Baroreceptor-sensitive neurons in the rat paratrigeminal nucleus

Yu, Yun-Guo; Lindsey, Charles Julian

doi:10.1016/s1566-0702(03)00022-5

Cited by 19 publications

(12 citation statements)

References 23 publications

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“…Our results point in the same direction. The abundance of m-opioid receptors in the nucleus of the solitary tract (Greenwell et al, 2007), which is particularly important for generating baroreflexes (de Sousa Buck et al, 2001;Yu and Lindsey, 2003) might explain the reduction of BRS in our study. The most likely explanation is via a baroreflex mechanism, which physiologically counteracts sympathetic activation.…”

Section: Which Mechanisms Link Opioid-dependent Analgesia and Sympathmentioning

confidence: 51%

Naloxone inhibits not only stress‐induced analgesia but also sympathetic activation and baroreceptor‐reflex sensitivity

Fechir

Breimhorst

Kritzmann

et al. 2012

European Journal of Pain

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Interactions between the sympathetic nervous system and pain are manifold and still have not been sufficiently characterized. Accordingly, several possible neuronal pathways have been described as being involved in mental stress-induced analgesia. We studied the role of the endogenous opioidergic system in stress-induced analgesia in 14 healthy participants in a double-blind cross-over trial. Naloxone or placebo was applied while electrical pain stimulation was started and electrical current increased. After reaching a constant stimulation at 30 mA, a color word interference test (Stroop task) was performed in a stressful and a non-stressful version. Blood pressure, heart rate and baroreflex sensitivity were continuously recorded to assess autonomic activation. Each participant was tested with naloxone and placebo with a randomized and balanced order of trials. The major results are that the opioid-receptor antagonist naloxone prevented (1) stress-induced reduction of tonic current-induced pain, (2) attenuated the simultaneous activation of the sympathetic nervous system, and (3) reduced the counteraction of sympathetic activation by vagal baroreceptor mechanisms. Thus, the opioidergic system not only modulates nociceptive input but also the interplay with vegetative responses. We conclude that acute stress, sympathetic activation and analgesia might be linked via vagal reflexes, which are disturbed when opioid receptors are blocked. This mechanism might underlie increased perception of noxious stimuli in patients with chronic pain or mood disorders.

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Section: Which Mechanisms Link Opioid-dependent Analgesia and Sympathmentioning

confidence: 51%

Naloxone inhibits not only stress‐induced analgesia but also sympathetic activation and baroreceptor‐reflex sensitivity

Fechir

Breimhorst

Kritzmann

et al. 2012

European Journal of Pain

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“…If the heart rate was increased after mechanical or thermal stimulation of the receptive fields, the percentage of halothane was increased. Enamel-coated tungsten microelectrodes (impedance =10–12 MΩ, 1000 Hz, FHC) were protruded perpendicularly to the brain surface into the Pa5 about 1.3 mm rostral to the obex and 2.5 mm lateral from the mid-line (Yu et al, 2003) in 2 μm steps ipsilateral to CFA injection. The Pa5 neurons were searched by applying mechanical stimulation (pressure or brush) to the facial skin.…”

Section: Methodsmentioning

confidence: 99%

“…Pa5 neurons are thought to be involved in autonomic functions such as controlling the cardiovascular system (Yu et al, 2002; Yu and Lindsey, 2003). The experimental TMJ inflammation results in expression of Fos proteins in Pa5 neurons as well as in the trigeminal spinal subnucleus caudalis (Vc) (Hathaway et al, 1995; Zhou et al, 1999; Bereiter et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…It is also known that modulation of Pa5 neuronal activity is associated with changes in arterial blood pressure (Balan et al, 2004; Yu and Lindsey 2003). Furthermore, esophageal acid stimulation or nociceptive stimuli to the tongue or laryngopharyngeal mucosa has been found to increase Fos protein expression in Pa5 neurons (Carstens et al, 1995; Suwanprathes et al, 2003; Boucher et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of paratrigeminal nociceptive neurons following temporomandibular joint inflammation in rats

Yamazaki

Ren

Shimada

et al. 2008

Experimental Neurology

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To evaluate the involvement of paratrigeminal nucleus (Pa5) nociceptive neurons in temporomandibular joint (TMJ) inflammation-induced pain and its autonomic correlates, we conducted behavioral, single unit recording and Fos immunohistochemical studies in anesthetized rats. Nocifensive behaviors to mechanical, heat or cold stimulation of the lateral face over the TMJ region were significantly enhanced in the TMJ-inflamed rats for 10–14 days after injection of complete Freund’s adjuvant (CFA) into the TMJ and gradually decreased at the end of the 14-day observation period. Lowering of the nocifensive threshold in TMJ-inflamed rats lasted longer in vagus nerve-transected rats than vagus nerve-intact rats. A large number of Fos-like immunoreactive (LI) cells were observed in the Pa5, and half of them were retrogradely labeled with Fluorogold (FG) injected into the parabrachial nucleus. Background activity of Pa5 wide dynamic range and nociceptive specific neurons was significantly higher in the TMJ-inflamed rats when compared with controls. Responses to mechanical stimuli were significantly higher in NS neurons in the TMJ-inflamed rats. All thermal responsive Pa5 neurons were exclusively sensitive to cold and the response to cold was significantly higher in the TMJ-inflamed rats compared with control rats. Vagus nerve stimulation significantly decreased responses to mechanical and cold stimuli as well as the background activity in TMJ-treated rats but not in TMJ-untreated rats. The present findings suggest that populations of Pa5 neurons are nociceptive and involved in TMJ inflammation-induced pain as well as in autonomic processes related to TMJ pain.

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“…Of course, to affect a change requires an anatomical route linking these C-fibers to cardiovascular control mechanisms. A major candidate pathway includes the jugular and nodose ganglia, which receive input from the pulmonary C-fiber populations and project to the cardiovascular control center in the medulla oblongata (48,55,112), including the solitary nucleus (Sol) and paratrigeminal nucleus (Pa5) (8,86,110,126) (Fig. 3B).…”

Section: Xenobiotic Particlesmentioning

confidence: 99%

Xenobiotic pulmonary exposure and systemic cardiovascular response via neurological links

Stapleton

Abukabda

Hardy

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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The cardiovascular response to xenobiotic particle exposure has been increasingly studied over the last two decades, producing an extraordinary scope and depth of research findings. With the flourishing of nanotechnology, the term "xenobiotic particles" has expanded to encompass not only air pollution particulate matter (PM) but also anthropogenic particles, such as engineered nanomaterials (ENMs). Historically, the majority of research in these fields has focused on pulmonary exposure and the adverse physiological effects associated with a host inflammatory response or direct particle-tissue interactions. Because these hypotheses can neither account entirely for the deleterious cardiovascular effects of xenobiotic particle exposure nor their time course, the case for substantial neurological involvement is apparent. Indeed, considerable evidence suggests that not only is neural involvement a significant contributor but also a reality that needs to be investigated more thoroughly when assessing xenobiotic particle toxicities. Therefore, the scope of this review is several-fold. First, we provide a brief overview of the major anatomical components of the central and peripheral nervous systems, giving consideration to the potential biologic targets affected by inhaled particles. Second, the autonomic arcs and mechanisms that may be involved are reviewed. Third, the cardiovascular outcomes following neurological responses are discussed. Lastly, unique problems, future risks, and hurdles associated with xenobiotic particle exposure are discussed. A better understanding of these neural issues may facilitate research that in conjunction with existing research, will ultimately prevent the untoward cardiovascular outcomes associated with PM exposures and/or identify safe ENMs for the advancement of human health.

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Baroreceptor-sensitive neurons in the rat paratrigeminal nucleus

Cited by 19 publications

References 23 publications

Naloxone inhibits not only stress‐induced analgesia but also sympathetic activation and baroreceptor‐reflex sensitivity

Naloxone inhibits not only stress‐induced analgesia but also sympathetic activation and baroreceptor‐reflex sensitivity

Modulation of paratrigeminal nociceptive neurons following temporomandibular joint inflammation in rats

Xenobiotic pulmonary exposure and systemic cardiovascular response via neurological links

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