Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

Wood, Susan K.; Verhoeven, Robert E; Savit, Aaron Zvi; Rice, Kenner C.; Fischbach, Peter S.; Woods, James H.

doi:10.1038/sj.npp.1301085

Cited by 14 publications

(13 citation statements)

References 49 publications

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“…However, there was an insignificant drop in MABP here that generally confirmed the results of others (1). Psychological studies also use swimming to induce stress levels in rodents naive to a water environment (102). However, there were no increases in HR or blood pressure in our swimming rats, suggesting that their training (58) since juveniles minimized their stress response.…”

Section: Voluntary Diving Versus Voluntary Swimmingsupporting

confidence: 88%

The rat: a laboratory model for studies of the diving response

Panneton

Gan

Juric

2010

Journal of Applied Physiology

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Underwater submersion in mammals induces apnea, parasympathetically mediated bradycardia, and sympathetically mediated peripheral vasoconstriction. These effects are collectively termed the diving response, potentially the most powerful autonomic reflex known. Although these physiological responses are directed by neurons in the brain, study of neural control of the diving response has been hampered since 1) it is difficult to study the brains of animals while they are underwater, 2) feral marine mammals are usually large and have brains of variable size, and 3) there are but few references on the brains of naturally diving species. Similar responses are elicited in anesthetized rodents after stimulation of their nasal mucosa, but this nasopharyngeal reflex has not been compared directly with natural diving behavior in the rat. In the present study, we compared hemodynamic responses elicited in awake rats during volitional underwater submersion with those of rats swimming on the water's surface, rats involuntarily submerged, and rats either anesthetized or decerebrate and stimulated nasally with ammonia vapors. We show that the hemodynamic changes to voluntary diving in the rat are similar to those of naturally diving marine mammals. We also show that the responses of voluntary diving rats are 1) significantly different from those seen during swimming, 2) generally similar to those elicited in trained rats involuntarily "dunked" underwater, and 3) generally different from those seen from dunking naive rats underwater. Nasal stimulation of anesthetized rats differed most from the hemodynamic variables of rats trained to dive voluntarily. We propose that the rat trained to dive underwater is an excellent laboratory model to study neural control of the mammalian diving response, and also suggest that some investigations may be done with nasal stimulation of decerebrate preparations to decipher such control.

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Section: Voluntary Diving Versus Voluntary Swimmingsupporting

confidence: 88%

The rat: a laboratory model for studies of the diving response

Panneton

Gan

Juric

2010

Journal of Applied Physiology

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“…Furthermore, CRF 1 receptor activation in select brain regions is also known to contribute to stress-induced sympathetic activation (Brown et al 1982; Chu et al 2004; Kurosawa et al 1986; Nijsen et al 2000). The dampening of sympathetic activation together with the para-sympathomimetic effect of CRF 1 antagonist treatment has been previously reported to be centrally mediated and likely contributes to the observed cardioprotective effects of NBI-30775 (Nijsen et al 2000; Wood et al 2006). Therefore the present study confirms our supposition that treatment with a centrally acting CRF 1 antagonist during exposure to social stress would prevent the development of stress-induced behavioral and autonomic dysfunction.…”

Section: Discussionmentioning

confidence: 93%

Depressive and cardiovascular disease comorbidity in a rat model of social stress: a putative role for corticotropin-releasing factor

et al. 2012

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Rationale Depression is associated with medical comorbidities, particularly cardiovascular disease. However, mechanisms linking depression and cardiovascular disease remain unclear. Objectives This study investigated whether the rat resident–intruder model of social stress would elicit behavioral dysfunctions and autonomic changes characteristic of psychiatric/cardiovascular comorbidity. Furthermore, the efficacy of the corticotropin-releasing factor-1 (CRF1) receptor antagonist, NBI-30775 (NBI), or the tricyclic antidepressant, desipramine (DMI), to prevent social stress-induced behavioral, neuroendocrine, and cardiovascular changes were evaluated. Methods Adult male rats were exposed to resident–intruder stress (seven consecutive days) and systemically administered NBI (10 mg/kg/7 days), DMI (10 mg/kg/14 days), or vehicle. The efficacy of NBI and DMI to alter the behavioral and neuroendocrine responses to social stress was assessed. Furthermore, their effects on stress-induced forced swim behavior (FST), bladder and adrenal weight, and heart rate variability (HRV) were examined. Results NBI, but not DMI, increased time spent in an upright, defensive posture and the latency to submit to the resident. Additionally, only NBI reduced social stress-induced adrenocorticotropic hormone and corticosterone release. Social stress increased FST immobility, caused bladder and adrenal hypertrophy, and decreased HRV. Both NBI and DMI blocked stress-induced increases in immobility during the FST. However, only NBI inhibited social stress-induced adrenal and bladder hypertrophy and decreases in heart rate variability. Conclusions Rat resident–intruder stress paradigm models aspects of psychiatric/medical comorbidity. Furthermore, the CRF system may contribute to both the behavioral response during social stress and its behavioral and autonomic consequences, offering insight into potential therapy to treat these comorbid conditions.

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“…Just before drowning they exhibit severe bradycardia, which can be prevented with atropine, lengthening the period they stay alive [14]. The first such experiments suggested hopelessness as a causal factor for this response [8].…”

Section: Vvs Represents a Design Faultmentioning

confidence: 97%

“…When rats are placed in a cylinder of water from which they cannot escape, they will ultimately drown [3,8,14]. Just before drowning they exhibit severe bradycardia, which can be prevented with atropine, lengthening the period they stay alive [14].…”

Section: Vvs Represents a Design Faultmentioning

confidence: 99%

Is there any point to vasovagal syncope?

Dijk

Sheldon

2008

Clin Auton Res

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Vasovagal fainting, i.e., neurally mediated syncope induced by slight pain, fear or merely standing, is a uniquely human characteristic. Other animals also fight over territory, make tools, make weapons, have culture, can use words and symbols, work together, have bosses, are monogamous or polygamous, and even have children who never seem to leave home. But we and we alone faint. And it is hardly uncommon: about 37% of people have at least one episode of vasovagal syncope (VVS) in their life up to age 70 [11].Why this is so is unknown. First, let's consider the broad features that have to be accommodated in an explanation. There are fainters and there are nonfainters. Those who faint usually start doing so in adolescence and remain prone to fainting throughout their lives. Few people have a first vasovagal syncopal spell after age 40. Women are more likely to faint than men (about 45 vs. 30%). Most fainters have multiple triggers. Fainters have a wide range of lifetime syncopal spells, and interestingly many have long quiescent epochs with interspersed clusters of faints. We do not know why any of this happens.

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Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

Cited by 14 publications

References 49 publications

The rat: a laboratory model for studies of the diving response

The rat: a laboratory model for studies of the diving response

Depressive and cardiovascular disease comorbidity in a rat model of social stress: a putative role for corticotropin-releasing factor

Is there any point to vasovagal syncope?

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