Sympathetic activity remains synchronized in presence of a glutamate antagonist.

Sun et al. like activity in the rostral ventrolateral medulla (RVLM) of the rat after an intracisternal injection of the glutamate receptor antagonist, kynurenate (KYN). They proposed that these neurons are primarily responsible for sympathetic nerve discharge (SND). The fact that RVLM pacemaker neurons discharge independently of each other after intracisternal KYN leads to the prediction that SND will be desynchronized by this drug. The results of the current study show that this is not the case. Postganglionic SND was recorded in rats and cats before and after intracisternal injection of KYN in doses that blocked the baroreceptor reflexes. Whereas the background level of SND was unchanged in rats, KYN markedly reduced SND in cats. Independent of this difference, KYN failed to desynchronize SND in either species. Power density spectra of SND in rats and cats contained sharp peaks between 2 and 10 Hz before and after intracisternal KYN. These results require a reassessment of the pacemaker hypothesis on the origin of SND. Moreover, KYN-induced depression of SND in the cat points to the importance of brain stem synaptic mechanisms in the genesis of sympathetic tone in this species.