Long-Term Potentiation of Excitatory Inputs to Brain Reward Areas by Nicotine

Mansvelder, Huibert D.; McGehee, Daniel S.

doi:10.1016/s0896-6273(00)00042-8

Cited by 658 publications

(709 citation statements)

References 46 publications

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“…First, changes in KYNA often parallel alterations in nAChR function/expression in a number of neurologic disorders (Perry et al, 1990;Hellstrom-Lindahl et al, 1999;Freedman et al, 2000;Court et al, 2001). Second, similarly to NMDA receptors, nAChRs are involved in regulating neuronal plasticity (Albuquerque et al, 1997;Broide and Leslie, 1999;Mansvelder and McGehee, 2000;Ji et al, 2001) and survival in the brain (Zoli et al, 1999;Kihara et al, 2001). Third, the overall effects of ␣7 nAChR antagonists and NMDA receptor antagonists on neuronal plasticity and viability are qualitatively similar and resemble those of KYNA.…”

Section: Kynurenic Acid (Kyna)mentioning

confidence: 99%

Unconventional ligands and modulators of nicotinic receptors

et al. 2002

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ABSTRACT:Evidence gathered from epidemiologic and behavioral studies have indicated that neuronal nicotinic receptors (nAChRs) are intimately involved in the pathogenesis of a number of neurologic disorders, including Alzheimer's disease, Parkinson's disease, and schizophrenia. In the mammalian brain, neuronal nAChRs, in addition to mediating fast synaptic transmission, modulate fast synaptic transmission mediated by the major excitatory and inhibitory neurotransmitters glutamate and GABA, respectively. Of major interest, however, is the fact that the activity of the different subtypes of neuronal nAChR is also subject to modulation by substances of endogenous origin such as choline, the tryptophan metabolite kynurenic acid, neurosteroids, and ␤-amyloid peptides and by exogenous substances, including the so-called nicotinic allosteric potentiating ligands, of which galantamine is the prototype, and psychotomimetic drugs such as phencyclidine and ketamine. The present article reviews and discusses the effects of unconventional ligands on nAChR activity and briefly describes the potential benefits of using some of these compounds in the treatment of neuropathologic conditions in which nAChR function/expression is known to be altered.

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Section: Kynurenic Acid (Kyna)mentioning

confidence: 99%

Unconventional ligands and modulators of nicotinic receptors

et al. 2002

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“…NMDA receptordependent LTP has been demonstrated at excitatory synapses on midbrain dopamine neurons (Bonci and Malenka, 1999;Overton et al, 1999;Mansvelder and McGehee, 2000;Liu et al, 2005). The demonstration of synaptic plasticity at excitatory synapses in mesolimbic dopaminergic structures, as well as the correlative evidence for changes in glutamate receptor expression and single unit responses to glutamate after in vivo exposure to drugs of abuse, support a role for synaptic plasticity at excitatory synapses in the development of addiction (Hyman and Malenka, 2001;Zhang et al, 1997;Carlezon and Nestler, 2002;Thomas and Malenka, 2003).…”

Section: Introductionmentioning

confidence: 95%

High-Frequency Afferent Stimulation Induces Long-Term Potentiation of Field Potentials in the Ventral Tegmental Area

Nugent

Hwong

Udaka

et al. 2007

Neuropsychopharmacol

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Excitatory synapses on dopamine neurons in the VTA can undergo both long-term potentiation and depression. Additionally, druginduced plasticity has been found at VTA synapses, and is proposed to play a role in reward-related learning and addiction by modifying dopamine cell firing. LTP at these synapses is difficult to generate experimentally in that it requires an undisturbed intracellular milieu and is often small in magnitude. Here, we demonstrate the induction of LTP as a property of evoked field potentials within the VTA. Excitatory field potentials were recorded extracellularly from VTA neurons in acute horizontal midbrain slices. Using extracellular and intracellular recording techniques, we found that evoked field potentials originate within the VTA itself and are largely composed of AMPA receptor-mediated EPSPs and action potentials triggered by activation of glutamatergic synapses on both dopamine and GABA neurons. High-frequency afferent stimulation (HFS) induced LTP of the field potential. The induction of this LTP was blocked by application of the NMDAR antagonist, d-APV, prior to HFS. As reported previously, glutamatergic synapses on GABA neurons did not express LTP while those on dopamine neurons did. We conclude that the potentiation of glutamatergic synapses on dopamine neurons is a major contributor to NMDA receptor-dependent LTP of the field potential. Field potential recordings may provide a convenient approach to explore the basic electrophysiological properties of VTA neurons and the development of addiction-related processes in this brain region.

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“…Activation of these somatic nAChRs increases the excitability, action potential firing, and Ca 2ϩ influx in these neurons (Pidoplichko et al, 1997;Picciotto et al, 1998;Klink et al, 2001). ␣7* nAChRs are expressed to a lesser degree on the midbrain neurons, and their presynaptic location on glutamatergic afferents to the midbrain serve to enhance long-term synaptic potentiation onto DA neurons (Mansvelder and McGehee, 2000;Mansvelder et al, 2002).…”

Section: Nicotinic Receptors In the Mesolimbic Dopamine System And Stmentioning

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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Long-Term Potentiation of Excitatory Inputs to Brain Reward Areas by Nicotine

Cited by 658 publications

References 46 publications

Unconventional ligands and modulators of nicotinic receptors

Unconventional ligands and modulators of nicotinic receptors

High-Frequency Afferent Stimulation Induces Long-Term Potentiation of Field Potentials in the Ventral Tegmental Area

Cholinergic interneuron characteristics and nicotinic properties in the striatum

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