Glutamate regulates the spontaneous and evoked release of dopamine in the rat striatum

Kulagina, N. V.; Zigmond, Michael J.; Michael, A.C

doi:10.1016/s0306-4522(00)00480-2

Cited by 90 publications

(101 citation statements)

References 51 publications

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“…However, the dosedependency of the effect was confirmed across the three concentrations tested through the highly significant linear trend in response suppression with concentration. These data support previous findings that agonists at ionotropic glutamate receptors generally 27,28 and specifically NMDA-R 12,24 in dorsal striatum caused a decrease in stimulated dopamine, across a similar dose range, albeit that unlike those of Wu et al…”

Section: Resultssupporting

confidence: 91%

N-Methyl-d-aspartate Modulation of Nucleus Accumbens Dopamine Release by Metabotropic Glutamate Receptors: Fast Cyclic Voltammetry Studies in Rat Brain Slices in Vitro

Yavas

Young

2017

ACS Chem. Neurosci.

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Abstract.The N-methyl-D-aspartate (NMDA) receptor antagonist, phencyclidine, induces behavioural changes in rodents mimicking symptoms of schizophrenia, possibly mediated through dysregulation of glutamatergic control of mesolimbic dopamine release. We tested the hypothesis that NMDA receptor activation modulates accumbens dopamine release, and that phencyclidine pretreatment altered this modulation. NMDA caused a receptor-specific, dosedependent decrease in electrically stimulated dopamine release in nucleus accumbens brain slices. This decrease was unaffected by picrotoxin, making it unlikely to be mediated through GABAergic neurones, but was decreased by the metabotropic glutamate receptor antagonist, (RS)-α-methyl-4-sulfonophenylglycine, indicating that NMDA activates mechanisms controlled by these receptors to decrease stimulated dopamine release. The effect of NMDA was unchanged by in vivo pretreatment with phencyclidine (twice daily for five days), with a washout period of at least seven days before experimentation, which supports the hypothesis that there is no enduring direct effect of PCP at NMDA receptors after this pretreatment procedure. We propose that NMDA depression of accumbal dopamine release is mediated by metabotropic glutamate receptors located pre-or peri-synaptically, and suggest that NMDA evoked increased extrasynaptic spill-over of glutamate is sufficient to activate these receptors that, in turn, inhibit dopamine release. Furthermore, we suggest that enduring functional changes brought about by sub-chronic phencyclidine pre-treatment, modelling deficits in schizophrenia, are downstream effects consequent on chronic blockade of NMDA receptors, rather than direct effects on NMDA receptors themselves.

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Section: Resultssupporting

confidence: 91%

N-Methyl-d-aspartate Modulation of Nucleus Accumbens Dopamine Release by Metabotropic Glutamate Receptors: Fast Cyclic Voltammetry Studies in Rat Brain Slices in Vitro

Yavas

Young

2017

ACS Chem. Neurosci.

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“…The actual value of the steady-state concentration from tonic firing will depend on the number of active dopaminergic neurons (Dai and Tepper 1998). In addition, our predictions only account for dopamine released by impulses; dopamine released by local factors such as activation of glutamate receptors might lead to higher basal concentrations (Kulagina et al 2001).…”

Section: Modeling Dopamine Diffusion In the Brainmentioning

confidence: 99%

Real‐time decoding of dopamine concentration changes in the caudate–putamen during tonic and phasic firing

Venton¹,

Zhang

Garris

et al. 2003

Journal of Neurochemistry

249

206

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The fundamental process that underlies volume transmission in the brain is the extracellular diffusion of neurotransmitters from release sites to distal target cells. Dopaminergic neurons display a range of activity states, from low-frequency tonic firing to bursts of high-frequency action potentials (phasic firing). However, it is not clear how this activity affects volume transmission on a subsecond time scale. To evaluate this, we developed a finite-difference model that predicts the lifetime and diffusion of dopamine in brain tissue. We first used this model to decode in vivo amperometric measurements of electrically evoked dopamine, and obtained rate constants for release and uptake as well as the extent of diffusion. Accurate predictions were made under a variety of conditions including different regions, different stimulation parameters and with uptake inhibited. Second, we used the decoded rate constants to predict how heterogeneity of dopamine release and uptake sites would affect dopamine concentration fluctuations during different activity states in the absence of an electrode. These simulations show that synchronous phasic firing can produce spatially and temporally heterogeneous concentration profiles whereas asynchronous tonic firing elicits uniform, steady-state dopamine concentrations. Keywords: amperometry, caudate-putamen, cocaine, diffusion, steady state, volume transmission. J. Neurochem. (2003Neurochem. ( ) 87, 1284Neurochem. ( -1295 Dopaminergic neurons fire in a low-frequency tonic mode and periodically exhibit bursts of high-frequency action potentials . Microdialysis studies have revealed that tonic dopamine concentrations are in the low nanomolar range (Justice 1993). Recently, naturally occuring increases in dopamine concentration have been detected on a subsecond time scale with carbon-fiber electrodes Phillips et al. 2003). These transients appear to arise from phasic firing because they are mimicked by high-frequency electrical stimulation of dopaminergic cell bodies. Like the phasic firing of dopaminergic neurons that occurs during salient stimuli (Schultz 1998), the dopamine transients can be matched to specific behaviors such as interaction with another animal (Robinson et al. 2001 or lever pressing to self-administer cocaine (Phillips et al. 2003).It is well documented that dopamine in the striatum communicates via volume transmission (Garris et al. 1994) which differs from the classic synaptic mode of wiring transmission because neurotransmitter can diffuse to target cells distant from release sites (Zoli et al. 1998;Vizi 2000). The existence of naturally occuring dopamine concentration transients in the brain raises several questions. Are there temporal differences in dopamine concentrations at release and target sites? Is dopamine volume transmission differentially affected by tonic and phasic firing patterns? To answer such questions, mathematical models that consider the rates of release, uptake and coupled diffusion are required. Although several models have been d...

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“…The interaction between glutamate and dopamine is widely documented Levine and Cepeda, 1998;Kulagina et al, 2001;West et al, 2003;David et al, 2005). In schizophrenia, dopaminergic dysregulation is thought to be the final common pathway resulting from an altered glutamatergic neurotransmission (Carlsson and Carlsson, 1990;Javitt and Zukin, 1991;Olney and Farber, 1995).…”

Section: Introductionmentioning

confidence: 99%

Higher Levels of Glutamate in the Associative-Striatum of Subjects with Prodromal Symptoms of Schizophrenia and Patients with First-Episode Psychosis

Fuente‐Sandoval

León-Ortíz

Favila

et al. 2011

Neuropsychopharmacol

208

157

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The glutamatergic and dopaminergic systems are thought to be involved in the pathophysiology of schizophrenia. Their interaction has been widely documented and may have a role in the neurobiological basis of the disease. The aim of this study was to compare, using proton magnetic resonance spectroscopy ( 1 H-MRS), glutamate levels in the precommissural dorsal-caudate (a dopamine-rich region) and the cerebellar cortex (negligible for dopamine) in the following: (1) 18 antipsychotic-naïve subjects with prodromal symptoms and considered to be at ultra high-risk for schizophrenia (UHR), (2) 18 antipsychotic-naïve first-episode psychosis patients (FEP), and (3) 40 age-and sex-matched healthy controls. All subjects underwent a 1 H-MRS study using a 3Tesla scanner. Glutamate levels were quantified and corrected for the proportion of cerebrospinal fluid and percentage of gray matter in the voxel. The UHR and FEP groups showed higher levels of glutamate than controls, without differences between UHR and FEP. In the cerebellum, no differences were seen between the three groups. The higher glutamate level in the precommissural dorsal-caudate and not in the cerebellum of UHR and FEP suggests that a high glutamate level (a) precedes the onset of schizophrenia, and (b) is present in a dopamine-rich region previously implicated in the pathophysiology of schizophrenia.

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Glutamate regulates the spontaneous and evoked release of dopamine in the rat striatum

Cited by 90 publications

References 51 publications

N-Methyl-d-aspartate Modulation of Nucleus Accumbens Dopamine Release by Metabotropic Glutamate Receptors: Fast Cyclic Voltammetry Studies in Rat Brain Slices in Vitro

N-Methyl-d-aspartate Modulation of Nucleus Accumbens Dopamine Release by Metabotropic Glutamate Receptors: Fast Cyclic Voltammetry Studies in Rat Brain Slices in Vitro

Real‐time decoding of dopamine concentration changes in the caudate–putamen during tonic and phasic firing

Higher Levels of Glutamate in the Associative-Striatum of Subjects with Prodromal Symptoms of Schizophrenia and Patients with First-Episode Psychosis

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