Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5859239 | Toxicology | 2013 | 8 Pages |
Abstract
The purpose of the present work was to assess the possible role of glutamatergic receptors and nitric oxide (NO) production on effects of glufosinate ammonium (GLA), an organophosphate pesticide structurally related to glutamate, on in vivo striatal dopamine release in awake and freely moving rats. For this, we used antagonists of NMDA (MK-801 and AP5) or AMPA/kainate (CNQX) receptors, or nitric oxide synthase (NOS) inhibitors (l-NAME and 7-NI), to study the effects of GLA on release of dopamine from rat striatum. So, intrastriatal infusion of 10 mM GLA significantly increased dopamine levels (1035 ± 140%, compared with basal levels) and administration of GLA to MK-801 (250 μM) or AP5 (650 μM) pretreated animals, produced increases in dopamine overflow that were â¼40% and â¼90% smaller than those observed in animals not pretreated with MK-801 or AP5. Administration of GLA to CNQX (500 μM) pretreated animals produced an effect that was not significantly different from the one produced in animals not pretreated with CNQX. On the other hand, administration of GLA to l-NAME (100 μM) or 7-NI (100 μM) pretreated animals, produced increases in dopamine overflow that were â¼80% and â¼75% smaller than those observed in animals not pretreated with these inhibitors. In summary, GLA appears to act, at least in part, through an overstimulation of NMDA (and not AMPA/kainate) receptors with possible NO production to induce in vivo dopamine release. Administration of NMDA receptor antagonists and NOS inhibitors partially blocks the release of dopamine from rat striatum.
Related Topics
Life Sciences
Environmental Science
Health, Toxicology and Mutagenesis
Authors
Lilian R.F. Faro, Brenda V. Ferreira Nunes, Miguel Alfonso, Vania M. Ferreira, Rafael Durán,