Glutamate in dopamine neurons: Synaptic versus diffuse transmission

Descarries, Laurent; Bérubé-Carrière, Noémie; Riad, Mustapha; Bo, Grégory Dal; Mendez, José Alfredo; Trudeau, Louis-Éric

doi:10.1016/j.brainresrev.2007.10.005

Cited by 106 publications

(126 citation statements)

References 83 publications

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“…Therefore, there is a certain chance that post-synaptic TRPV 1 R triggered the production of a retrograde messenger (e.g. NO) that The present electrophysiological and neurochemical evidence do not necessarily argue for glutamate release modulation at cortico-or thalamostriatal terminals: it is known that glutamate serves as a cotransmitter to dopamine in mesolimbic efferents, helping axonal guidance and target selection (Descarries et al, 2008). It is therefore plausible that the effect of capsaicin seen by us is restricted to such developing terminals in the striatum, thus capsaicin can evoke sustained release of glutamate and dopamine from nerve terminals of the same mesolimbic origin.…”

Section: Age-dependence Of Presynaptic Trpv 1 R Functionality In the mentioning

confidence: 74%

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Köles

Garção

Zádori

et al. 2013

Brain Research Bulletin

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Neocortical and striatal TRPV1 (vanilloid or capsaicin) receptors (TRPV1Rs) are excitatory ligand-gated ion channels, and are implicated in psychiatric disorders. However, the purported presynaptic neuromodulator role of TRPV1Rs in glutamatergic, serotonergic or dopaminergic terminals of the rodent forebrain remains little understood. With the help of patch-clamp electrophysiology and neurochemical approaches, we mapped the age-dependence of presynaptic TRPV1R function, and furthermore, we aimed at exploring whether the presence of CB1 cannabinoid receptors (CB1Rs) influences the function of the TRPV1Rs, as both receptor types share endogenous ligands. We found that the major factor which affects presynaptic TRPV1R function is age: by post-natal day 13, the amplitude of capsaicin-induced release of dopamine and glutamate is halved in the rat striatum, and two weeks later, capsaicin already loses its effect. However, TRPV1R receptor function is not enhanced by chemical or genetic ablation of the CB1Rs in dopaminergic, glutamatergic and serotonergic terminals of the mouse brain. Altogether, our data indicate a possible neurodevelopmental role for presynaptic TRPV1Rs in the rodent brain, but we found no cross-talk between TRPV1Rs and CB1Rs in the same nerve terminal. AbstractNeocortical and striatal TRPV 1 (vanilloid or capsaicin) receptors (TRPV 1 Rs) are excitatory ligandgated ion channels, and are implicated in psychiatric disorders. However, the purported presynaptic neuromodulator role of TRPV 1 Rs in glutamatergic, serotonergic or dopaminergic terminals of the rodent forebrain remains little understood. With the help of patch-clamp electrophysiology and neurochemical approaches, we mapped the age-dependence of presynaptic TRPV 1 R function, and furthermore, we aimed at exploring whether the presence of CB 1 cannabinoid receptors (CB 1 Rs) influences the function of the TRPV 1 Rs, as both receptor types share endogenous ligands.We found that the major factor which affects presynaptic TRPV 1 R function is age: by post-natal day 13, the amplitude of capsaicin-induced release of dopamine and glutamate is halved in the rat striatum, and two weeks later, capsaicin already loses its effect. However, TRPV 1 R receptor function is not enhanced by chemical or genetic ablation of the CB 1 Rs in dopaminergic, glutamatergic and serotonergic terminals of the mouse brain.Altogether, our data indicate a possible neurodevelopmental role for presynaptic TRPV 1 Rs in the rodent brain, but we found no cross-talk between TRPV 1 Rs and CB 1 Rs in the same nerve terminal.

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Section: Age-dependence Of Presynaptic Trpv 1 R Functionality In the mentioning

confidence: 74%

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Köles

Garção

Zádori

et al. 2013

Brain Research Bulletin

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“…It was shown recently that VGLUT3 and the vesicular acetylcholine transporter colocalize on the same vesicular surface and that gene targeting of Vglut3 leads to loss of cholinergic transmission resulting from the reduced vesicular transport activity of acetylcholine, a feature referred to as "vesicular synergy" (36). In mDA neurons, it is not known whether VGLUT2 and VMAT2 localize to the same synaptic vesicle, although in electron microscopy analysis they appear to be at least in close proximity to each other (32). The close proximity provides a basis for possible mechanisms by which VGLUT2-mediated cotransmission affects amphetamine-provoked DA release.…”

Section: Discussionmentioning

confidence: 99%

VGLUT2 in dopamine neurons is required for psychostimulant-induced behavioral activation

Birgner

Nordenankar

Lundblad

et al. 2009

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

119

151

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The "One neuron-one neurotransmitter" concept has been challenged frequently during the last three decades, and the coexistence of neurotransmitters in individual neurons is now regarded as a common phenomenon. The functional significance of neurotransmitter coexistence is, however, less well understood. Several studies have shown that a subpopulation of dopamine (DA) neurons in the ventral tegmental area (VTA) expresses the vesicular glutamate transporter 2 (VGLUT2) and has been suggested to use glutamate as a cotransmitter. The VTA dopamine neurons project to limbic structures including the nucleus accumbens, and are involved in mediating the motivational and locomotor activating effects of psychostimulants. To determine the functional role of glutamate cotransmission by these neurons, we deleted VGLUT2 in DA neurons by using a conditional gene-targeting approach in mice. A DAT-Cre/Vglut2Lox mouse line (Vglut2 f/f;DAT-Cre mice) was produced and analyzed by in vivo amperometry as well as by several behavioral paradigms. Although basal motor function was normal in the Vglut2 f/f;DAT-Cre mice, their risk-taking behavior was altered. Interestingly, in both home-cage and novel environments, the gene targeted mice showed a greatly blunted locomotor response to the psychostimulant amphetamine, which acts via the midbrain DA system. Our results show that VGLUT2 expression in DA neurons is required for normal emotional reactivity as well as for psychostimulant-mediated behavioral activation.amphetamine | midbrain | neurotransmission | reward | striatum

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“…Thus, if also co-released from DA somata or dendrites, glutamate or GABA could provide autoregulation of somatodendritic DA release. In support of this possibility, vesicular glutamate transporters (vGluT2) are found in VTA DA neurons [148,157], and co-released GABA appears to be stored via VMAT2 [152], which is found in all midbrain DA cells [78].…”

Section: Modulation Of Somatodendritic Dopamine Release By Synaptic Imentioning

confidence: 99%

“…Long-standing evidence, primarily from cultured DA neurons, had indicated that glutamate could be synthesized and released by DA neurons [147,148]. Using optogenetic methods with selective expression of channelrhodopsin (ChR2) in DA neurons, several groups have now shown that glutamate released from DA axons produces glutamate receptor-dependent excitatory postsynaptic currents in striatal neurons in ex vivo slices [149][150][151][152][153][154] and mediates behavioural consequences in vivo [155].…”

Section: Modulation Of Somatodendritic Dopamine Release By Synaptic Imentioning

confidence: 99%

Somatodendritic dopamine release: recent mechanistic insights

Rice

Patel

2015

Phil. Trans. R. Soc. B

101

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One contribution of 16 to a discussion meeting issue 'Release of chemical transmitters from cell bodies and dendrites of nerve cells'. Dopamine (DA) is a key transmitter in motor, reward and cogitative pathways, with DA dysfunction implicated in disorders including Parkinson's disease and addiction. Located in midbrain, DA neurons of the substantia nigra pars compacta project via the medial forebrain bundle to the dorsal striatum (caudate putamen), and DA neurons in the adjacent ventral tegmental area project to the ventral striatum (nucleus accumbens) and prefrontal cortex. In addition to classical vesicular release from axons, midbrain DA neurons exhibit DA release from their cell bodies and dendrites. Somatodendritic DA release leads to activation of D2 DA autoreceptors on DA neurons that inhibit their firing via G-protein-coupled inwardly rectifying K þ channels. This helps determine patterns of DA signalling at distant axonal release sites. Somatodendritically released DA also acts via volume transmission to extrasynaptic receptors that modulate local transmitter release and neuronal activity in the midbrain. Thus, somatodendritic release is a pivotal intrinsic feature of DA neurons that must be well defined in order to fully understand the physiology and pathophysiology of DA pathways. Here, we review recent mechanistic aspects of somatodendritic DA release, with particular emphasis on the Ca 2þ dependence of release and the potential role of exocytotic proteins.

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Glutamate in dopamine neurons: Synaptic versus diffuse transmission

Cited by 106 publications

References 83 publications

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

Presynaptic TRPV1 vanilloid receptor function is age- but not CB1 cannabinoid receptor-dependent in the rodent forebrain

VGLUT2 in dopamine neurons is required for psychostimulant-induced behavioral activation

Somatodendritic dopamine release: recent mechanistic insights

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