Ionotropic glutamate-receptor antagonists inhibit the aversive effects of nitric oxide donor injected into the dorsolateral periaqueductal gray of rats

Abstract

The results suggest that the aversive reactions induced by an NO donor in the dlPAG depend on ionotropic glutamate receptor activation.

Benzodiazepine receptor and serotonin 2A receptor modulate the aversive-like effects of nitric oxide in the dorsolateral periaqueductal gray of rats

“…The mechanisms of this flight reaction are not completely understood but may involve facilitation of glutamate release (Moreira et al 2004). This is in accordance with electrophysiological data in which excitatory post-synaptic potentials induced by NO donors in the dorsal PAG are inhibited by ionotropic glutamate-receptor antagonists (Hall and Behbehani 1998).…”

“…In a previous study, we showed that these effects were completely prevented by pre-treatment with ionotropic glutamate-receptor antagonists (Moreira et al 2004). These results, therefore, suggest that the aversive-like effects of NO in the dlPAG may be mediated by glutamate and modulated by GABA and 5-HT-mediated neurotransmission.…”

Fine-tuning of defensive behaviors in the dorsal periaqueductal gray by atypical neurotransmitters

“…Electrophysiological data showed that excitatory postsynaptic potentials induced by NO in dPAG slices are reduced by antagonists of ionotropic glutamate receptors (41). Reinforcing the possibility that NO effects in the PAG depend on facilitation of glutamate-mediated neurotransmission, we showed that local pretreatment with AP7, an NMDA receptor antagonist, blocked the aversive-like reaction induced by linsidomine chlorhydrate (SIN-1) (42) and reduced the activation of NOS neurons induced by predator exposure (36). More recently, we determined if the defensive reactions induced by NMDA in the dlPAG would depend of endogenous NO.…”

Anxiolytic effects induced by inhibition of the nitric oxide–cGMP pathway in the rat dorsal hippocampus

“…This is probably reflecting complex interactions of NO with several neurotransmitter systems and may also help to explain the contradictory results regarding its role in anxiety. Although NO could exert a facilitatory role in defensive reactions by potentiating the release of glutamate (Moreira et al 2004), its excessive production may negatively modulate NMDA function (Contestabile 2000). A reduction in glutamate release induced by an increase in cGMP levels or administration of a NO donor has also been described (Sisitaga et al 1997).…”