Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sympathetic and enteric divisions of the autonomic nervous system are interactive in the determination of the functional state of the digestive tract. Activation of the sympathetic input suppresses digestive function primarily through release of norepinephrine at its synaptic interface with the enteric nervous system. The enteric nervous system functions like an independent minibrain in the initiation of the various programmed patterns of digestive tract behavior and moment-to-moment control as the neural microcircuits carry-out the behavioral patterns. Most of the postganglionic projections from sympathetic prevertebral ganglia terminate as synapses in myenteric and submucous ganglia of the enteric nervous system. Two primary actions of the sympathetic input are responsible for suppression of motility and secretion. First is presynaptic inhibitory action of norepinephrine to suppress release of neurotransmitters at fast and slow excitatory synapses in the enteric neural microcircuits and this effectively shuts-down the circuit. Second is inhibitory synaptic input to submucosal secretomotor neurons to the intestinal crypts. The alpha, adrenergic receptor subtype mediates both actions. Axons of secretomotor neurons to the crypts bifurcate to innervate and dilate the submucosal vasculature. Dilitation of the vasculature increases blood flow in support of increased secretion. Sympathetic inhibitory input to the secretomotor neurons therefore suppresses both secretion and blood flow. Activation of the sympathetic nervous system cannot explain the symptoms of secretory diarrhea and abdominal discomfort associated with psychologic and other forms of stress. Current evidence suggests that brain to mast cell connections account for stress-induced gastrointestinal symptoms. Degranulation of enteric mast cells by neural inputs releases inflammatory mediators that enhance excitability of intestinal secretomotor neurons while suppressing the release of norepinephrine from postganglionic sympathetic axons. This is postulated to underlie the secretory diarrhea and abdominal discomfort associated with stress.
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PMID:Neurotransmission at the interface of sympathetic and enteric divisions of the autonomic nervous system. 1070 95

Until now, Irritable Bowel Syndrome (IBS) has been one of gastrointestinal disorders which have not been fully understood. Clinically, there are some findings that indicate the role of inflammatory process in pathogenesis of IBS; such as, the onset of IBS that occurs after an episode of gastroenteritis (post-infective IBS (PI-IBS)). Although there is less evidence supporting genetic factors in pathogenesis of IBS, there are some reports about serotonin release in the plasma correlated to predominant constipation symptom. In contrast, increased serotonin release in IBS cases correlated to predominant diarrhea symptom. The stress-mast cell axis is one of pathophysiologic pathway that is expected to be able to explain the correlation between stress and characteristics found in IBS symptoms. Psychosocial factor has been well-considered to have important role in pathogenesis of IBS. Diagnosis of IBS is based on history of pain or abdominal discomfort that correlated to abnormal defecation pattern, without any obvious alarm sign. Nowadays, there is no specific laboratory test or physical or biochemical marker pathognomonic for IBS; therefore, clinical symptoms become the main modality in diagnosing IBS. This article will discuss the pathophysiology and diagnosis of IBS which will be helpful for clinicians in the management of IBS in daily practice.
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PMID:Irritable bowel syndrome: current review on pathophysiology and diagnotic aspects. 1915 51