Effects of d-amphetamine administration on the release of endogenous excitatory amino acids in the rat nucleus accumbens

Labarca, Rafael; Gajardo, Maria Ines; Seguel, Mario; Silva, Hernán; Jerez, Sonia; Ruiz, Aida; Bustos, Gonzalo

doi:10.1016/0278-5846(94)00027-f

Cited by 16 publications

(8 citation statements)

References 24 publications

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“…Similarly, dopamine, acting through D 1 receptors, has been found to potentiate neuronal responses to N-methyl-D-aspartate (NMDA), a glutamate receptor agonist, in striatal slices (Cepeda et al 1993). Amphetamine, moreover, is known to enhance striatal glutamate release (Labarca et al 1995), and the destruction of corticostriatal fibers, which removes a major source of glutamatergic input, damps the excitatory effects of amphetamine on striatal neurons . Furthermore, glutamate receptor antagonists have been reported to block amphetamine-induced stereotyped behavior (Karler et al 1994;Segal et al 1995).…”

Section: Discussionmentioning

confidence: 97%

Responses of neurons in dorsal striatum during amphetamine-induced focused stereotypy

1997

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The phase of highly focused, repetitive behavior (stereotypy) induced by amphetamine in rats emerges after an initial period of locomotor activation. To assess the neuronal correlates of this behavioral transition, single-unit activity was recorded from the dorsal striatum of awake, unrestrained rats. Units were first characterized in terms of their responsiveness to spontaneous movement. Various types of motor-related neurons were identified. Some increased activity above resting baseline during specific movements such as forward locomotion or turning of the head, while others were excited during periods of general behavioral activation. Neurons that showed no consistent change in firing rate during overt movement were classified separately. Administration of 5.0 mg/kg d-amphetamine caused a steady increase in the overall neuronal response through both the locomotor and stereotypy phases. An analysis of specific neuronal types, however, revealed distinct, phase-related shifts in firing rate. Locomotor-related neurons discharged rapidly during the early phase of the amphetamine response and then declined toward baseline as focused stereotypy emerged. Cells found to be excited primarily during head movements showed relatively small changes shortly after drug administration but increased markedly in conjunction with intense head-movement activity associated with focused stereotypy. Other neurons, which increased activity nonselectively to a wide range of movements, showed progressive increases in firing rate during both behavioral phases elicited by the drug. Subsequent administration of 1.0 mg/kg haloperidol typically reversed the neuronal changes and blocked amphetamine-induced focused stereotypy. Nonmotor-related cells responded inconsistently to amphetamine, showing an inhibition, excitation, or no change in rate. Previous assessments of neuron-behavior relationships have shown that changes in motor-related neuronal activity are not secondary to amphetamine-induced behavioral changes, though this finding may not apply in all cases. At doses capable of eliciting focused stereotypy, therefore, amphetamine appears to trigger a complex pattern of striatal activity that governs the behavioral response. This conclusion supports steadily increasing evidence that the role of striatal neurons in amphetamine-induced focused stereotypy is shaped by multiple synaptic mechanisms.

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Section: Discussionmentioning

confidence: 97%

Responses of neurons in dorsal striatum during amphetamine-induced focused stereotypy

1997

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“…(1997), which showed that haloperidol increases aspartate release in the entopeduncular nucleus of the rat. In addition, Labarca et al . (1995) showed that d‐amphetamine inhibits K + ‐induced release of aspartate in nucleus accumbens of the rat, an effect which is antagonized by haloperidol.…”

Section: Discussionmentioning

confidence: 99%

On the mechanism of d‐amphetamine‐induced changes in glutamate, ascorbic acid and uric acid release in the striatum of freely moving rats

Miele

Mura

Enrico

et al. 2000

British J Pharmacology

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1 The e ects of systemic, intrastriatal or intranigral administration of d-amphetamine on glutamate, aspartate, ascorbic acid (AA), uric acid, dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in dialysates from the striatum of freely-moving rats were evaluated using microdialysis. 2 d-Amphetamine (2 mg kg 71 ) given subcutaneously (s.c.) increased DA, AA and uric acid and decreased DOPAC+HVA, glutamate and aspartate dialysate concentrations over a 3 h period after d-amphetamine. 5-HIAA concentrations were una ected. Individual changes in glutamate and AA dialysate concentrations were negatively correlated. 3 d-Amphetamine (0.2 mM), given intrastriatally, increased DA and decreased DOPAC+HVA and aspartate dialysate concentrations, but failed to change those of glutamate, AA uric acid or 5-HIAA, over a 2 h period after d-amphetamine. Haloperidol (0.1 mM), given intrastriatally, increased aspartate concentrations without a ecting those of glutamate or AA. 4 d-Amphetamine (0.2 mM), given intranigrally, increased AA and uric acid dialysate concentrations and decreased those of glutamate, aspartate and DA; DOPAC+HVA and 5-HIAA concentrations were una ected. 5 These results suggest that d-amphetamine-induced increases in AA and uric acid and decreases in glutamate concentrations are triggered at nigral sites. The changes in aspartate levels may be evoked by at least two mechanisms: striatal (mediated by inhibitory dopaminergic receptors) and nigral (activation of amino acid carrier-mediated uptake).

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“…mGluR also mediate VTA neuron 8/48 plasticity induced by amphetamine [28]. Glutamatergic neurotransmission has been correlated with the neurotoxic effects of high doses of amphetamine [29]. However, the marked differences in glutamatergic neurotransmission caused by acute and chronic amphetamine exposures rise several questions related the plasticity of the glutamatergic synapse [30][31][32].…”

Section: Abusementioning

confidence: 99%

Drug Abuse, Brain Calcification and Glutamate-Induced Neurodegeneration

Rodrı́guez

Pugliese²,

Mahy³

2009

CDAR

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Effects of d-amphetamine administration on the release of endogenous excitatory amino acids in the rat nucleus accumbens

Cited by 16 publications

References 24 publications

Responses of neurons in dorsal striatum during amphetamine-induced focused stereotypy

Responses of neurons in dorsal striatum during amphetamine-induced focused stereotypy

On the mechanism of d‐amphetamine‐induced changes in glutamate, ascorbic acid and uric acid release in the striatum of freely moving rats

Drug Abuse, Brain Calcification and Glutamate-Induced Neurodegeneration

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