Sympathoexcitatory neurons

Sun M-K, Jeske IT, Reis DJ. Cyanide excites medullary sympathoexcitatory neurons in rats. Am J Physiol 1992 262 R182-R189. 

Further studies by Sun and Reis with the in vitro medullary slice preparation provide additional evidenee for a direet excitatory effect of hypoxia on these neurons (69). In this redueed preparation, the RVLM sympathoexeitatory neurons retain exeitability by hypoxia and foeal NaCN. When synaptie transmission is blocked by applieation of tetrodotoxin (TTX), both hypoxia and NaCN eontinue to elieit neuronal membrane depolarization while the membrane response is abolished by applieation of Co +, a nonseleetive Ca +-ehannel bloeker (68-70). These observations argue for intrinsie hypoxic chemosensitivity of these sympathoexcitatory neurons of the RVLM. 

Depressant effects (other than those from neuronal failure due to energy depletion) may well reflect a residue of mechanisms that have evolved to deal with the peculiar challenge of the perinatal period. Nonspecific effects of brain hypoxia have been described, but more recent work points to direct excitation of medullary neurons by hypoxia as seen in both the sympathoexcitatory neurons of the RVLM and the putative pacemaker neurons of the pre-BdtC. In our view, the role of the excitation of the pre-BdtC in the genesis of gasping has been established and the possibility that hypoxia may modulate eupneic breathing has been raised. 

There is substantial evidence fi om studies in the intact animal that these neurons are directly stimulated by hypoxia. Sun and colleagues have shown that microinjection of cyanide into the RVLM of rats evokes a pressor response (68). The RVLM reticulospinal sympathoexcitatory vasomotor neurons, many of which exhibit pacemaker-hke activity, are rapidly and reversibly excited in a dose-dependent manner when the cyanide is delivered by either microinjection or microiontophoresis (63,66,68,69). This excitation is not altered by blockade of ionotropic excitatory amino acid (EAA) receptors in this region (70). Fiuiher, during hypoxic excitation of these RVLM reticulospinal sympathoexcitatory vasomotor neurons, their response to baroreceptor stimulation is preserved, suggesting that the... 

Ramirez et al. (82) produced bilateral synaptic blockade within the pre-BotC in pentobarbitone-anesthetized cats by injection of TTX and abolished eupneic ouQ)ut without eliminating the gasping response to severe hypoxia or asphyxia. It is important to note in this regard that Sun and Reis have shown that hypoxic excitation of reticulospinal sympathoexcitatory vasomotor neurons seems to be independent of synaptic transmission, or, at least, TTX-sensitive mechanisms (63,69,70 described above). If similar mechanisms exist in the pre-BotC, the inability of TTX to block hypoxia-induced gasping is not unexpected. 

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