Research reportSympathoexcitatory neurons of rostral ventrolateral medulla exhibit pacemaker properties in the presence of a glutamate-receptor antagonist
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Cited by (135)
Rostral ventrolateral medulla, retropontine region and autonomic regulations
2022, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Consistent with the pacemaker theory, injecting large doses of kynurenic acid, a broad-spectrum ionotropic glutamate receptor antagonist into the RVLM blocks sympathoexcitatory reflexes but produces little or no effect on SNA and BP in anesthetized rats (reviewed in (Guyenet et al., 2018)). In addition, injecting this drug into the fourth ventricle of anesthetized rats blocks all tested inputs to RVLM presympathetic neurons but these cells retain a high and extremely regular discharge whose rhythm can only be reset by evoking an antidromic spike therefore excluding a neuronal oscillator as the cause of the rhythmic activity (Sun et al., 1988a). These observations are consistent with auto-depolarization properties under these specific conditions.
Essential hypertension as a result of neurochemical changes at the rostral ventrolateral medulla
2013, Journal of Clinical NeuroscienceCitation Excerpt :Sympathoexcitatory neurons of the RVLM send direct projections to the intermediolateral cell column of the spinal cord (Fig. 1). They are functionally organized into target-specific topographic subgroups controlling sympathetic outflow to the blood vessels, heart, and adrenal gland.13 These sympathoexcitatory neurons also mediate the baroreflex.6
C1 catecholamine neurons form local circuit synaptic connections within the rostroventrolateral medulla of rat
2012, NeuroscienceCitation Excerpt :It is well established that both C1 and non-C1 reticulospinal RVLM neurons exhibit cardiac- and respiratory-related activity (McAllen, 1985, 1986a–c, 1987; Haselton and Guyenet, 1989; Guyenet, 1990). Some investigations suggest that this activity is pacemaker related (Sun et al., 1988a,b; Guyenet, 1990; Kangrga and Loewy, 1995) while others have advanced a “network hypothesis” in which individual action potentials are driven by excitatory postsynaptic potentials (Barman and Gebber, 1987; Lipski et al., 1996). Both theories are consistent with an integrative function for C1 neurons that would enable coordinated activity throughout the C1 column as well as within the larger network of central neurons devoted to the control of cardiovascular function.
Asymmetrical changes in lumbar sympathetic nerve activity following stimulation of the sciatic nerve in rat
2011, Brain ResearchCitation Excerpt :A decrease in the pressor response, elicited by SN stimulation, was previously observed after antagonism of glutamate receptors in the RVLM (Kiely and Gordon, 1993). Intracisternal injection of kynurenic acid causes a 70% attenuation of the SSR evoked in the lumbar nerve (Sun et al., 1988). Finally, microinjection of kynurenate in the RVLM of cats abolishes the excitatory component of the SSR (Zanzinger et al., 1994).
Is augmented central respiratory-sympathetic coupling involved in the generation of hypertension?
2010, Respiratory Physiology and NeurobiologyCitation Excerpt :Many other nuclei including the nucleus of the solitary tract (NTS), the raphé nuclei, A5, caudal pressor area, parabrachial nucleus the hypothalamic paraventricular nucleus, perifornical lateral hypothalamus, amygdala and cortical regions also project to and influence the activity of RVLM neurons in different situations (reviewed by Guyenet, 2006). The activity of pre-sympathetic RVLM neurons is therefore dependent on the balance of inhibitory and excitatory inputs as well as potentially the intrinsic pacemaker-like properties displayed by these neurons in vitro (Sun et al., 1988). The ontogeny of essential hypertension is not fully understood but it is becoming clear that an alteration in SNA is associated with this pathology in both humans and animal models (Guyenet, 2006; Paton et al., 2009).