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Bhattacharjee, A.K. et al.

Abesh K. Bhattacharjee, Lisa Chang, Mei Chen, Laura White, Jane M. Bell, Richard P. Bazinet, Stanley I. Rapoport,

Chronic d-amphetamine depresses an imaging marker of arachidonic acid metabolism in rat brain.

Acute d-amphetamine (d-Amph) administration to rats leads to the release of arachidonic acid (AA, 20:4n-6) as a second messenger following indirect agonism at dopamine D2-like receptors in the brain. We hypothesized that chronically administered d-Amph in rats also would alter brain AA metabolism and signalling. To test this, adult male rats were injected i.p. daily for 2 wk with saline or 2.5 mg/kg d-Amph. After a 1-d washout, the unanaesthetized rats were injected acutely with i.v. saline, 1 mg/kg quinpirole (a D2-like receptor agonist) or 5.0 mg/kg SKF-38393 (a D1-like receptor agonist), followed by i.v. [1-14C]AA. The AA incorporation coefficient k* (brain radioactivity/integrated plasma radioactivity), a marker of AA signalling and metabolism, was quantified using autoradiography in each of 62 brain regions. Compared with chronic saline, chronic d-Amph widely decreased baseline values of k* in brain regions having D2-like receptors. On the other hand, chronic amphetamine did not alter the k* responses to quinpirole seen in chronic saline-treated rats. SKF-38393 had minimal effects on k* in both chronic saline-treated and amphetamine-treated rats, consistent with D1-like receptors not being coupled to AA signalling. The ability of chronic d-Amph after 1-d washout to down-regulate baseline values of k* probably reflects neuroplastic changes in brain AA signalling, and may correspond to depressive behaviours noted following withdrawal from chronic amphetamine in humans and in rats.[1]

References

Chronic d-amphetamine depresses an imaging marker of arachidonic acid metabolism in rat brain. Bhattacharjee, A.K., Chang, L., Chen, M., White, L., Bell, J.M., Bazinet, R.P., Rapoport, S.I. Int. J. Neuropsychopharmacol. (2008) [Pubmed]

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