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

Abstract

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).

Design and Construction of a Distributed Sensor NET for Biotelemetric Monitoring of Brain Energetic Metabolism Using Microsensors and Biosensors

“…19). This result is consistent with the activation of the AA/glutamate heteroexchange system (Rice, 2000) in which AA release is related to glutamate release and uptake subsequent to neural activation (Miele et al, 2000). Glucose biosensor in-vivo experiments were carried out using the same procedures as oxygen and AA ones.…”

“…In brief, in normal conditions both neurons and astrocytes use glucose as energetic substrate. After neural activation, cortico-striatal endings release glutamate (1) in the striatal extracellular compartment (Miele et al, 2000). Immediately after, GLU is taken by astrocytes from the synaptic cleft and exchanged (Rice, 2000) with AA (2).…”

Dopamine Modulates Release from Corticostriatal Terminals

“…In control mice, microdialysis demonstrated a decrease in extracellular glutamate after exposure to amphetamine, as shown by others (Miele et al, 2000). This was anticipated because FM1-43 destaining from corticostriatal terminals in the presence of amphetamine suggested a reduction in vesicular release of glutamate.…”

Investigation of the effects of ‘piperazine-containing party pills’ and dexamphetamine on interhemispheric communication using electroencephalography

“…Our findings of a lack of IHTT asymmetry in the groups given either BZP, BZP + TFMPP or dexamphetamine may suggest that enhanced DA release induced by these drugs promotes neural connectivity between the hemispheres which cancels out the asymmetry usually observed in healthy adults. Evidence shows that BZP and the combination of BZP + TFMPP selectively elevate dialysate DA levels in vivo (Baumann et al 2004), and dexamphetamine increases dialysate DA concentrations up to 15 times above baseline in vivo (Miele et al 2000). Conversely, TFMPP reduces extracellular DA via 5-HT 2c receptor binding, leading to the enhanced directional asymmetry.…”