schelling, 1992;Stolerman and Jarvis, 1995;Rose and Corrigall, 1997;Mansvelder and McGehee, 2000).Nicotinic receptors are found in the cell bodies, dendrites, and within the presynaptic domains of neurons. Recent electrophysiological studies have provided direct evidence that nAChRs mediate synaptic transmission at central synapses (for review, see Jones et al., 1999). In addition, nAChRs are targeted to synaptic terminal and preterminal domains, consistent with demonstrated effects of ACh and nicotine on the release of a wide variety of neurotransmitters (Rapier et al., 1990;Grady et al., 1992;McGehee et al., 1995;Dani and Heinemann, 1996;Gray et al., 1996;McGehee and Role, 1996;Role and Berg, 1996;Wonnacott, 1997;MacDermott et al., 1999).Nicotine interaction with nAChRs facilitates the induction of long-term potentiation of glutamatergic neurotransmission in the hippocampus (Fujii et al., 1999...

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Section: Nicotinic Ach Receptor-mediated Facilitationmentioning

confidence: 99%

Long-Lasting Enhancement of Glutamatergic Synaptic Transmission by Acetylcholine Contrasts with Response Adaptation after Exposure to Low-Level Nicotine

Girod

Role

2001

J. Neurosci.

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“…Indeed, stimulation of PFC synaptosomes with a β2-selective agonist increases the release of . In the rat PFC α7 nAChRs have also been localised to glutamatergic terminals, as well as GABAergic terminals and cell bodies [103]. α7 nAChR agonists also induce [ A c c e p t e d M a n u s c r i p t…”

Section: Nicotinic Receptor-mediated Facilitation Of Dopamine Releasementioning

confidence: 99%

Nicotinic acetylcholine receptors and the ascending dopamine pathways

Livingstone

Wonnacott

2009

Biochemical Pharmacology

125

114

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Nicotinic acetylcholine receptors (nAChRs) are widely expressed in midbrain dopamine neurons that project to dorsal striatum, nucleus accumbens and prefrontal cortex. Thus nAChRs can influence the functions of these three pathways; notably motor control, 'reward' and executive function, respectively. Diverse subtypes of nAChRs have been identified on dopamine cell bodies and terminals as well as on neighbouring afferents and interneurons. Here we review the molecular and cellular mechanisms through which nAChRs exert their influence on these pathways in rodents. Page 4 of 40A c c e p t e d M a n u s c r i p t A c c e p t e d M a n u s c r i p t 5 IntroductionThe association of nicotine with tobacco addiction has stimulated particular interest in how nicotine interacts with the 'reward' pathways of the brain. Most attention has been given to the ascending dopaminergic pathways that arise in the midbrain and project to aspects of the basal ganglia and prefrontal cortex (PFC; Fig. 1). In addition to mediating the reinforcing properties of addictive substances, dopamine is also central to the fine control of movement governed by the basal ganglia, whereas its actions in the PFC are critically important to 'executive' function [1,2]. This includes working memory, behavioural flexibility and decision making, and the PFC is also involved with the anticipation of reward [3,4]. FIGURE ONE NEAR HERENicotine interacts with the dopamine systems via nicotinic acetylcholine receptors (nAChRs), a family of ligand-gated pentameric cation channels constituted from at least nine α and β subunits (α2-7 and β2-4) expressed in the mammalian brain [5]. nAChR subtypes can differ in their sensitivities to nicotine or acetylcholine (ACh), their channel characteristics (including their propensity to desensitise) and their cellular distribution. A high relative permeability to Ca 2+ , a notable characteristic of the α7 nAChR subtype, enables nAChRs to interface with a variety of intracellular Ca 2+ -dependent mechanisms [6]. The localisation of nAChRs on dopamine cell bodies in the ventral tegmental area (VTA) or substantia nigra pars compacta (SNc) allows nicotine to directly modulate dopaminergic cell firing. Additionally, nAChRs on dopamine terminals can influence transmitter release. nAChRs present on afferents projecting to the VTA and SNc or to the terminal fields can also influence the activity of dopaminergic neurons. The nicotinic modulation of dopamine release has generated interest in nAChRs as therapeutic targets for conditions involving dopaminergic dysfunction, including schizophrenia, attention deficit hyperactivity disorder, Parkinson's disease, Alzheimer's disease and age-related cognitive impairment [7][8][9][10].In this review we focus on the mechanisms through which nAChRs modulate the activity of dopamine neurones of the principal ascending pathways (Fig. 1). We will considerPage 6 of 40A c c e p t e d M a n u s c r i p t 6 nicotinic influences on somatodendritic and terminal fields, with the aim of integratin...

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“…These nicotinic mechanisms differ from the mechanisms by which nicotine A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 12 increases excitatory transmission in the hippocampus and VTA, where activation of 7* receptors leads to a direct stimulation of glutamate release [51,60]. Support for modulatory effects of presynaptic nAChRs activation in the PFC comes from a variety of approaches including electrophysiological recordings and assay of release from isolated nerve terminals [72][73][74]. A recent study testing the relative contribution of β2*nAChRs vs. α7*nAChRs on glutamatergic synaptosomes from PFC [72] demonstrated that both α7* and non α7*nAChRs appear to be important although each modulates excitatory amino acid (EAA) release via distinct mechanisms.…”

Section: Nicotinic Modulation Of Thalamocortical Communicationmentioning

confidence: 99%

Nicotinic actions on neuronal networks for cognition: General principles and long-term consequences

Poorthuis

Goriounova

Couey

et al. 2009

Biochemical Pharmacology

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Ultrastructural Immunolocalization of the α7 nAChR Subunit in Guinea Pig Medial Prefrontal Cortex

Cited by 34 publications

References 10 publications

Long-Lasting Enhancement of Glutamatergic Synaptic Transmission by Acetylcholine Contrasts with Response Adaptation after Exposure to Low-Level Nicotine

Long-Lasting Enhancement of Glutamatergic Synaptic Transmission by Acetylcholine Contrasts with Response Adaptation after Exposure to Low-Level Nicotine

Nicotinic acetylcholine receptors and the ascending dopamine pathways

Nicotinic actions on neuronal networks for cognition: General principles and long-term consequences

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