Elsevier

Brain Research

Volume 653, Issues 1–2, 8 August 1994, Pages 57-65
Brain Research

Amphetamine induces excess release of striatal acetylcholine in vivo that is independent of nigrostriatal dopamine

https://doi.org/10.1016/0006-8993(94)90372-7Get rights and content

Abstract

The effect of amphetamine on striatal acetylcholine (ACh) release was studied by an in vivo intrastriatal microdialysis technique. Although we expected systemic amphetamine to inhibit baseline striatal ACh release, the opposite was found. In addition, we found that the amphetamine-induced striatal ACh release did not depend on nigrostriatal DA since 6-hydroxy-dopamine (6-OHDA) lesions had no effect on amphetamine-induced ACh release. Local intrastriatal injection of amphetamine via the microdialysis probe had no effect on striatal ACh release even when the probe was located more laterally in striatum to take advantage of the medial to lateral gradient of striatal ACh and D2 receptors. The hypothesis that amphetamine increased extracellular striatal ACh by increasing the release of biogenic amines besides dopamine was tested by pharmacological manipulations designed to specifically increase local striatal norepinephrine or serotonin levels. The serotonergic and noradrenergic manipulations had no effect on striatal ACh levels. These results indicate that amphetamine-induced release of ACh in striatum is mediated via distal brain regions that are functionally connected with the striatum.

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  • Cited by (21)

    • Chapter 2.4 Dopamine-acetylcholine interactions in the brain studied by in vivo microdialysis

      2006, Handbook of Behavioral Neuroscience
      Citation Excerpt :

      The distal sites that are involved in the tonic DA-D1 regulation of striatal ACh efflux include the parafascicular thalamic nucleus, the FC, and the SN (pars reticulata), possibly through an increase in glutamatergic neurotransmission via N-methyl-d-aspartate (NMDA)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors, whereas a local striatal neuronal circuit through an increase in γ-aminobutyric acid (GABA)/neurokininA/substanceP neurotransmission (via GABAA/tachykinin receptors) also seems to be implicated (see Fig. 1; Damsma et al., 1991; Zocchi and Pert, 1993; Anderson et al., 1994; Consolo et al., 1996; Abercrombie and DeBoer, 1997; Acquas et al., 1997; Steinberg et al., 1995, 1998; Zackheim and Abercrombie, 2005). In addition, DA seems to exert a tonic inhibitory control over spontaneous ACh efflux within the NAcc/Str complex that is directly mediated by DA-D2 receptors (Fig. 1; Bertorelli and Consolo, 1990; Damsma et al., 1990a, b, 1991; De Boer et al., 1992; Robertson et al., 1992, 1993; Russi et al., 1993; Imperato et al., 1994a, b; Mandel et al., 1994; De Boer and Abercrombie, 1996; Abercrombie and DeBoer, 1997; Acquas et al., 1997; Ikarashi et al., 1997a, b; Acquas and Fibiger, 1998; Keys and Mark, 1998; Acquas and Di Chiara, 1999a, b). Similarly to DA-D2 receptors, stimulation of DA-D3 receptors with selective ligands appears to mediate an inhibitory action on striatal ACh efflux (Sato et al., 1994; Millan et al., 2004).

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