Nitric oxide induces calcium‐dependent release of [³H]dopamine release from striatal slices

Abstract

Hydroxylamine (0.01-30 mM), a nitric oxide (NO) generator, produced a concentration-dependent release of [3H]dopamine ([3H]DA) from rat striatal slices. Hemoglobin (10 microM), a NO scavenger, reduced basal [3H]DA release and blocked hydroxylamine (100 microM)-stimulated [3H]DA efflux. Tetrodotoxin (0.5 microM) had no significant effect. Sodium cyanide was used as a model compound to test the possibility that NO acted through blockade of mitochondrial electron transport. Calcium-free experimental buffer (1 mM EGTA) reduced basal release and the hydroxylamine response, while sodium cyanide-induced release did not change under these experimental conditions. Cadmium (200 microM), a non-selective inhibitor of voltage-dependent calcium channels, reduced the hydroxylamine response by 69%. Methylene blue (10 microM), an inhibitor of guanylate cyclase, produced a 3-fold increase in the basal release but had no significant effect on the hydroxylamine response. These data suggest that NO induces calcium-dependent [3H]DA release from the striatum via a mechanism which is independent of blockade of electron transport or activation of guanylate cyclase.

The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia

“…Abnormalities in NO synthesis have been implicated in neurodevelopment and increasing the vulnerability to develop SCH (Akbarian et al 1993;Black et al 1999). Nitric oxide has been shown to increase the release of DA and influence the activity of the DA transporter in the striatum (Lonart et al 1993, Kiss et al 1999. It is possible that excessive NO synthesis might be involved in some more basic aspects of SCH along with contributing to the deficit in cortisol response to APO.…”

Increased striatal dopamine efflux in vivo following inhibition of cerebral nitric oxide synthase by the novel monosodium salt of 7‐nitro indazole

“…However, there is confusion over the manner in which NO modulates dopamine release. In vitro studies using tissue slices have shown NO to increase dopamine efflux in the striatum (Lonart et al, 1993), whereas in vivo microdialysis studies using NO synthase inhibitors or exogenous NO suggest the opposite to be true (Guevara-Guzman et al, 1994;Rose et al, 1994b).…”

Nitric Oxide Synthase Inhibitors Attenuate Phencyclidine-Induced Disruption of Prepulse Inhibition

“…First, nitric oxide is intimately connected with dopamine and glutamate, two neurotransmitter systems that are dysfunctional in schizophrenia (Lonart et al 1993;Montague et al 1994;Pogun et al 1994). Further, nitric oxide's dual action as mediator and negative modulator of glutamate neurotransmission at the NMDA receptor complex give this system a unique role in regulating the balance of excitatory and inhibitory influences.…”