Nitric oxide and potassium chloride-facilitated striatal dopamine efflux in vivo: role of calcium-dependent release mechanisms

West, Anthony R.; Galloway, M. P.

doi:10.1016/s0197-0186(98)00054-0

Cited by 62 publications

(27 citation statements)

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“…−: inhibition; +: activation; 0: no effect. studies suggest that, under physiological conditions, NO increases striatal dopamine by facilitating its release (Black et al, 1994;Stewart et al, 1996;Iravani et al, 1998;West and Galloway, 1998;West et al, 2002) and/or by decreasing its reuptake (Guevara-Guzman et al, 1994;Kiss and Vizi, 2001). The effects of NO may vary depending on several factors such as the functional state of the target neurons and the instant composition of the extracellular fluid.…”

Section: Motor Effects Of Nos Inhbitors: Possible Mechanisms Of Actionmentioning

confidence: 99%

“…Striatal NO tone regulates the basal activity and responsiveness of dopamine (DA) neurons to cortical and striatal inputs (Sandor et al, 1995;West and Galloway, 1998;West et al, 2002). Therefore, striatal NO signaling may play an important role in the integration of information transmitted to basal ganglia output centers via corticostriatal and striatal efferent pathways (West et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, striatal NO signaling may play an important role in the integration of information transmitted to basal ganglia output centers via corticostriatal and striatal efferent pathways (West et al, 2002). Although the influence of NO on striatal neuronal activity remains to be thoroughly characterized, evidence has accumulated suggesting that NO signaling may mediate and/or regulate multiple aspects of striatal neurotransmission (West and Galloway, 1998;West et al, 2002). (PPTg).…”

Section: Introductionmentioning

confidence: 99%

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Role of Nitric Oxide on Motor Behavior

et al. 2005

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The present review paper describes results indicating the influence of nitric oxide (NO) on motor control. Our last studies showed that systemic injections of low doses of inhibitors of NO synthase (NOS), the enzyme responsible for NO formation, induce anxiolytic effects in the elevated plus maze whereas higher doses decrease maze exploration. Also, NOS inhibitors decrease locomotion and rearing in an open field arena. These results may involve motor effects of this compounds, since inhibitors of NOS, NG-nitro-L-arginine (L-NOARG), N(G)-nitro-L-arginine methylester (L-NAME), N(G)-monomethyl-L-arginine (L-NMMA), and 7-Nitroindazole (7-NIO), induced catalepsy in mice. This effect was also found in rats after systemic, intracebroventricular or intrastriatal administration. Acute administration of L-NOARG has an additive cataleptic effect with haloperidol, a dopamine D2 antagonist. The catalepsy is also potentiated by WAY 100135 (5-HT1a receptor antagonist), ketanserin (5HT2a and alfal adrenergic receptor antagonist), and ritanserin (5-HT2a and 5HT2c receptor antagonist). Atropine sulfate and biperiden, antimuscarinic drugs, block L-NOARG-induced catalepsy in mice. L-NOARG subchronic administration in mice induces rapid tolerance (3 days) to its cataleptic effects. It also produces cross-tolerance to haloperidol-induced catalepsy. After subchronic L-NOARG treatment there is an increase in the density NADPH-d positive neurons in the dorsal part of nucleus caudate-putamen, nucleus accumbens, and tegmental pedunculupontinus nucleus. In contrast, this treatment decreases NADPH-d neuronal number in the substantia nigra compacta. Considering these results we suggest that (i) NO may modulate motor behavior, probably by interfering with dopaminergic, serotonergic, and cholinergic neurotransmission in the striatum; (ii) Subchronic NO synthesis inhibition induces plastic changes in NO-producing neurons in brain areas related to motor control and causes cross-tolerance to the cataleptic effect of haloperidol, raising the possibility that such treatments could decrease motor side effects associated with antipsychotic medications. Finally, recent studies using experimental Parkinson's disease models suggest an interaction between NO system and neurodegenerative processes in the nigrostriatal pathway. It provides evidence of a protective role of NO. Together, our results indicate that NO may be a key participant on physiological and pathophysiological processes in the nigrostriatal system.

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Section: Motor Effects Of Nos Inhbitors: Possible Mechanisms Of Actionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of Nitric Oxide on Motor Behavior

et al. 2005

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“…In the dorsal striatum, NO interacts with dopamine (Hanbauer et al, 1992;Zhu and Luo, 1992;Lonart et al, 1993;Guevara Guzman et al, 1994;Ishida et al, 1994;Silva, et al, 1995;Shibata et al, 1996;West and Galloway, 1998) and other neurotransmitters (Guevara Guzman et al, 1994;Moller et al, 1995;Bogdanov and Wurtman, 1997;Hanania and Johnson, 1998;Ikarashi et al, 1998;Segovia and Mora, 1998). Little is known of the effects of NO in the nucleus accumbens, although it seems likely that the interactions between NO and various transmitters that occur in the dorsal striatum also take place in the nucleus accumbens.…”

mentioning

confidence: 99%

Ultrastructural features of the nitric oxide synthase-containing interneurons in the nucleus accumbens and their relationship with tyrosine hydroxylase-containing terminals

Hidaka

Totterdell

2001

J. Comp. Neurol.

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The ultrastructural features of neuronal nitric oxide synthase (NOS) -immunoreactive interneurons of rat nucleus accumbens shell and core were studied and compared. The NOS-containing subpopulation displayed characteristics similar to those previously described for nicotinamide adenine dinucleotide phosphate diaphorase-, neuropeptide Y, or somatostatin-containing striatal neurons, but also showed properties not previously associated with them, particularly the formation of both asymmetric and symmetric synaptic junctions. Inputs derived mainly from unlabeled terminals, but some contacts were made by NOS-immunolabeled terminals, by means of asymmetric synapses. Immunopositive endings that formed symmetric synapses were mainly onto dendritic shafts, whereas those that formed asymmetric synapses targeted spine heads. Morphometric analysis revealed that the core and shell NOS-stained neurons had subtly different innervation patterns and that immunostained terminals were significantly larger in the shell. A parallel investigation explored synaptic associations with dopaminergic innervation identified by labeling with an antibody against tyrosine hydroxylase (TH). In both shell and core, TH-positive boutons formed symmetric synapses onto NOS-containing dendrites, and in the core, TH- and NOS-immunolabeled terminals converged on both a single spiny dendrite and a spine. These results suggest that, in the rat nucleus accumbens, NOS-containing neurons may be further partitioned into subtypes, with differing connectivities in shell and core regions. These NOS-containing neurons may be influenced by a dopaminergic input. Recent studies suggest that nitric oxide potentiates dopamine release and the current study identifies the medium-sized, densely spiny neurons as a possible site of such an interaction.

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“…These results suggest that a part of the COinduced increase in extracellular DA may be due to enhancement of DA release depending on the influx of external Na + , but not to nonspecific leakage of DA from nerve terminals. Evidence has been accumulated that CO endogenously generated via degradation of heme has physiological functions as a neurotransmitter or neuromodulator, like nitric oxide (Marks et al 1991;Maines 1993;Snyder et al 1998;Sharma et al 1998), which is involved in regulation of DA release in the striatum (Kahn et al 1995;West and Galloway 1999). In addition, exogenous CO is able to influence physiological functions by mimicking the role of endogenous CO (Trischmann et al 1991;Wang et al 1997;Steiner et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Modification of the striatal dopaminergic neuron system by carbon monoxide exposure in free-moving rats, as determined by in vivo brain microdialysis

Hara

Mukai

Kurosaki

et al. 2002

Archives of Toxicology

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Acute carbon monoxide (CO) intoxication in humans results in motor deficits, which resemble those in Parkinson's disease, suggesting possible disturbance of the central dopaminergic (DAergic) neuronal system by CO exposure. In the present study, therefore, we explored the effects of CO exposure on the DAergic neuronal system in the striatum of freely moving rats by means of in vivo brain microdialysis. Exposure of rats to CO (up to 0.3%) for 40 min caused an increase in extracellular dopamine (DA) levels and a decrease in extracellular levels of its major metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in the striatum depending on the CO concentration. Reoxygenation following termination of the CO exposure resulted in a decline of DA to the control level and an overshoot in the recovery of DOPAC and HVA to levels higher than the control. A monoamine oxidase type A (MAO-A) inhibitor, clorgyline, significantly potentiated the CO-induced increase in DA and completely abolished the subsequent overshoot in the recovery of DOPAC and HVA. Tetrodotoxin, a Na(+) channel blocker, completely abolished both the CO-induced increase in DA and the overshoot of DOPAC and HVA. A DA uptake inhibitor, nomifensine, strongly potentiated the CO-induced increase in DA without affecting the subsequent overshoot of DOPAC and HVA. Clorgyline further potentiated the effect of nomifensine on the CO-induced increase in DA, although a slight overshoot of DOPAC and HVA appeared. These findings suggest that (1) CO exposure may stimulate Na(+)-dependent DA release in addition to suppressing DA metabolism, resulting in a marked increase in extracellular DA in rat striatum, and (2) CO withdrawal and subsequent reoxygenation may enhance the oxidative metabolism, preferentially mediated by MAO-A, of the increased extracellular DA. In the light of the neurotoxicity of DA per se and reactive substances, such as quinones and activated oxygen species, generated via DA oxidation, the significant modification of the striatal DAergic neuronal system by CO exposure might participate in the neurological outcome following acute CO intoxication.

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Nitric oxide and potassium chloride-facilitated striatal dopamine efflux in vivo: role of calcium-dependent release mechanisms

Cited by 62 publications

References 29 publications

Role of Nitric Oxide on Motor Behavior

Role of Nitric Oxide on Motor Behavior

Ultrastructural features of the nitric oxide synthase-containing interneurons in the nucleus accumbens and their relationship with tyrosine hydroxylase-containing terminals

Modification of the striatal dopaminergic neuron system by carbon monoxide exposure in free-moving rats, as determined by in vivo brain microdialysis

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