Gastrocardiac Afferent Convergence in Upper Thoracic Spinal Neurons: A Central Mechanism of Postprandial Angina Pectoris

Qin, Chao; Farber, Jay P.; Foreman, Robert D.

doi:10.1016/j.jpain.2007.02.428

Cited by 6 publications

(8 citation statements)

References 47 publications

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“…Thus, the postprandial increment of BDNF might be associated with cardiovascular diseases and postprandial angina. [ 43–45 ] In the present study, a high serum BDNF level was observed within 2 hours of OGTT in subjects with obesity and metabolic syndrome. The abated postprandial BDNF observed after short-term body-weight reduction might, therefore, reflect cardiovascular improvement.…”

Section: Discussionsupporting

confidence: 60%

Relationship between body weight and the increment in serum brain-derived neurotrophic factor after oral glucose challenge in men with obesity and metabolic syndrome

Lee

Wang

et al. 2016

Medicine

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Brain-derived neurotrophic factor (BDNF) plays a role in energy homeostasis. However, the postprandial BDNF change has not been well investigated. We hypothesized that the BDNF increment after oral glucose challenge is associated with body weight.To address this possibility, man adults with obesity in conjunction with metabolic syndrome were compared with normal weight controls at baseline in the initial cross-sectional protocol. The obese subjects then underwent a 12-week program for body-weight reduction in the prospective protocol. The area under the curve (AUC) of serum BDNF was recorded during a 75 g oral glucose tolerant test and the BDNF AUC index was defined as [(AUC of BDNF) − (fasting BDNF∗2 hours)]/(fasting BDNF∗2 hours).A total of 25 controls and 36 obese subjects completed the study assessments. In the cross-sectional protocol, the BDNF AUC index was significantly higher in the obese subjects than in the controls (9.0 ± 16.5% vs. − 8.0 ± 22.5%, P = 0.001). After weight reduction (from 97.0 ± 12.5 kg to 88.6 ± 12.9 kg, P < 0.001), the percentage change of body weight was significantly associated with the BDNF AUC index after the study (95% CI between 0.21 and 1.82, P = 0.015). Using 6% weight reduction as a cut-off value, a larger weight reduction was able to reliably predict a negative BDNF AUC index.In conclusion, a high BDNF AUC index was observed for obese men in this study, whereas the index value significantly decreased after body-weight reduction. These findings suggest that postprandial BDNF increment may be associated with obesity.

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Section: Discussionsupporting

confidence: 60%

Relationship between body weight and the increment in serum brain-derived neurotrophic factor after oral glucose challenge in men with obesity and metabolic syndrome

Lee

Wang

et al. 2016

Medicine

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“…The contribution of primary afferent reflex pathway in colon-to-bladder cross-sensitization has been investigated and well documented. Several anatomic pathways have been suggested including sensory convergence projection to DRG neurons and the spinal cord dorsal horn, which denotes input from both organs onto the same sensory neurons named dichotomizing neurons (Christianson et al, 2007; Qiao and Grider, 2007; Qin et al, 2007). Neuronal tracing studies from independent laboratories reveal that colonic and bladder afferent neurons locate in the same spinal segments, however, the number of dichotomizing sensory neurons project to both colon and urinary bladder ranges 5–27 %, in rat, and 21 %, in mouse, of traced neurons (Christianson et al, 2007; Qiao and Grider, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Several theories have been formed to explain the cross-organ sensitization or the referred pain suggestive of the involvement of spinal segments receiving inputs from different organs (Brumovsky and Gebhart, 2010). It is described that convergent neural input via dichotomizing primary afferents to the sensory limb including dorsal root ganglia (DRG) and spinal dorsal horn occurs between the heart and the stomach or the gallbladder (Ammons and Foreman, 1984; Qin et al, 2007), the colon and the urethra (Peng et al, 2010), as well as the distal colon and the urinary bladder (Qiao and Grider, 2007; Qin et al, 2005). However, the majority of the colonic afferent neurons do not overlap with bladder afferent neurons in the DRG (Chaban, 2008; Christianson et al, 2007; Qiao and Grider, 2007).…”

Section: Introductionmentioning

confidence: 99%

Colitis-induced bladder afferent neuronal activation is regulated by BDNF through PLCγ pathway

Xia

Shen

Hashmi

et al. 2016

Experimental Neurology

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Patients with inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS) often experience increased sensory responsiveness in the urinary bladder reflecting neurogenic bladder overactivity. Here we demonstrate that colitis-induced up-regulation of the phospholipase C gamma (PLCγ) pathway downstream of brain-derived neurotrophic factor (BDNF) in bladder afferent neurons in the dorsal root ganglia (DRG) plays essential roles in activating these neurons thereby leading to bladder hyperactivity. Upon induction of colitis with 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats, we found that the phosphorylation (activation) level of cAMP responsive element-binding (p-CREB) protein, a molecular switch of neuronal plasticity, was increased in specifically labeled bladder afferent neurons in the thoracolumbar and lumbosacral DRGs. In rats having reduced levels of BDNF (BDNF+/−), colitis failed to elevate CREB protein activity in bladder afferent neurons. Physiological examination also demonstrated that colitis-induced urinary frequency was not shown in BDNF+/− rats, implicating an essential role of BDNF in mediating colon-to-bladder sensory cross-sensitization. We further implemented in vivo and in vitro studies and demonstrated that BDNF-mediated colon-to-bladder sensory cross-activation involved the TrkB - PLCγ-calcium/calmodulin-dependent protein kinase II (CaMKII) cascade. In contrast, the PI3K/Akt pathway was not activated in bladder afferent neurons during colitis and was not involved in BDNF action in the DRG. Our results suggest that colon-to-bladder sensory cross-sensitization is regulated by specific signal transduction initiated by the up-regulation of BDNF in the DRG.

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“…Studies in cat (Ammons and Foreman, 1984), monkey (Ammons et al, 1984) and rat (Qin et al, 2007c) have shown that distension of the gallbladder (Ammons et al, 1984; Ammons and Foreman, 1984) or stomach (Qin et al, 2007c) activates thoracic spinothalamic tract neurons responsive to noxious chemical stimulation of the heart. Likewise, airway irritants (e.g., ammonia, cigarette smoke) have been shown to excite rat thoracic spinal neurons that also respond to esophageal distension (Hummel et al, 1997) or intrapericardial administration of bradykinin (Euchner-Wamser et al, 1994; Qin et al, 2007d).…”

Section: Clinical and Experimental Evidence Of Cross-organ Sensitizationmentioning

confidence: 99%

Visceral organ cross-sensitization — An integrated perspective

Brumovsky¹,

Gebhart²

2010

Autonomic Neuroscience

118

109

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Viscero-somatic referral and sensitization has been well documented clinically and widely investigated, whereas viscero-visceral referral and sensitization (termed cross-organ sensitization) has only recently received attention as important to visceral disease states. Because second order neurons in the CNS have been extensively shown to receive convergent input from different visceral organs, it has been assumed that cross-organ sensitization arises by the same convergence-projection mechanism as advanced for viscero-somatic referral and sensitization. However, increasing evidence also suggests participation of peripheral mechanisms to explain referral and sensitization. We briefly summarize behavioral, morphological and physiological support of and focus on potential mechanisms underlying cross-organ sensitization.

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Gastrocardiac Afferent Convergence in Upper Thoracic Spinal Neurons: A Central Mechanism of Postprandial Angina Pectoris

Cited by 6 publications

References 47 publications

Relationship between body weight and the increment in serum brain-derived neurotrophic factor after oral glucose challenge in men with obesity and metabolic syndrome

Relationship between body weight and the increment in serum brain-derived neurotrophic factor after oral glucose challenge in men with obesity and metabolic syndrome

Colitis-induced bladder afferent neuronal activation is regulated by BDNF through PLCγ pathway

Visceral organ cross-sensitization — An integrated perspective

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