Modulation of Sensory and Excitatory Amino Acid Responses by Nitric Oxide Donors and Glutathione in the Ventrobasal Thalamus of the Rat

Abstract

Nitric oxide has been identified as having a role in synaptic transmission in the central nervous system. In the ventrobasal complex of the thalamus (VB), the precursor of nitric oxide synthesis, L-arginine, causes enhancement of excitatory amino acid responses and somatosensory transmission. In this study, the nitric oxide donors sodium nitroprusside, 3-morpholinosydnonimine and S-nitrosoglutathione were applied to VB relay neurons by iontophoresis and responses of single neurons were recorded extracellularly. Sodium nitroprusside caused selective inhibition of responses to NMDA, probably mediated by a by-product, ferrocyanide, as described in previous studies. 3-Morpholinosydnonimine and S-nitrosoglutathione, however, caused potentiation of responses to sensory stimuli and to excitatory amino acids. In contrast, glutathione in both its reduced and oxidized forms reduced such responses, and this suggests that the potentiating effect of S-nitrosoglutathione could be due to nitric oxide production. These results are consistent with the hypothesis that nitric oxide may have a local modulatory role in the thalamus. Data are presented which suggest that glutathione may have a negative modulatory influence on neurotransmission and excitatory amino acid responses in the ventrobasal thalamus.

Nitric oxide synthase-containing neurons in the amygdaloid nuclear complex of the rat

“…The role of nitric oxide in the central somatosensory system is less elucidated. Shaw and Salt (1997) found that iontophoretically applied nitric oxide donors can potentiate transmission in the ventrobasal thalamus. Moreover, nitric oxide levels in the rat thalamus are dependent on its behavioral state, raising the possibility of this agent modulating the sensory alertness (Williams et al 1997).…”

The sleep relay—the role of the thalamus in central and decentral sleep regulation

“…Sensory responses and responses to excitatory amino acids are facilitated after NO-induced increases of the intracellular cGMP concentration in TC neurons [160], interrupting oscillatory burst activity and enhancing the relay mode of activity in TC neurons, as described in detail above. Additionally, NO causes a robust, long-lasting depolarisation in NRT neurons via an ACh and cGMP-dependent pathway, this time inhibiting burst activity [192,193].…”

“…Sensory responses and responses to excitatory amino acids are facilitated after NO-induced increases of the intracellular cGMP concentration in TC neurons [160], interrupting oscillatory burst activity and enhancing the relay mode of activity in TC neurons. An increase of cGMP levels can be assumed to also result in an increased production of cyclic ADP ribose, facilitating CICR [20], and thus further strengthening the relay mode of activity.…”

Nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat

“…NO is a versatile gaseous molecule, able to modulate both the neuronal excitability and the release of neurotransmitters in many structures of the CNS of mammalians (Cudeiro et al, 1997;Shaw and Salt, 1997;Ferraro et al, 1999;Trabace and Kendrick, 2000;Prast and Philippu, 2001;Ahern et al, 2002;Li et al, 2004;Garthwaite, 2008). Clear NO-mediated actions have been shown in the BG (Cox and Johnson, 1998;Calabresi et al, 1999;Centonze et al, 2001): in this regard, strong modulatory effects exerted by NO-active drugs on the bioelectric activity of striatal, pallidal, subthalamic and nigral cells have been recently demonstrated (Sardo et al, 2002a(Sardo et al, ,b, 2003(Sardo et al, , 2006aCarletti et al, 2009), as well as a marked influence of NOactive drugs on GABA-and GLU-evoked responses in the STN .…”