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OBJECTIVES: Empathy is an essential ability that allows us to tune into how others are feeling or thinking. Empathy makes it possible to resonate with others' positive and negative feelings alike so that we can thus feel happy when we vicariously share the joy of others and we can share the experience of suffering when we empathize with someone in pain. Empathy training not only promotes prosocial behaviour, but also augments positive affect and resilience, which in turn fosters better coping with stressful situations. The Empathy Quotient (EQ) is a self-report questionnaire that was developed to measure the cognitive, affective, and behavioural aspects of empathy. Here, we aimed to examine the validity, reliability, and factor structure of the EQ in a Turkish sample. METHODS: Participants were 436 mostly college students and civil servants (195 female, 241 male). Sociodemographic information, the Turkish version of the EQ, Marlowe-Crowne Social Desirability Scale (MC-SDS) 33-item full version and MC-SDS 13-item shorter versions were administered. All statistical analyses were performed by using SPSS version 23 for Windows. RESULT: EQ scores were significantly higher in female participants ((X) over bar (Female)=46.45, SDFemale=0.62) compared to the male participants ((X) over bar (Male)=43.68, SD (Male)=0.56). The Cronbach's alpha coefficient for the scale was 0.76, Guttman's split-half reliability coefficient was 0.61, and test-retest reliability coefficient was 0.95. A positive and statistically significant correlation was found between the Turkish EQ and MC-SDS Full version (r=0.299, p

Mammalian tissues express the cannabinoid 1 (CB(1)) receptor and the cannabinoid 2 (CB(2)) receptor, the latter being involved in inflammation and pain. In somatic nerve pathways, the analgesic effects of CB(2) agonism are well documented. Two papers published in the Journal have provided evidence that CB(2) receptor activation inhibits visceral afferent nerve activity in rodents. These exciting findings are discussed in the context of recent data highlighting the emerging role of CB(2) receptor as a critical target able to counteract hypermotility in pathophysiological states, gut inflammation and possibly colon cancer.

Postoperative gastro-intestinal motility disorders are of major importance for patient management following abdominal surgery both for clinical and economic reasons. In recent years, new pathophysiological links have been identified that contribute to postoperative ileus. The activation of sympathetic efferent neurons by visceral afferent nerve fibers, catecholamines, the stimulation of beta 3 -receptors in the gut wall, an inflammatory response of the gut wall with the consecutive release of nitric oxide, and opioids given for postoperative analgesia seem to be of major importance regarding the development of postoperative ileus. The pharmacological reduction of visceral afferent nerve fiber activity, non-steroidal anti-inflammatory drugs (NSAIDs) instead of opioids for postoperative pain, peripheral opioid receptor antagonists together with opioids for postoperative analgesia, motilides and 5-HT4 receptor agonists as prokinetic drugs are strategies that are currently evaluated to treat postoperative ileus. Our review summarizes the present knowledge on the pathophysiology of postoperative ileus and new experimental treatments that might be of importance in the future.

Introduction: Postoperative gastric ileus interferes with postoperative recovery of the patients. Previous studies suggest that capsaicin-sensitive afferent neurons are involved in the mediation of postoperative gastric ileus. Methods: A group of rats were equipped with a strain gauge transducer sutured to the gastric wall. Gastric motility was recorded after intraperitoneal injection of capsaicin (0.1 µmol/kg and 1 µmol/kg) or vehicle. The rats were given 2 days of recovery before gastric motility was investigated in a postoperative ileus model. Results: Pretreatment with capsaicin 2 days prior to abdominal surgery significantly increased postoperative gastric motility, with complete recovery of gastric motility at 30 min postoperatively (with the baseline motility index set at 100±4%, the gastric motility index 30–45 min postoperatively was 64±4% for the vehicle, 138±20% for capsaicin 0.1 µmol/kg, and 110±12% for capsaicin 1 µmol/kg: P=0.0008 vehicle vs capsaicin). In contrast, capsaicin treatment 2 h prior to abdominal surgery did not increase postoperative gastric motility (gastric motility index 30–45 min postoperatively was 64±4% for the vehicle and 51±8% for capsaicin 0.1 µmol/kg). The acute intraperitoneal injection of capsaicin decreased gastric motility by about 50–60%, the response lasting for 15–30 min. Conclusions: Intraperitoneal capsaicin treatment 2 days prior to abdominal surgery resulted in immediate recovery of postoperative gastric motility, indicating an important role for serosal visceral afferent nerve fibers in the mediation of postoperative gastric ileus. Possibly, capsaicin or vanilloid (capsaicin) receptor agonists can be used to treat postoperative ileus in the future.

To define the route of influenza virus invasion into the central nervous system (CNS), an avian influenza A (H5N3) virus was inoculated into mice intranasally or intravenously. Only the intranasal infection group mice showed depression and retention of gas in the digestive system. Pathological findings in the animals were bronchointerstitial pneumonia and non-suppurative encephalitis restricted to the brain stem. The nerve nucleus primarily affected was the nucleus of solitary tract. Prior to the development of the CNS lesions, viral antigen was detected in vagal and trigeminal ganglia. These results suggest that the primarily replicated virus in the respiratory mucosa ascended to the CNS via sensory nerve routes, inducing lesions in the brain stem, and then spread trans-synaptically in the CNS.

Brief mesenteric ischemia (10 min) can stimulate both visceral A delta- and C-fiber afferents and evoke reflex excitation of the cardiovascular system. We have shown that exogenous histamine causes reflex cardiovascular responses and that intra-arterial injection of 5-hydroxytryptamine (5- HT) into a mesenteric artery stimulates visceral A delta- and C-fiber afferents. We therefore hypothesized that brief abdominal ischemia is associated with release of histamine and 5-HT into the interstitium, where these mediators could stimulate or sensitize ischemically sensitive visceral afferent nerve endings. Accordingly, we measured concentrations of histamine and 5-HT in portal venous blood plasma and intestinal lymph fluid in cats. Cannulas were placed in a portal vein and in an intestinal lymphatic duct distal to the lymph node. Lymph and plasma histamine and 5-HT concentrations were measured by high-performance liquid chromatography before, during, and immediately after 10-min occlusion of the descending thoracic aorta. Histamine concentration increased significantly (P < 0.01) in portal venous blood plasma from a preocclusion level of 2.2 +/- 0.6 to 4.6 +/- 1.0 and 6.4 +/- 1.3 nmol/ml and in lymph fluid from a preocclusion level of 3.4 +/- 1.0 to 6.3 +/- 1.3 and 6.4 +/- 1.3 nmol/ml (n = 18) during brief ischemia and reperfusion, respectively. Also, the 5-HT concentration was significantly (P < 0.01) elevated in portal venous blood plasma from a preocclusion concentration of 1.1 +/- 0.5 to 2.7 +/- 0.8 and 2.5 +/- 0.8 nmol/ml and in lymph from a preocclusion level of 1.8 +/- 0.7 to 4.0 +/- 1.4 and 4.6 +/- 1.3 nmol/ml (n = 13) during brief ischemia and reperfusion, respectively. Because visceral afferent nerve endings are located in the interstitium, elevation of the interstitial concentration of histamine and 5-HT may contribute to the stimulation or sensitization of these nerve terminals during the brief ischemia and reperfusion period.

Mesenteric ischemia of short duration (5-10 min) can stimulate A delta- and C-fiber afferent nerve endings in the viscera to reflexly activate the cardiovascular system. The mechanism of activation of abdominal visceral afferents is probably multifactorial and may involve prostaglandins (PGs), which have been shown to directly stimulate and/or sensitive visceral afferents when administered exogenously. We hypothesized that brief visceral ischemia is accompanied by release of PGI2 and PGE2 into the interstitium, where these cyclooxygenase products could stimulate or sensitize visceral afferent nerve endings. Accordingly, we measured immunoreactive PGE2 (iPGE2) and 6-keto-PGF1 alpha (i6-keto-PGF1 alpha), the stable metabolite of PGI2, in lymph draining the ischemic viscera as well as in portal venous blood. An intestinal lymph duct distal to the lymph node was cannulated in pentobarbital sodium-anesthetized cats. Lymph and plasma iPGE2 and i6-keto-PGF1 alpha concentrations were measured by radioimmunoassay before, during, and immediately after a 5- to 10-min occlusion of the descending aorta. The i6-keto-PGF1 alpha concentration increased significantly (P < 0.001) in portal venous plasma (61 +/- 12 to 107 +/- 18 pg/0.1 ml; n = 14) but not in lymph (148 +/- 30 to 159 +/- 24 pg/0.1 ml; n = 16). In contrast, iPGE2 concentration was significantly (P < 0.01) elevated in both venous plasma (156 +/- 16 to 207 +/- 26 pg/0.1 ml; n = 19) and lymph (520 +/- 48 to 590 +/- 52 pg/0.1 ml; n = 20).(ABSTRACT TRUNCATED AT 250 WORDS)

Cranial visceral afferent nerve transfers information about visceral organs to nucleus tractus solitarii (NTS) by releasing the excitatory neurotransmitter glutamate. Various endogenous modulators affect autonomic reflex responses by changing glutamatergic responses in the NTS. Although the expression of GABA(A) and GABA(B) receptors in glutamatergic terminals is known, their functional contribution on glutamate release is poorly characterized. Here, we used mechanically isolated NTS neurons to examine the mechanisms by which presynaptic GABA(A) and GABA(B) receptors modulate glutamatergic excitatory postsynaptic currents (EPSCs). EPSC were isolated by clamping voltage at equilibrium potential for chloride (-49 mV) without any GABA receptors antagonists. In all neurons, GABA(A) agonist, muscimol (1 and 10 μM), increased EPSC frequency (284.1±57% and 278.4±87% of control, respectively), but the GABA(B) agonist, baclofen (10 μM), decreased EPSC frequency (43±8% of control). The GABA(A) antagonist, gabazine (18 μM), decreased EPSC frequency in 50% of tested neurons, whereas GABA(B) antagonist, CGP (5 μM), increased the EPSC frequency in 36% of tested neurons. External application of GABA (1 and 30 μM) facilitating the EPSC frequency. The facilitation of the GABA(A) receptor-mediated release of glutamate was blocked by Na⁺-K⁺-Cl⁻ cotransporter type 1 antagonist or Na⁺ and Ca²⁺ channel inhibitors indicating GABA(A) presynaptic depolarization. Thus, tonically released GABA activates GABA(A) and GABA(B) receptors to modulate the release of glutamate. These findings provide cellular mechanisms of heterosynaptic GABA-glutamate integration of peripheral visceral afferent signals in the NTS.

Abdominal pain is one of the most difficult to treat symptoms in patients suffering from IBS. Recent evidence shows that abnormal perception of visceral stimuli, or visceral hypersensitivity, represents an important underlying mechanism. Of interest, similar mechanisms may be involved in abdominal pain reported by UC and Crohn's disease patients in remission. Although the underlying mechanisms are not fully understood, it becomes increasingly clear that intestinal inflammation may provide an initial stimulus for a persistent state of visceral hypersensitivity. Most insight in the role of inflammation in chronic abdominal pain comes from studies evaluating patients with postinfectious (PI)-IBS. Colonic biopsies of patients with PI-IBS reveal no signs of overt inflammation but show persistent minor increases in epithelial T lymphocytes and mast cells,1 suggesting that long-term inflammatory changes may be responsible for colonic hypersensitivity. To date, mast cells are considered to play a key role in this process. Supernatant of mucosal biopsies of visceral hypersensitive patients with IBS indeed contains more mast cell mediators such as serotonin, histamine and proteases, which are able to activate visceral afferent nerve fibres.2 Moreover, abdominal pain in patients with IBS was reported to be correlated with …

We investigated the effects of BTX-A on visceral afferent nerve transmission by measuring bladder tissue NGF levels in patients with neurogenic detrusor overactivity before and after intravesical treatment with BTX-A. We also compared the bladder tissue NGF content with clinical and urodynamic data.A total of 23 patients underwent clinical evaluation and urodynamics with detection of the UDC threshold, maximum pressure and maximum cystometric capacity before, and at the 1 and 3-month followups. Endoscopic bladder wall biopsies were also obtained at the same time points. NGF levels were measured in tissue homogenate by enzyme-linked immunosorbent assay (Promega, Madison, Wisconsin).At 1 and 3 months mean catheterization and incontinent episodes were significantly decreased (p0.05 and0.001, respectively). On urodynamics we detected a significant increase in the UDC threshold and maximum cystometric capacity, and a significant decrease in UDC maximum pressure at the 1 and 3-month follow-ups compared to baseline (each p0.001). At the same time points we detected a significant decrease in NGF bladder tissue content (each p0.02).BTX-A intravesical treatment induces a state of NGF deprivation in bladder tissue that persists at least up to 3 months. As caused by BTX-A, the decrease in acetylcholine release at the presynaptic level may induce a decrease in detrusor contractility and in NGF production by the detrusor muscle. Alternatively BTX-A can decrease the bladder level of neurotransmitters that normally modulate NGF production and release.

Neurokinin-1 (NK(1)) receptors activated by substance P (SP) are involved in the processing of nociceptive information and are a potential target for therapy of visceral pain. We have evaluated the role of NK(1) receptors using a selective antagonist of NK(1) receptors in two animal models of colorectal hypersensitivity. The behavioral response to colorectal distension was assessed in freely moving guinea pigs by recording visceromotor reflex contractions of the abdominal musculature. Colonic hypersensitivity was induced by intracolonic administration of a chemical irritant (0.6% of acetic acid), or by acute partial restraint stress. Sensitization was characterized by an exaggerated visceromotor response to a low level of colorectal distension (10 mm Hg). In both models of colonic hypersensitivity, oral administration of TAK-637 (0.1-10 mg/kg) normalized visceromotor responses. The intracerebroventricular (10 microg/kg) or intrathecal (10 microg/kg) administration of TAK-637 inhibited colonic hypersensitivity, suggesting an interaction with central NK(1) receptors. In contrast, TAK-637 had no effect on visceromotor responses to colorectal distension at 40 mm Hg in guinea pigs with normosensitive (nonsensitized) colons. In conclusion, central NK(1) receptors play a significant role in colonic hypersensitivity induced by visceral afferent nerve sensitization from gastrointestinal origin or acute psychosomatic stress, but not in the perception of colorectal distension in animals with normosensitive colons.

Abdominal ischemia reflexly activates the cardiovascular system by stimulating abdominal visceral afferent nerve endings. Whereas many ischemic metabolites responsible for activating these nerves have been identified (e.g., bradykinin), their precise mechanism of action is unclear. Protein kinase C (PKC) is an important part of the signal transduction process underlying the action of metabolites such as bradykinin and is a regulator of neuronal activity. Therefore, we hypothesized that PKC contributes to stimulation of ischemically sensitive abdominal visceral afferents. Single-unit activity was recorded from the right thoracic sympathetic chain of anesthetized cats. Exogenous activation of PKC using phorbol 12,13-dibutyrate (PDBu, 5 μg/kg ia) increased the impulse activity of ischemically sensitve C-fiber afferents from 0.04 ± 0.01 to 0.67 ± 0.23 impulses/s ( n = 11; P < 0.05). The influence of endogenous activation of PKC also was evaluated during 10 min of mesenteric ischemia. Inhibition of PKC using PKC-(19—36) (20 μg/kg iv) reduced ischemia-induced increases in afferent activity from 0.46 ± 0.11 to 0.19 ± 0.08 impulses/s ( n = 7, P < 0.05). Moreover, PKC-(19—36) (20 μg/kg iv) reduced the response of ischemically sensitive C fibers to bradykinin (0.5–1.0 μg/kg ia) from 1.18 ± 0.20 to 0.66 ± 0.14 impulses/s ( n = 13, P < 0.05). These results indicate that PKC contributes to activation of abdominal visceral afferents during ischemia and specifically to part of the bradykinin-induced activation of these afferents.

Background: Calcitonin gene-related peptide (CGRP) is a widely distributed neuropeptide contained in intrinsic and extrinsic neurons of the gastrointestinal wall that has been shown to be released by noxious stimulation, to be involved in nociception, to inhibit gastrointestinal motility, and to partly mediate postoperative gastric ileus. We hypothesized that abdominal surgery-induced release of CGRP might inhibit postoperative colonic motility and food intake. Methods: Colonic transit, stool pellet number, stool pellet weight, and food intake were measured for 48 hours after induction of postoperative ileus in rats. CGRP was immunoneutralized by preoperative injection of CGRP monoclonal antibody, or visceral afferent nerve fibers containing CGRP were functionally ablated by topical capsaicin treatment of the vagus nerves or of the celiac/superior mesenteric ganglia before abdominal surgery. Results: Abdominal surgery increased colonic transit time and decreased 24-hour cumulative stool pellet number, stool pellet weight, and food intake. CGRP immunoneutralization reversed postoperative inhibition of colonic transit, 24-hour cumulative stool pellet number, stool pellet weight, and food intake by 77%, 82%, 80%, and 52%, respectively. Whereas ablation of vagal afferent nerve fibers had no effect, spinal afferent nerve fiber ablation reversed postoperative inhibition of 24-hour cumulative stool pellet number, stool pellet weight, and food intake by 41%, 38%, and 19%, respectively. Conclusions: CGRP and spinal afferent nerve fibers partly mediate postoperative colonic ileus and inhibition of food intake in the rat. By the magnitude of reversal of postoperative ileus, CGRP seems to be an important mediator of postoperative colonic ileus. Our results for the first time show involvement of a neuropeptide and spinal afferents in the mediation of postoperative colonic ileus and postoperative inhibition of food intake in rats. (Surgery 1998;123:518-27.)

There is evidence for a pathway involving small intestinal CCK-producing entero-endocrine cells and visceral afferent nerve fibers in signaling the effect of luminal nutrients on gastrointestinal and food intake regulation. In order to investigate the type of anatomical apposition that exists between CCK cells and vagal afferents, CCK immunocytochemistry was performed on tissue from rats whose vagal afferent fibers to the abdomen had previously been labeled in vivo by injecting the fluorescent carbocyanine dye Dil into the nodose ganglia. CCK immunoreactive (CCK-IR) cells were more abundant than vagal afferent fibers, but both were present throughout the small intestine as well as in crypts and villi. Few CCK-IR cells were in close (

An antibody specific for the C-terrainus of rat alpha calcitonin gene-related peptide has been used in radioimmunoassay to measure concentrations of immunoreactive peptide in the upper gastrointestinal tract of capsaicin-treated and coeliac ganglionectomized rats and to measure axonal transport velocities in the vagus and splanchnic nerves. In adult rats that had been treated soon after birth with capsaicin, immunoreactive calcitonin gene-related peptide in the stomach and duodenum was undetectable (