Cutaneous vasodilation elicited by disinhibition of the caudal portion of the rostral ventromedial medulla of the free-behaving rat

Cerri, Matteo; Zamboni, Giovanni; Tupone, Domenico; Dentico, Daniela; Luppi, Marco; Martelli, Davide; Perez, Emanuele; Amici, Roberto

doi:10.1016/j.neuroscience.2009.10.068

Cited by 30 publications

(23 citation statements)

References 24 publications

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“…In studies using jackets perfused with cold water on rats, the threshold skin temperature to activate BAT sympathetic nerve activity is 37.5 °C (Ootsuka and McAllen, 2006), while the threshold skin temperature to activate tail sympathetic nerve activity is higher, 38.8–40.1 °C (Tanaka et al, 2007). At an ambient temperature of 24 °C, rat tail skin temperature has been measured to be between 26 °C to 27 °C (Sakurada et al, 1993; Cerri et al, 2010). Thus, it is likely that 19 °C and to some extent 25 °C water temperature conditions in our study resulted in activation of these two sympathetic pathways involved in cold defense.…”

Section: Discussionmentioning

confidence: 99%

Swim stress activates serotonergic and nonserotonergic neurons in specific subdivisions of the rat dorsal raphe nucleus in a temperature-dependent manner

et al. 2011

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Physical (exteroceptive) stimuli and emotional (interoceptive) stimuli are thought to influence stress-related physiologic and behavioral responses through different neural mechanisms. Previous studies have demonstrated that stress-induced activation of brainstem serotonergic systems is influenced by environmental factors such as temperature. In order to further investigate the effects of environmental influences on stress-induced activation of serotonergic systems, we exposed adult male Wistar rats to either home cage control conditions or a 15 min swim in water maintained at 19 °C, 25 °C, or 35 °C and conducted dual immunohistochemical staining for c-Fos, a marker of immediate-early nuclear activation, and tryptophan hydroxylase (TPH), a marker of serotonergic neurons. Changes in core body temperature were documented using biotelemetry. As expected, exposure to cold (19 °C) swim, relative to warm (35 °C) swim, increased c-Fos expression in the external lateral part of the parabrachial nucleus (LPBel), an important part of the spinoparabrachial pathway involved in sensation of cold, cutaneous stimuli, and in serotonergic neurons in the raphe pallidus nucleus (RPa), an important part of the efferent mechanisms controlling thermoregulatory warming responses. In addition, exposure to cold (19 °C) swim, relative to 35 °C swim, increased c-Fos expression in the dorsal raphe nucleus, ventrolateral part/periaqueductal gray (DRVL/VLPAG) and dorsal raphe nucleus, interfascicular part (DRI). Both of these subregions of the dorsal raphe nucleus (DR) have previously been implicated in thermoregulatory responses. Altogether, the data are consistent with the hypothesis that midbrain serotonergic neurons, possibly via activation of afferents to the DR by thermosensitive spinoparabrachial pathways, play a role in integration of physiologic and behavioral responses to interoceptive stress-related cues involved in forced swimming and exteroceptive cues related to cold ambient temperature.

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Section: Discussionmentioning

confidence: 99%

Swim stress activates serotonergic and nonserotonergic neurons in specific subdivisions of the rat dorsal raphe nucleus in a temperature-dependent manner

et al. 2011

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“…Verner and colleagues (2004; 2008) proposed that the dramatic apnea, bradycardia, and hypotension resulting from stimulation of raphé magnus was caused by activation of inhibitory (likely GABA) neurons that project to brain respiratory and cardiovascular sites. Consistent with this concept, when GABA activity is disrupted in the medullary raphé the resulting disinhibition increases sympathetic outflow (Cerri et al, 2010; Morrison, 1999; 2001a; b). The potential role of raphé GABA inhibition of sympathetic response is supported by neuroanatomical studies demonstrating projections of GAD-ir raphé cells to sympathetic spinal cord regions (Antal et al, 1996; Blessing, 1990; Blessing et al, 1987; Jones et al, 1991; Reichling and Basbaum, 1990; Stornetta and Guyenet, 1999; Stornetta et al, 2005; reviewed by Stornetta, 2009).…”

Section: Discussionmentioning

confidence: 66%

CO2-inhibited neurons in the medullary raphé are GABAergic

Iceman

Corcoran

Taylor

et al. 2014

Respiratory Physiology & Neurobiology

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Previous studies have reported subsets of medullary raphé neurons that are either stimulated or inhibited by CO2/pH in vitro, in situ, and in vivo. We tested the hypothesis that medullary raphé CO2-inhibited neurons are GABAergic. Extracellular recordings in unanesthetized juvenile in situ rat preparations showed reversible hypercapnia-induced suppression of 19% (63/323) of medullary raphé neurons, and this suppression persisted after antagonism of NMDA, AMPA/kainate, and GABAA receptors. We stained a subset of CO2-inhibited cells and found that most (11/12) had glutamic acid decarboxylase 67 immunoreactivity (GAD67-ir). These data indicate that the majority of acidosis-inhibited medullary raphé neurons are GABAergic, and that their chemosensitivity is independent of major fast synaptic inputs. Thus, CO2-sensitive GABAergic neurons may play a role in central CO2/pH chemoreception.

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“…4,9 These studies proposed that efferent projections from the PVN could influence sympathetic tone via connections with spinally projecting neurons, as well as with the rostral ventrolateral medulla. 26,27 This region contains populations of pre-motor neurons influencing sympathetic activation, including to the kidneys and the skin. 26,27 In context of this background, in the present study, lidocaine was bilaterally injected to block traffic, both neuronally generated and that carried by fibers of passage in the PVN during heat stress.…”

Section: Discussionmentioning

confidence: 99%

Contribution of the paraventricular nucleus in autonomic adjustments to heat stress

Leite

Zheng

Coimbra

et al. 2012

Exp Biol Med (Maywood)

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We assessed the contribution of the paraventricular nucleus (PVN) in the heat stress-mediated changes in sympathetic nerve activity and blood flow redistribution from the core to the skin surface. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), heart rate (HR), body and tail temperatures were recorded in anesthetized rats after bilateral microinjection of CSF, lidocaine or L-NMMA into the PVN during heat stress. Heat stress was induced by a graded increase in the temperature of a heating pad for 30 min. Heat stimulus after blockade of the PVN with lidocaine resulted in a blunted RSNA response (ΔRSNA: 117.6 ± 17.0 % vs. 11.3 ± 7.3 %), as well as blunted MAP and HR (ΔMAP: 22 ± 2 mmHg vs. −0.04 ± 7.2 mmHg; ΔHR: 93.4 ± 9.3 bpm vs. 43.4 ± 18.8 bpm). Body temperature threshold for tail vasodilation was unaffected by lidocaine treatment. The increase in RSNA, MAP and HR due to heat stress in L-NMMA-treated rats reached similar levels as CSF treated control rats. However, a higher body temperature threshold for tail vasodilation was observed after L-NMMA injection (37.3 ± 0.1 °C vs. 37.8 ± 0.2°). In conclusion, an intact PVN contributes to an increase in renal sympathetic activity provoked by heat stress, resulting in cardiovascular adjustments that influence core blood redistribution to the periphery. Furthermore, during heat stress, the effect of the PVN on cutaneous vasodilation is dependent on a nitric oxide mechanism.

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Cutaneous vasodilation elicited by disinhibition of the caudal portion of the rostral ventromedial medulla of the free-behaving rat

Cited by 30 publications

References 24 publications

Swim stress activates serotonergic and nonserotonergic neurons in specific subdivisions of the rat dorsal raphe nucleus in a temperature-dependent manner

Swim stress activates serotonergic and nonserotonergic neurons in specific subdivisions of the rat dorsal raphe nucleus in a temperature-dependent manner

CO2-inhibited neurons in the medullary raphé are GABAergic

Contribution of the paraventricular nucleus in autonomic adjustments to heat stress

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