The Experts below are selected from a list of 7434 Experts worldwide ranked by ideXlab platform
Jorge Aceves - One of the best experts on this subject based on the ideXlab platform.
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GABAB receptors modulate depolarization-stimulated [3H]glutamate release in slices of the Pars reticulata of the rat substantia nigra
European Journal of Pharmacology, 2010Co-Authors: Hernán Cortés, David Erlij, Jorge Aceves, Francisco Paz, Benjamín FloránAbstract:GABA(B) receptors decrease the release of GABA from the striatal terminals within the Pars reticulata of the substantia nigra by opposing the increase in the release caused by dopamine D₁ receptors. The dopamine D₁ receptors also increase the release of glutamate from subthalamic terminals in the Pars reticulata. Because GABA(B) receptors decrease the glutamate release from these terminals, we have explored if the effect of GABA(B) receptors also opposed the effect of the dopamine D₁ receptors. The effect of baclofen, a selective GABA(B)-receptor agonist, was tested on the release of [³H]glutamate caused by highly (40 mM) concentrated K(+) solutions in slices of the Pars reticulata. Baclofen decreased (the concentration causing 50% inhibition, IC₅₀, was 8.15 μM) the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors and it also decreased (IC₅₀ was 0.51 μM) this release in the absence of the activation of the dopamine D₁ receptors. The GABA(B) receptors appear then to inhibit glutamate release in two ways; one dependent on the activation of the dopamine D₁ receptors and the other independent of such activation. The protein kinase A-inhibitor H89 blocked the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors, though it did not block the dopamine D₁ receptor-independent baclofen inhibition of the release. This finding indicates that this inhibition was not via the protein kinase A signal-transduction pathway. N-ethylmaleimide, an alkylating agent that inactivates pertussis toxin-sensitive Gi proteins, eliminated both the dopamine D₁ receptor-dependent and -independent baclofen inhibition, showing that both were mediated by these proteins. The injection of baclofen into the Pars reticulata of unanesthetized rats caused contralateral rotation, suggesting a reduced glutamate release from the subthalamic terminals, thereby stopping the inhibition of the premotor thalamic nuclei, causing locomotion. Our data suggest that GABA(B) receptors restrain the excitatory input from the subthalamic nucleus and stimulate motor behavior.
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GABA(B) receptors modulate depolarization-stimulated [³H]glutamate release in slices of the Pars reticulata of the rat substantia nigra.
European journal of pharmacology, 2010Co-Authors: Hernán Cortés, David Erlij, Jorge Aceves, Francisco Paz, Benjamín FloránAbstract:GABA(B) receptors decrease the release of GABA from the striatal terminals within the Pars reticulata of the substantia nigra by opposing the increase in the release caused by dopamine D₁ receptors. The dopamine D₁ receptors also increase the release of glutamate from subthalamic terminals in the Pars reticulata. Because GABA(B) receptors decrease the glutamate release from these terminals, we have explored if the effect of GABA(B) receptors also opposed the effect of the dopamine D₁ receptors. The effect of baclofen, a selective GABA(B)-receptor agonist, was tested on the release of [³H]glutamate caused by highly (40 mM) concentrated K(+) solutions in slices of the Pars reticulata. Baclofen decreased (the concentration causing 50% inhibition, IC₅₀, was 8.15 μM) the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors and it also decreased (IC₅₀ was 0.51 μM) this release in the absence of the activation of the dopamine D₁ receptors. The GABA(B) receptors appear then to inhibit glutamate release in two ways; one dependent on the activation of the dopamine D₁ receptors and the other independent of such activation. The protein kinase A-inhibitor H89 blocked the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors, though it did not block the dopamine D₁ receptor-independent baclofen inhibition of the release. This finding indicates that this inhibition was not via the protein kinase A signal-transduction pathway. N-ethylmaleimide, an alkylating agent that inactivates pertussis toxin-sensitive Gi proteins, eliminated both the dopamine D₁ receptor-dependent and -independent baclofen inhibition, showing that both were mediated by these proteins. The injection of baclofen into the Pars reticulata of unanesthetized rats caused contralateral rotation, suggesting a reduced glutamate release from the subthalamic terminals, thereby stopping the inhibition of the premotor thalamic nuclei, causing locomotion. Our data suggest that GABA(B) receptors restrain the excitatory input from the subthalamic nucleus and stimulate motor behavior.
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Control of the Subthalamic Innervation of Substantia Nigra Pars reticulata by D1 and D2 Dopamine Receptors
Journal of neurophysiology, 2005Co-Authors: Osvaldo Ibáñez-sandoval, Benjamín Florán, Jorge Aceves, Elvira Galarraga, Adán Hernández, Dagoberto Tapia, René Valdiosera, David Erlij, José BargasAbstract:The effects of activating dopaminergic D1 and D2 class receptors of the subthalamic projections that innervate the Pars reticulata of the subtantia nigra (SNr) were explored in slices of the rat br...
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histamine h3 receptor activation selectively inhibits dopamine d1 receptor dependent 3h gaba release from depolarization stimulated slices of rat substantia nigra Pars reticulata
Neuroscience, 1997Co-Authors: M Garcia, J.m. Young, Benjamín Florán, Joseantonio Ariasmontano, Jorge AcevesAbstract:The release of [3H]GABA from slices of rat substantia nigra Pars reticulata induced by increasing extracellular K+ from 6 to 15 mM in the presence of 10 microM sulpiride was inhibited by 73 +/- 3% by 1 microM SCH 23390, consistent with a large component of release dependent upon D1 receptor activation. The histamine H3 receptor-selective agonist immepip (1 microM) and the non-selective agonist histamine (100 microM) inhibited [3H]GABA release by 78 +/- 2 and 80 +/- 2%, respectively. The inhibition by both agonists was reversed by the H3 receptor antagonist thioperamide (1 microM). However, in the presence of 1 microM SCH 23390 depolarization-induced release of [3H]GABA was not significantly decreased by 1 microM immepip. In rats depleted of dopamine by pretreatment with reserpine, immepip no longer inhibited control release of [3H]GABA, but in the presence of 1 microM SKF 38393, which produced a 7 +/- 1-fold stimulation of release, immepip reduced the release to a level not statistically different from that in the presence of immepip alone. Immepip (1 microM) also inhibited the depolarization-induced release of [3H]dopamine from substantia nigra Pars reticulata slices, by 38 +/- 3%. The evidence is consistent with the proposition that activation of histamine H3 receptors leads to the selective inhibition of the component of depolarization-induced [3H]GABA release in substantia nigra Pars reticulata slices which is dependent upon D1 receptor activation. This appears to be largely an action at the terminals of the striatonigral GABA projection neurons, which may be enhanced by a partial inhibition of dendritic [3H]dopamine release.
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RECIPROCAL INTERACTION BETWEEN GLUTAMATE AND DOPAMINE IN THE Pars reticulata OF THE RAT SUBSTANTIA NIGRA: A MICRODIALYSIS STUDY
Neuroscience, 1997Co-Authors: M.g. Rosales, Benjamín Florán, G Flores, D Martínez-fong, R Morales, A Nuñez, José L. Góngora-alfaro, Jorge AcevesAbstract:We studied the interactions between glutamate and dopamine in the Pars reticulata of the substantia nigra by using microdialysis in unanaesthetized rats. Increased extracellular levels of glutamate in the Pars reticulata were obtained by microinjecting the muscarinic agonist carbachol into the ipsilateral subthalamic nucleus. The increase of glutamate levels was followed by increments in extracellular levels of dopamine and GABA. Increased levels of the three neurotransmitters were also observed during the administration of N-methyl-d-aspartate through the microdialysis probe. The increase in glutamate and GABA caused by N-methyl-d-aspartate was blocked by SCH 23390, a selective D1 antagonist. However, the D1 antagonist did not prevent the increase in dopamine levels. The selective D1 agonist SKF 38393, added to the microdialysis probe, increased the levels of the three neurotransmitters. However, after the lesion of the subthalamic nucleus with kainic acid, SKF 38393 increased only the level of GABA but not those of glutamate and dopamine. In addition, the lesion of the subthalamic nucleus produced a drastic (80%) fall in the extracellular levels of glutamate. These data suggest that glutamate, through N-methyl-d-aspartate receptors, stimulates the release of dopamine from dopaminergic dendrites present in the substantia nigra Pars reticulata, and that dopamine in turn stimulates the release of glutamate and GABA. Both effects are mediated by D1 dopamine receptors present on subthalamonigral and striatonigral axon terminals, respectively.
James M. Tepper - One of the best experts on this subject based on the ideXlab platform.
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Striatal, pallidal, and Pars reticulata evoked inhibition of nigrostriatal dopaminergic neurons is mediated by GABAA receptors in vivo
Neuroscience, 1999Co-Authors: Carlos A. Paladini, Pau Celada, James M. TepperAbstract:Abstract Dopaminergic neurons express both GABAA and GABAB receptors and GABAergic inputs play a significant role in the afferent modulation of these neurons. Electrical stimulation of GABAergic pathways originating in neostriatum, globus pallidus or substantia nigra Pars reticulata produces inhibition of dopaminergic neurons in vivo. Despite a number of prior studies, the identity of the GABAergic receptor subtype(s) mediating the inhibition evoked by electrical stimulation of neostriatum, globus pallidus, or the axon collaterals of the projection neurons from substantia nigra Pars reticulata in vivo remain uncertain. Single-unit extracellular recordings were obtained from substantia nigra dopaminergic neurons in urethane anesthetized rats. The effects of local pressure application of the selective GABAA antagonists, bicuculline and picrotoxin, and the GABAB antagonists, saclofen and CGP-55845A, on the inhibition of dopaminergic neurons elicited by single-pulse electrical stimulation of striatum, globus pallidus, and the thalamic axon terminals of the substantia nigra Pars reticulata projection neurons were recorded in vivo. Striatal, pallidal, and thalamic induced inhibition of dopaminergic neurons was always attenuated or completely abolished by local application of the GABAA antagonists. In contrast, the GABAB antagonists, saclofen or CGP-55845A, did not block or attenuate the stimulus-induced inhibition and at times even increased the magnitude and/or duration of the evoked inhibition. Train stimulation of globus pallidus and striatum also produced an inhibition of firing in dopaminergic neurons of longer duration. However this inhibition was largely insensitive to either GABAA or GABAB antagonists although the GABAA antagonists consistently blocked the early portion of the inhibitory period indicating the presence of a GABAA component. These data demonstrate that dopaminergic neurons of the substantia nigra Pars compacta are inhibited by electrical stimulation of striatum, globus pallidus, and the projection neurons of substantia nigra Pars reticulata in vivo. This inhibition appears to be mediated via the GABAA receptor subtype, and all three GABAergic afferents studied appear to possess inhibitory presynaptic GABAB autoreceptors that are active under physiological conditions in vivo.
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GABAergic control of rat substantia nigra dopaminergic neurons: role of globus pallidus and substantia nigra Pars reticulata.
Neuroscience, 1999Co-Authors: Pau Celada, Carlos A. Paladini, James M. TepperAbstract:Abstract Dopaminergic neurons in vivo fire spontaneously in three distinct patterns or modes. It has previously been shown that the firing pattern of substantia nigra dopaminergic neurons can be differentially modulated by local application of GABA A and GABA B receptor antagonists. The GABA A antagonists, bicuculline or picrotoxin, greatly increase burst firing in dopaminergic neurons whereas GABA B antagonists cause a modest shift away from burst firing towards pacemaker-like firing. The three principal GABAergic inputs to nigral dopaminergic neurons arise from striatum, globus pallidus and from the axon collaterals of nigral Pars reticulata projection neurons, each of which appear to act in vivo primarily on GABA A receptors (see preceding paper). In this study we attempted to determine on which afferent pathway(s) GABA A antagonists were acting to cause burst firing. Substantia nigra dopaminergic neurons were studied by single unit extracellular recordings in urethane anesthetized rats during pharmacologically induced inhibition and excitation of globus pallidus. Muscimol-induced inhibition of pallidal neurons produced an increase in the regularity of firing of nigral dopaminergic neurons together with a slight decrease in firing rate. Bicuculline-induced excitation of globus pallidus neurons produced a marked increase in burst firing together with a modest increase in firing rate. These changes in firing rate were in the opposite direction to what would be expected for a monosynaptic GABAergic pallidonigral input. Examination of the response of Pars reticulata GABAergic neurons to similar manipulations of globus pallidus revealed that the firing rates of these neurons were much more sensitive to changes in globus pallidus neuron firing rate than dopaminergic neurons and that they responded in the opposite direction. Pallidal inhibition produced a dramatic increase in the firing rate of Pars reticulata GABAergic neurons while pallidal excitation suppressed the spontaneous activity of Pars reticulata GABAergic neurons. These data suggest that globus pallidus exerts significant control over the firing rate and pattern of substantia nigra dopaminergic neurons through a disynaptic pathway involving nigral Pars reticulata GABAergic neurons and that at least one important way in which local application of bicuculline induces burst firing of dopaminergic neurons is by disinhibition of this tonic inhibitory input.
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GABAA receptor-mediated inhibition of rat substantia nigra dopaminergic neurons by Pars reticulata projection neurons
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1995Co-Authors: James M. Tepper, L. P. Martin, D. R. AndersonAbstract:Evidence from electrophysiological studies has suggested an inhibitory interaction between GABAergic neurons in substantia nigra Pars reticulata and dopaminergic neurons in Pars compacta. However, that this inhibitory interaction is due to a projection from Pars reticulata to Pars compacta has never been demonstrated directly, nor has the GABAergic neuron that mediates the interaction been identified either electrophysiologically or anatomically. To more closely examine interactions between substantia nigra Pars reticulata GABA neurons and dopaminergic neurons, single unit extracellular recordings were obtained from antidromically identified nigrostriatal neurons and their response to antidromic activation of nigral GABAergic projection neurons observed. Stimulation of superior colliculus or thalamus produced a short latency inhibition of dopaminergic neurons. This inhibition was blocked by local application of bicuculline but not 2-hydroxysaclofen. Bicuculline caused most dopaminergic neurons to fire in a bursty mode, whereas saclofen caused most dopaminergic neurons to fire in a pacemaker-like mode. The thalamicevoked inhibition was not affected by kainate lesions of the globus pallidus, but these lesions produced effects on firing pattern identical to those produced by saclofen. These data demonstrate a short latency inhibition of nigral dopaminergic neurons mediated by GABA, receptors that arises from the axon collaterals of Pars reticulata projection neurons. We propose a model in which the firing pattern of nigral dopaminergic neurons in viva is modulated differentially by disinhibition of GABA, inputs arising from Pars reticulata projection neuron axon collaterals and disinhibition of pallidonigral GABAergic inputs mediated by GABA, receptors.
Benjamín Florán - One of the best experts on this subject based on the ideXlab platform.
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GABAB receptors modulate depolarization-stimulated [3H]glutamate release in slices of the Pars reticulata of the rat substantia nigra
European Journal of Pharmacology, 2010Co-Authors: Hernán Cortés, David Erlij, Jorge Aceves, Francisco Paz, Benjamín FloránAbstract:GABA(B) receptors decrease the release of GABA from the striatal terminals within the Pars reticulata of the substantia nigra by opposing the increase in the release caused by dopamine D₁ receptors. The dopamine D₁ receptors also increase the release of glutamate from subthalamic terminals in the Pars reticulata. Because GABA(B) receptors decrease the glutamate release from these terminals, we have explored if the effect of GABA(B) receptors also opposed the effect of the dopamine D₁ receptors. The effect of baclofen, a selective GABA(B)-receptor agonist, was tested on the release of [³H]glutamate caused by highly (40 mM) concentrated K(+) solutions in slices of the Pars reticulata. Baclofen decreased (the concentration causing 50% inhibition, IC₅₀, was 8.15 μM) the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors and it also decreased (IC₅₀ was 0.51 μM) this release in the absence of the activation of the dopamine D₁ receptors. The GABA(B) receptors appear then to inhibit glutamate release in two ways; one dependent on the activation of the dopamine D₁ receptors and the other independent of such activation. The protein kinase A-inhibitor H89 blocked the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors, though it did not block the dopamine D₁ receptor-independent baclofen inhibition of the release. This finding indicates that this inhibition was not via the protein kinase A signal-transduction pathway. N-ethylmaleimide, an alkylating agent that inactivates pertussis toxin-sensitive Gi proteins, eliminated both the dopamine D₁ receptor-dependent and -independent baclofen inhibition, showing that both were mediated by these proteins. The injection of baclofen into the Pars reticulata of unanesthetized rats caused contralateral rotation, suggesting a reduced glutamate release from the subthalamic terminals, thereby stopping the inhibition of the premotor thalamic nuclei, causing locomotion. Our data suggest that GABA(B) receptors restrain the excitatory input from the subthalamic nucleus and stimulate motor behavior.
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GABA(B) receptors modulate depolarization-stimulated [³H]glutamate release in slices of the Pars reticulata of the rat substantia nigra.
European journal of pharmacology, 2010Co-Authors: Hernán Cortés, David Erlij, Jorge Aceves, Francisco Paz, Benjamín FloránAbstract:GABA(B) receptors decrease the release of GABA from the striatal terminals within the Pars reticulata of the substantia nigra by opposing the increase in the release caused by dopamine D₁ receptors. The dopamine D₁ receptors also increase the release of glutamate from subthalamic terminals in the Pars reticulata. Because GABA(B) receptors decrease the glutamate release from these terminals, we have explored if the effect of GABA(B) receptors also opposed the effect of the dopamine D₁ receptors. The effect of baclofen, a selective GABA(B)-receptor agonist, was tested on the release of [³H]glutamate caused by highly (40 mM) concentrated K(+) solutions in slices of the Pars reticulata. Baclofen decreased (the concentration causing 50% inhibition, IC₅₀, was 8.15 μM) the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors and it also decreased (IC₅₀ was 0.51 μM) this release in the absence of the activation of the dopamine D₁ receptors. The GABA(B) receptors appear then to inhibit glutamate release in two ways; one dependent on the activation of the dopamine D₁ receptors and the other independent of such activation. The protein kinase A-inhibitor H89 blocked the increase in the release of the [³H]glutamate caused by the dopamine D₁ receptors, though it did not block the dopamine D₁ receptor-independent baclofen inhibition of the release. This finding indicates that this inhibition was not via the protein kinase A signal-transduction pathway. N-ethylmaleimide, an alkylating agent that inactivates pertussis toxin-sensitive Gi proteins, eliminated both the dopamine D₁ receptor-dependent and -independent baclofen inhibition, showing that both were mediated by these proteins. The injection of baclofen into the Pars reticulata of unanesthetized rats caused contralateral rotation, suggesting a reduced glutamate release from the subthalamic terminals, thereby stopping the inhibition of the premotor thalamic nuclei, causing locomotion. Our data suggest that GABA(B) receptors restrain the excitatory input from the subthalamic nucleus and stimulate motor behavior.
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Control of the Subthalamic Innervation of Substantia Nigra Pars reticulata by D1 and D2 Dopamine Receptors
Journal of neurophysiology, 2005Co-Authors: Osvaldo Ibáñez-sandoval, Benjamín Florán, Jorge Aceves, Elvira Galarraga, Adán Hernández, Dagoberto Tapia, René Valdiosera, David Erlij, José BargasAbstract:The effects of activating dopaminergic D1 and D2 class receptors of the subthalamic projections that innervate the Pars reticulata of the subtantia nigra (SNr) were explored in slices of the rat br...
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histamine h3 receptor activation selectively inhibits dopamine d1 receptor dependent 3h gaba release from depolarization stimulated slices of rat substantia nigra Pars reticulata
Neuroscience, 1997Co-Authors: M Garcia, J.m. Young, Benjamín Florán, Joseantonio Ariasmontano, Jorge AcevesAbstract:The release of [3H]GABA from slices of rat substantia nigra Pars reticulata induced by increasing extracellular K+ from 6 to 15 mM in the presence of 10 microM sulpiride was inhibited by 73 +/- 3% by 1 microM SCH 23390, consistent with a large component of release dependent upon D1 receptor activation. The histamine H3 receptor-selective agonist immepip (1 microM) and the non-selective agonist histamine (100 microM) inhibited [3H]GABA release by 78 +/- 2 and 80 +/- 2%, respectively. The inhibition by both agonists was reversed by the H3 receptor antagonist thioperamide (1 microM). However, in the presence of 1 microM SCH 23390 depolarization-induced release of [3H]GABA was not significantly decreased by 1 microM immepip. In rats depleted of dopamine by pretreatment with reserpine, immepip no longer inhibited control release of [3H]GABA, but in the presence of 1 microM SKF 38393, which produced a 7 +/- 1-fold stimulation of release, immepip reduced the release to a level not statistically different from that in the presence of immepip alone. Immepip (1 microM) also inhibited the depolarization-induced release of [3H]dopamine from substantia nigra Pars reticulata slices, by 38 +/- 3%. The evidence is consistent with the proposition that activation of histamine H3 receptors leads to the selective inhibition of the component of depolarization-induced [3H]GABA release in substantia nigra Pars reticulata slices which is dependent upon D1 receptor activation. This appears to be largely an action at the terminals of the striatonigral GABA projection neurons, which may be enhanced by a partial inhibition of dendritic [3H]dopamine release.
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RECIPROCAL INTERACTION BETWEEN GLUTAMATE AND DOPAMINE IN THE Pars reticulata OF THE RAT SUBSTANTIA NIGRA: A MICRODIALYSIS STUDY
Neuroscience, 1997Co-Authors: M.g. Rosales, Benjamín Florán, G Flores, D Martínez-fong, R Morales, A Nuñez, José L. Góngora-alfaro, Jorge AcevesAbstract:We studied the interactions between glutamate and dopamine in the Pars reticulata of the substantia nigra by using microdialysis in unanaesthetized rats. Increased extracellular levels of glutamate in the Pars reticulata were obtained by microinjecting the muscarinic agonist carbachol into the ipsilateral subthalamic nucleus. The increase of glutamate levels was followed by increments in extracellular levels of dopamine and GABA. Increased levels of the three neurotransmitters were also observed during the administration of N-methyl-d-aspartate through the microdialysis probe. The increase in glutamate and GABA caused by N-methyl-d-aspartate was blocked by SCH 23390, a selective D1 antagonist. However, the D1 antagonist did not prevent the increase in dopamine levels. The selective D1 agonist SKF 38393, added to the microdialysis probe, increased the levels of the three neurotransmitters. However, after the lesion of the subthalamic nucleus with kainic acid, SKF 38393 increased only the level of GABA but not those of glutamate and dopamine. In addition, the lesion of the subthalamic nucleus produced a drastic (80%) fall in the extracellular levels of glutamate. These data suggest that glutamate, through N-methyl-d-aspartate receptors, stimulates the release of dopamine from dopaminergic dendrites present in the substantia nigra Pars reticulata, and that dopamine in turn stimulates the release of glutamate and GABA. Both effects are mediated by D1 dopamine receptors present on subthalamonigral and striatonigral axon terminals, respectively.
G Flores - One of the best experts on this subject based on the ideXlab platform.
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RECIPROCAL INTERACTION BETWEEN GLUTAMATE AND DOPAMINE IN THE Pars reticulata OF THE RAT SUBSTANTIA NIGRA: A MICRODIALYSIS STUDY
Neuroscience, 1997Co-Authors: M.g. Rosales, Benjamín Florán, G Flores, D Martínez-fong, R Morales, A Nuñez, José L. Góngora-alfaro, Jorge AcevesAbstract:We studied the interactions between glutamate and dopamine in the Pars reticulata of the substantia nigra by using microdialysis in unanaesthetized rats. Increased extracellular levels of glutamate in the Pars reticulata were obtained by microinjecting the muscarinic agonist carbachol into the ipsilateral subthalamic nucleus. The increase of glutamate levels was followed by increments in extracellular levels of dopamine and GABA. Increased levels of the three neurotransmitters were also observed during the administration of N-methyl-d-aspartate through the microdialysis probe. The increase in glutamate and GABA caused by N-methyl-d-aspartate was blocked by SCH 23390, a selective D1 antagonist. However, the D1 antagonist did not prevent the increase in dopamine levels. The selective D1 agonist SKF 38393, added to the microdialysis probe, increased the levels of the three neurotransmitters. However, after the lesion of the subthalamic nucleus with kainic acid, SKF 38393 increased only the level of GABA but not those of glutamate and dopamine. In addition, the lesion of the subthalamic nucleus produced a drastic (80%) fall in the extracellular levels of glutamate. These data suggest that glutamate, through N-methyl-d-aspartate receptors, stimulates the release of dopamine from dopaminergic dendrites present in the substantia nigra Pars reticulata, and that dopamine in turn stimulates the release of glutamate and GABA. Both effects are mediated by D1 dopamine receptors present on subthalamonigral and striatonigral axon terminals, respectively.
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Activation of subthalamic neurons produces NMDA receptor-mediated dendritic dopamine release in substantia nigra Pars reticulata: a microdialysis study in the rat.
Brain research, 1994Co-Authors: M G Rosales, G Flores, S Hernández, D Martínez-fong, J AcevesAbstract:Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the Pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe was implanted in the medial aspect of the Pars reticulata to collect samples of the perfusate. Carbachol (1 microgram/0.25 microliter saline) enhanced (58 +/- 8% over basal values) nigral DA release. The enhancement was fully blocked by the NMDA antagonist AP5 added to the microdialysis medium perfusing the Pars reticulata. Perfusion of the Pars reticulata with NMDA also increased (125 +/- 25% over basal) nigral DA release. Again, AP5 reversed the effect. These results suggest that activation of the glutamatergic subthalamonigral pathway enhances dendritic DA release by activating NMDA receptors present on dopaminergic dendrites.
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Activation of subthalamic neurons produces NMDA receptor-mediated dendritic dopamine release in substantia nigra Pars reticulata: a microdialysis study in the rat
Brain Research, 1994Co-Authors: M G Rosales, G Flores, S Hernández, D Martínez-fong, Jorge AcevesAbstract:Abstract Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the Pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe was implanted in the medial aspect of the Pars reticulata to collect samples of the perfusate. Carbachol (1 μg/0.25 μl saline) enhanced (58 ± 8% over basal values) nigral DA release. The enhancement was fully blocked by the NMDA antagonist AP5 added to the microdialysis medium perfusing the Pars reticulata. Perfusion of the Pars reticulata with NMDA also increased (125 ± 25% over basal) nigral DA release. Again, AP5 reversed the effect. These results suggest that activation of the glutamatergic subthalamonigral pathway enhances dendritic DA release by activating NMDA receptors present on dopaminergic dendrites.
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Activation of D1 receptors stimulates accumulation of γ-aminobutyric acid in slices of the Pars reticulata of 6-hydroxydopamine-lesioned rats
Neuroscience letters, 1992Co-Authors: Jorge Aceves, Benjamín Florán, D Martínez-fong, Joaquin Benitez, Arturo Sierra, G FloresAbstract:Abstract D 1 dopamine receptors are present on terminals of striatal neurons to the Pars reticulata of the substantia nigra in the rat. Here we have studied the effect of the activation of these receptors on the synthesis of γ-aminobutyric acid (GABA) in slices of the Pars reticulata of the substantia nig isolated from 6-hydroxydopamine-lesioned rats. The synthesis was judged by the accumulation of GABA after inhibiting GABA transaminase with aminooxyacetic acid. Both dopamine and SCH 23390, a D 1 agonist, stimulated the synthesis. The effect of both compounds was blocked by SCH 23390, a D 1 antagonist, but not by sulpiride, a D 2 antagonist. In the absence of receptor activation, the synthesis was very slow. The results a trophic influence of dopamine upon the synthesis of GABA via D 1 receptors.
Wing-ho Yung - One of the best experts on this subject based on the ideXlab platform.
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Modulation of synaptic GABAA receptor function by zolpidem in substantia nigra Pars reticulata.
Acta pharmacologica Sinica, 2008Co-Authors: Li-li Zhang, Lei Chen, Yan Xue, Wing-ho YungAbstract:Modulation of synaptic GABA A receptor function by zolpidem in substantia nigra Pars reticulata 1
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Inhibitory postsynaptic currents of rat substantia nigra Pars reticulata neurons: role of GABA receptors and GABA uptake.
Brain Research, 1999Co-Authors: Priscilla K.y Chan, Wing-ho YungAbstract:Abstract Whole-cell patch-clamp recordings were made from substantia nigra Pars reticulata neurons in midbrain slices of young rats to study the characteristics of spontaneous and evoked inhibitory postsynaptic currents and factors which govern their decay kinetics. In the presence of the glutamate receptor antagonists d , l -2-amino-5-phosphonopentanoic acid (20 μM) and 6-cyano-7-nitroquinoxaline-2,3-dione (20 μM), bicuculline-sensitive spontaneous inward inhibitory postsynaptic currents were often observed using high Cl− electrodes. Application of the selective GABAB receptor antagonist CGP55845A (2 μM) did not alter the half decay time of these inhibitory postsynaptic currents, which however was prolonged by the potent GABA uptake blocker tiagabine (1 μM). In addition, the frequencies and amplitudes of the inhibitory postsynaptic currents were significantly reduced by tiagabine but these effects were prevented by CGP55845A. Inhibitory postsynaptic currents with similar sensitivity to bicuculline could also be evoked intranigrally. Similar to the spontaneous currents, the decay time of evoked inhibitory postsynaptic currents was not affected by 2 μM CGP55845A. However, in the absence of CGP55845A, tiagabine shortened the IPSC decay time but had an opposite effect if CGP55845A was present. These data suggest that the spontaneous and evoked inhibitory postsynaptic currents recorded from substantia nigra Pars reticulata neurons are mediated mainly by GABAA receptors. Uptake of GABA helps to terminate these currents. When the uptake mechanism is blocked, accumulation of GABA would lead to activation of presynaptic GABAB receptors and reduction in GABA release. The role of postsynaptic GABAB receptors in substantia nigra Pars reticulata of young rats seems to be minimal.
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Differential expression of pre- and postsynaptic GABAB receptors in rat substantia nigra Pars reticulata neurones
European Journal of Pharmacology, 1998Co-Authors: Priscilla K.y Chan, Christopher Kai-shun Leung, Wing-ho YungAbstract:Whole-cell recordings were made from substantia nigra Pars reticulata in rat midbrain slices to study the functional expression of pre- and postsynaptic GABAB receptors in GABA output neurones. Baclofen (up to 300 μM) dose-dependently activated a weak current which was insensitive to tetrodotoxin and Ca2+-free solution but blocked by Ba2+ and 2-OH-saclofen. The maximum current activated by baclofen (30 μM) was 43.0±4.5 pA (n=27), representing only 23% of that in dopamine neurones. Baclofen (1–30 μM) also reduced the frequency of the GABAA receptor-mediated miniature inhibitory postsynaptic currents while the distribution of their amplitudes was unaffected. This presynaptic effect of baclofen, prominent at a concentration as low as 1 μM, was sensitive to 2-OH-saclofen and occluded by Cd2+, but was unaffected by Ba2+. The results suggest a predominant role of the presynaptic GABAB receptors in substantia nigra Pars reticulata. The relative abundance of pre- and postsynaptic GABAB receptor subtypes in this brain region may also be important in mediating the anticonvulsant effect of baclofen in rats.