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PubMed1994

Effects of central losartan on plasma renin and centrally mediated natriuresis.

Because intracerebroventricular (ICV) infusion of hypertonic saline or angiotensin II (Ang II) both induce water drinking, vasopressin secretion, natriuresis and increased arterial pressure, the possibility that common neural pathways mediate responses to ICV Ang II and hypertonic saline has been investigated. This was done by testing the effect of ICV infusion of the Ang II antagonist losartan on the natriuretic and pressor responses to ICV hypertonic NaCl in sheep. The effect of ICV losartan on plasma renin concentration (PRC) was also investigated. Infusion of losartan (1 mg/hr) into a lateral ventricle prevented both natriuretic and pressor responses to infusion of 0.6 mol/liter NaCl into a lateral ventricle at 1 ml/hr. In another experiment, ICV losartan at 1 mg/hr caused a pronounced increase in the PRC of Na-depleted sheep, while ICV Ang II at 3 micrograms/hr decreased PRC. The results suggest that: (i) a central angiotensinergic pathway may mediate osmoregulatory responses to centrally administered hypertonic saline, and (ii) a central angiotensinergic pathway may have a tonic inhibitory influence on renin secretion in Na-depleted animals.

Angiotensin II↗

PubMed2005

Leptin regulation of bone resorption by the sympathetic nervous system and CART.

Bone remodelling, the mechanism by which vertebrates regulate bone mass, comprises two phases, namely resorption by osteoclasts and formation by osteoblasts; osteoblasts are multifunctional cells also controlling osteoclast differentiation. Sympathetic signalling via beta2-adrenergic receptors (Adrb2) present on osteoblasts controls bone formation downstream of leptin. Here we show, by analysing Adrb2-deficient mice, that the sympathetic nervous system favours bone resorption by increasing expression in osteoblast progenitor cells of the osteoclast differentiation factor Rankl. This sympathetic function requires phosphorylation (by protein kinase A) of ATF4, a cell-specific CREB-related transcription factor essential for osteoblast differentiation and function. That bone resorption cannot increase in gonadectomized Adrb2-deficient mice highlights the biological importance of this regulation, but also contrasts sharply with the increase in bone resorption characterizing another hypogonadic mouse with low sympathetic tone, the ob/ob mouse. This discrepancy is explained, in part, by the fact that CART ('cocaine amphetamine regulated transcript'), a neuropeptide whose expression is controlled by leptin and nearly abolished in ob/ob mice, inhibits bone resorption by modulating Rankl expression. Our study establishes that leptin-regulated neural pathways control both aspects of bone remodelling, and demonstrates that integrity of sympathetic signalling is necessary for the increase in bone resorption caused by gonadal failure.

Activating Transcription Factor 4↗

PubMed2004

Behavioral equivalence, but not neural equivalence--neural evidence of alternative strategies in mathematical thinking.

In a functional magnetic resonance imaging study, we investigated how people solve mathematically equivalent problems presented in two alternative formats: verbal, story format or symbolic, equation format. Although representation format had no effect on behavior, anterior prefrontal activation was greater in the story condition and posterior parietal activation was greater in the equation condition. These results show that there exist alternative neural pathways that implement different and yet equally efficient problem-solving strategies.

Behavior↗

PubMed2006

Perspective on the central control of appetite.

Within the last 10 to 15 years, a number of discoveries have revised the way in which scientists view the role of the brain in the control of food intake (1). One aspect of the brain's influence is often characterized as the control of energy homeostasis. This term accounts for a number of factors arising from experimental studies on molecules and food consumption but seems to stop well short of explaining how brain processes articulate the variety of patterns of human feeding. It should be kept in mind that eating is 100% behavior, and this activity links the internal world of molecules and physiological processes with the external world of physical and cultural systems. It is not always clear the extent to which human eating patterns are a function of physiological or environmental pressure; this is, of course,the subject of extensive experimental study and debate. Because much of the current scientific activity on neural control of feeding is driven by the need to understand (and deal with) the causes of obesity, it will be necessary, at some stage, to reconcile the effects of the physiological mechanism believed to be responsible for eating control in the obese with the actual patterns of eating displayed (eating phenotypes) by obese people. Ultimately, the mechanisms and the behavioral phenotypes must match up. Initially, it is useful to consider which components of energy homeostasis are codified in specific molecular processes and neural pathways and to describe how the integration of diverse signaling systems (the codification) is translated into the expression of behavior and the accompanying subjective sensations.

Appetite Regulation↗

PubMed2003

Update on central function relevant to sex: remodeling the basis of drug treatments for sex and the brain.

Sexual function draws on a complex network of peripheral and central neural pathways. The standard focus on erectile difficulties and peripheral therapies has been highly successful clinically but there are many unresolved issues in men and newly discussed issues in women that will likely benefit from improved understanding of the central nervous system and sexual function. The spectrum of future therapies, based on evolving central neurophysiological understanding, will include the management of problems related to orgasm, ejaculation, desire, motivation, anxiety, and pleasure. This new range of therapies will employ old and new neurochemicals and pathways singly or in combination. The capability of hormones to modulate many of the sexual pathways will also contribute to the rise of multiagent therapy. The expanded understanding, in combination with enhanced imaging technologies, will renew the role of diagnosis and cause-specific treatment.

Animals↗

PubMed2004

The Effects of dizocilpine and phencyclidine on prepulse inhibition of the acoustic startle reflex and on prepulse-elicited reactivity in C57BL6 mice.

Prepulse inhibition (PPI) of the acoustic startle response refers to the reduction in startle reaction to a startle-eliciting stimulus when it is shortly preceded by a subthreshold prepulse stimulus. Here, we evaluated the possible effects on prepulse-elicited reactivity by dizocilpine (MK-801) and phencyclidine (PCP) in the PPI of acoustic startle paradigm in C57BL6/J mice. The aim was to ascertain whether these two drugs would affect prepulse-elicited reactivity in a manner similar to apomorphine, which enhances prepulse-elicited reactivity at doses that disrupt PPI. In two dose-response studies, we showed that both drugs exhibited a tendency to attenuate prepulse-elicited reaction at higher doses when PPI was severely disrupted. On the other hand, at lower doses when PPI was marginally disrupted, reaction to the prepulse, if anything, tended to increase. It is concluded that PPI disruption induced by noncompetitive NMDA receptor antagonists can be distinguished from apomorphine-induced PPI disruption by their concomitant effects on prepulse-elicited reactivity. Our data support the suggestion that dopamine receptor agonists and NMDA receptor antagonists disrupt PPI via interference with distinct neural pathways or neuronal systems.

Acoustic Stimulation↗

PubMed1998

Characterization of prostate size, PSA and endocrine profiles in patients with spinal cord injuries.

Aims of this study: From cross-sectional and longitudinal population based studies as well as from autopsy studies it is well documented that total prostate volume increases with advancing age. However, it is not well known (1) which factors are ultimately responsible for this growth phenomenon; or (2) at what time in a persons life the growth tends to occur. At present at least a permissive role for testicular androgens is assumed to be involved in growth regulation. Other factors such as growth factors, epithelial-mesenchymal interaction, and the role of intact neural pathways are still poorly understood. We aimed to study a group of men with spinal cord injuries to determine whether the pattern of prostate enlargement would be different in men with partially or completely interrupted innervation of the pelvis and the prostate gland. Materials and methods: Forty-three men from the Spinal Cord Injury (SCI) Service at the VA North Texas Health Care System ranging in age from 27-73 y (mean 51 y) were recruited to participate in this study. Time since SCI ranged from 2-47 (mean 19 y). All patients underwent standardized questionnaire, physical examination, transrectal ultrasonography (TRUS) measurements of total and transition zone volume of the prostate, serum PSA, testosterone (T), dihydrotestosterone (DHT), FSH and LH measurements, some had TRUS guided biopsies taken. Results: By all the measured criteria there were no abnormalities regarding the pituitary-gonadal axis observed in these men. Testicular volume, serum T, DHT and LH were within normal ranges, and when the patients were stratified by age, no differences were identified. There was an age related increase in FSH which has been described in neurologically intact men. Serum PSA increased slightly with advancing age. While total (TPV) and transition zone (TZV) prostate volume increased with age, the groupwise differences by decades of life were not significant. Moreover, when compared to a group of community dwelling men without known prostatic diseases and a clinic cohort of men with BPH, TPV was substantially lower for each decade of life except for men in their 40s, while TZV was substantially lower for men in their 60s. Conclusions: We observed normal age related changes regarding serum PSA and serum FSH without significant changes in other hormonal parameters. All parameters behaved consistent with changes described in neurologically intact populations. However, we did not observe the typical increase in TPV and TZV of the prostate as seen in population, autopsy and clinic patient studies. This interesting finding indicates that factors other than an intact pituitary-gonadal axis and male steroid hormones may be responsible for the normal age related growth of the prostate. Further studies in larger cohorts are needed to corroborate our findings.

Journal Article↗

PubMed2006

Coordination training in individuals with incomplete spinal cord injury: consideration of motor hierarchical structures.

STUDY DESIGN: Clinical commentary. OBJECTIVE: To discuss the method of coordination training to enhance motor skills in persons after spinal cord injury (SCI). METHOD: From the literature and clinical experience, we learn that basic motor skills like walking are refined and maintained through the millions of repetitions that take place as part of normal development. These coordinated patterns function effectively as a form of training to the system because of the presence of neural pathways that mediate commands between higher and lower levels of the central nervous system (CNS). When these pathways are disrupted as a result of a lesion, the question that arises is whether retraining can be effective. RESULTS/DISCUSSION: The question is directed at the common practice among rehabilitation professionals to prescribe and carry out tireless repetitions of coordinated motor activities in people with SCI lesions. We discuss this fundamental question from the perspective of understanding differences in maturation and function of higher motor centres and lower motor centres.

Central Nervous System↗

PubMed2006

Reduced sleep efficiency in cervical spinal cord injury; association with abolished night time melatonin secretion.

STUDY DESIGN: Case-controlled preliminary observational study. OBJECTIVE: Melatonin is usually secreted only at night and may influence sleep. We previously found that complete cervical spinal cord injury (SCI) interrupts the neural pathway required for melatonin secretion. Thus, we investigated whether the absence of night time melatonin in cervical SCI leads to sleep disturbances. SETTING: General Clinical Research Center, Brigham and Women's Hospital, Boston, USA. METHODS: In an ancillary analysis of data collected in a prior study, we assessed the sleep patterns of three subjects with cervical SCI plus absence of nocturnal melatonin (SCI levels: C4A, C6A, C6/7A) and two control patients with thoracic SCI plus normal melatonin rhythms (SCI levels: T4A, T5A). We also compared those results to the sleep patterns of 10 healthy control subjects. RESULTS: The subjects with cervical SCI had significantly lower sleep efficiency (median 83%) than the control subjects with thoracic SCI (93%). The sleep efficiency of subjects with thoracic SCI was not different from that of healthy control subjects (94%). There was no difference in the proportion of the different sleep stages, although there was a significantly increased REM-onset latency in subjects with cervical SCI (220 min) as compared to subjects with thoracic SCI (34 min). The diminished sleep in cervical SCI was not associated with sleep apnea or medication use. CONCLUSION: We found that cervical SCI is associated with decreased sleep quality. A larger study is required to confirm these findings. If confirmed, the absence of night time melatonin in cervical SCI may help explain their sleep disturbances, raising the possibility that melatonin replacement therapy could help normalize sleep in this group.

Adolescent↗

PubMed1998

Neural and non-neural activation of electrogenic secretion by 5-hydroxytryptamine in the rat ileum in vitro.

5-hydroxytryptamine (5-HT) stimulates electrogenic Cl- secretion in rat ileum stripped of its outer smooth musculature and myenteric plexus. The myenteric plexus, however, is a site of 5-HT synthesis in the gut, and the plexus mediates electrogenic ion secretion activated by luminal enterotoxin STa and taurocholate. Thus, we investigated the role of the myenteric plexus in 5-HT-induced electrogenic secretion in vitro by measuring short-circuit current (Isc, microamps) with voltage-clamp apparatus as an index of electrogenic Cl-secretion in rat ileum which was either stripped of the myenteric plexus or was left intact. Serosally added 5-HT stimulated electrogenic Cl- secretion in muscle-stripped and intact ileum in a concentration-dependent manner. Pre-treatment of stripped ileum with atropine (1 micron), hexamethonium (100 microns), tetrodotoxin (1.25 microns) and capsaicin (1 micron) for 15 min did not effect the maximum Isc induced by 5-HT which would implicate a direct action on the enterocyte. In intact ilea, however, tetrodotoxin (TTX) and capsaicin reduced significantly the maximum values of Isc stimulated by 5-HT, and the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) caused a significant decrease in the maximum response to 5-HT. These results suggest that electrogenic secretion induced by 5-HT in rat ileum in vitro occurs partly by activation of a non-neural pathway probably involving a direct interaction with the enterocyte, and partly via a nitrinergic-myenteric secretory reflex activated by sensory afferent fibres. These data highlight the danger of characterising intestinal secretory activity from in vitro experiments by using muscle-stripped tissue only.

Animals↗

PubMed1998

Influence of arterial baroreceptors and intracerebroventricular guanabenz on synchronized renal nerve activity.

The contributions of changes in the number of active fibres and the peak interval of synchronized neural discharges to arterial baroreflex regulated alterations in renal sympathetic nerve activity were examined in intact conscious rats. Stimulation of central nervous system alpha 2 adrenoreceptors with intracerebroventricular guanabenz (10, 20, 40 micrograms) was used to alter renal sympathetic nerve activity by a non-reflex mechanism in both intact and sinoaortic denervated (SAD) rats. Synchronized renal sympathetic nerve discharge was analysed with the sympathetic peak detection algorithm. When arterial pressure was increased from 50 mmHg to 150 mmHg in intact rats, the peak height (number of simultaneously active fibres) of synchronized discharges decreased in a sigmoidal fashion while the peak interval remained unchanged. Guanabenz produced a dose dependent inhibition of renal sympathetic nerve activity due to both a decrease in peak height and an increase in peak interval of synchronized discharges in both intact and SAD rats. Arterial baroreflex mediated changes in renal sympathetic nerve activity are due to changes in the number of simultaneously active nerve fibres. Central nervous system alpha 2 adrenoreceptor stimulation decreases renal sympathetic nerve activity by decreasing the number of active fibres and increasing the peak interval, acting on additional neural pathways not involved in buffering acute arterial pressure changes.

Adrenergic alpha-Agonists↗

PubMed2001

Review article: Helicobacter pylori, mucosal inflammation and symptom perception--new insights into an old hypothesis.

The role of Helicobacter pylori and the accompanying mucosal inflammatory response in functional dyspepsia is still undefined. Human and animal studies have clearly demonstrated a link between intestinal mucosal inflammation and changes in sensory-motor function. Growing clinical and basic evidence supports the concept that a similar paradigm may occur in H. pylori-related dyspepsia. The infection may both induce gastric dysmotility and trigger neuroplastic changes in the afferent neural pathways leading to visceral hyperalgesia. A reduction of central antinociceptive control systems may also play a pathophysiological role. H. pylori eradication has provided disappointing results in terms of improvement of symptoms. This may reflect the long-term recovery of neuroplastic changes occurring in the afferent nervous system or, alternatively, the incomplete resolution of gastritis and the persistent production of inflammatory mediators by resident cells in the muscularis externa. The identification of these mechanisms may provide a better understanding of the pathophysiology of H. pylori-related dyspepsia and prompt innovative therapeutic approaches.

Animals↗

PubMed2002

Transient lower oesophageal sphincter relaxations--a pharmacological target for gastro-oesophageal reflux disease?

The oesophago-gastric junction functions as an anti-reflux barrier preventing increased exposure of the oesophageal mucosa to gastric contents. Failure of this anti-reflux barrier results in gastro-oesophageal reflux disease, and may lead to complications such as oesophagitis, Barrett's oesophagus and eventually oesophageal carcinoma. Recent studies have suggested that transient lower oesophageal sphincter relaxation is the main mechanism underlying gastro-oesophageal reflux. It involves a prolonged relaxation of the lower oesophageal sphincter, mediated by a vago-vagal neural pathway, synapsing in the brainstem. Several drugs, such as atropine, baclofen and loxiglumide, have been shown to reduce the rate of transient lower oesophageal sphincter relaxations and concomitantly the number of reflux episodes. These findings illustrate that transient lower oesophageal sphincter relaxations may represent a potential new target for the pharmacological treatment of gastro-oesophageal reflux disease. It is possible that the reduction in the number of transient lower oesophageal sphincter relaxations may also contribute to the beneficial effect of fundoplication and new endoscopic anti-reflux procedures. It should be emphasized, however, that other factors, such as low lower oesophageal sphincter pressure, the presence of a hiatal hernia and impaired oesophageal peristalsis, are also of great importance. Therefore, whether the targeting of transient lower oesophageal sphincter relaxations is the 'golden bullet' in anti-reflux therapy remains to be proven, as evidence of an effective control of gastro-oesophageal reflux in reflux patients is still lacking.

Atropine↗

PubMed1997

Absence of desensitization by hexarelin to subsequent GH releasing hormone-mediated GH secretion in patients with anorexia nervosa.

OBJECTIVE: Both the basal levels and the neuroregulation of GH secretion are perturbed in patients with anorexia nervosa. It is unknown if these alterations are due to severe undernutrition or if they reflect basic neurotransmitter alterations of the patient's neural pathways. On the other hand, prior administration of the GH secretagogue hexarelin in normal subjects blocks the GH-releasing capability of GH releasing hormone (GHRH) administered 2 hours later. In the present work a sequential test was performed using the administration of hexarelin as first stimulus followed 120 minutes later by GHRH. The two aims of the study were: (a) to evaluate the interaction of GHRH and hexarelin, and (b) to further understand the alterations in GH neuroregulation in patients with anorexia nervosa. DESIGN: The GH stimuli used were hexarelin (1 micrograms/kg i.v.), a GH stimulus whose main action is hypothalamic, followed 120 minutes later by GHRH (1 micrograms/kg i.v.) as a pituitary stimulus. Each woman was tested once. PATIENTS: Thirty-two woman matched for age participated in the study: six normal-weight women as controls, 14 women with anorexia nervosa, seven women with secondary amenorrhoea due to voluntary weight loss for aesthetic reasons, and five normal-weight women after 72 hours of a controlled hypocaloric diet (800 cal/day). MEASUREMENTS: Plasma GH levels were measured by time-resolved fluoroimmunosasay, each value shown is the mean +/- SE in mU/l. RESULTS: The administration of hexarelin to the normal-weight women induced a clear-cut GH secretion (expressed as mean +/- SE of GH peak in mU/l of 77.5 +/- 21.8, but blocked the GH-releasing capability of GHRH administered 120 minutes later (6.6 +/- 2.8, P < 0.05). In contrast, the women with anorexia nervosa showed a normal GH response after the two stimuli: hexarelin 64.8 +/- 9.2. GHRH 71.1 +/- 14.2. The absence of heterologous desensitization was specific to anorexia nervosa, because the women with amenorrhoea due to voluntary weight loss but with a normal energy intake showed a pattern similar to the controls (GH after hexarelin 60.3 +/- 9.5 and to GHRH 120 minutes later 6.2 +/- 1.0 (P < 0.05)). Similarly, the women after the short-term hypocaloric diet showed a hexarelin-mediated GH secretion of 99.6 +/- 17.8, which blunted the subsequent administration of GHRH (GH mean peak of 9.9 +/- 2.9, P < 0.05 vs hexarelin). CONCLUSIONS: In the normal subjects, the administration of hexarelin induced clear-cut GH secretion, but inhibited the action of GHRH when administered 120 min later, while this heterologous desensitization was not observed in the patients with anorexia nervosa. This sequentially delayed test may be of some value in the clinical setting for assessing the status of patients with anorexia nervosa.

Adult↗

PubMed2000

Neuroendocrinology briefings 10: biological timekeeping.

The existence of biological clocks was once the subject of considerable debate. However, research has confirmed that a 24 h (circadian) clock in our brain has a pronounced influence on when we sleep, eat, drink, etc. Disruptions in clock function compromise normal daily patterns of hormone release, sleep and body temperature, and can affect mental and physical well-being. The recent identification of clock genes and the neural pathways to the clock will facilitate the development of effective strategies to treat disorders of circadian function.

Animals↗

PubMed2002

Photoperiodic control of oestrous cycles in Syrian hamsters: mediation by the mediobasal hypothalamus.

To assess whether the mediobasal hypothalamus (MBH) is necessary for photoperiodic control of oestrous cycles and prolactin secretion, we tested intact female Syrian hamsters (controls) and those that had sustained unilateral or bilateral lesions of the MBH. All hamsters displayed 4-day oestrous cycles postoperatively in the long-day photoperiod (14 h light/day); control females and those with unilateral MBH damage ceased to undergo oestrous cycles approximately 8 weeks after transfer to a short-day photocycle (10 h light/day), whereas 12 of 15 females with bilateral MBH lesions continued to generate 4-day oestrous cycles throughout 22 weeks in short days. Serum prolactin concentrations were either undetectable or low in all hamsters 8 or 14 weeks after the transfer to short-day lengths, but increased above long-day baseline values by week 22. We conclude that melatonin-binding sites in the MBH mediate suppression of oestrous cycles but not prolactin secretion by short-day lengths; recovery of prolactin secretion in females during prolonged exposure to short-day lengths reflects development of refractoriness to melatonin in a substrate distinct from the MBH. These findings suggest that separate neural pathways mediate photoperiodic control of gonadotropin and prolactin secretion in female hamsters.

Animals↗

PubMed2003

The melanocortin agonist Melanotan-II reduces the orexigenic and adipogenic effects of neuropeptide Y (NPY) but does not affect the NPY-driven suppressive effects on the gonadotropic and somatotropic axes in the male rat.

Neuropeptide Y (NPY) is a strong orexigenic neurotransmitter also known to modulate several neuroendocrine axes. alpha-Melanocyte-stimulating hormone (MSH) is an essential anorectic neuropeptide, acting on hypothalamic MC3/4 receptor subtypes. When given as an intracerebroventricular bolus injection, Melanotan-II (MT-II), a non selective MC receptor agonist, inhibits feeding, suppresses the NPY orexigenic action, and reduces basal insulinaemia. We evaluated the effects of a 7-day central infusion of MT-II (15 nmol/day) given either alone or in association with NPY (5 nmol/day) in male Sprague-Dawley rats. MT-II produced almost full anorexia for 1-2 days but then feeding gradually returned to normal despite continued MT-II infusion. When coinfused with NPY, MT-II also produced the same initial anorectic episode but then maintained feeding to upper normal levels, thus cancelling the hyperphagia driven by NPY. Whereas NPY infusion produced a doubling of fat pad weight, MT-II reduced adiposity by a factor of two compared to pair-fed rats, and vastly curtailed the NPY-driven increase in fat pad weight. MT-II infusion also significantly curtailed the NPY-induced rise in insulin and leptin secretions. NPY infusion significantly inhibited hypothalamic pro-opiomelanocortin mRNA expression, most likely cancelling the alpha-MSH anorectic activity. As expected from previous studies, chronic NPY infusion strongly inhibited both the gonadotropic and somatotropic axes, and coinfusion of MT-II did not reverse these NPY-driven effects, in sharp contrast with that seen for the metabolic data. MT-II infusion alone had little effect on these axes. In conclusion, chronic MT-II infusion generated a severe but transient reduction in feeding, suggesting an escape phenomenon, and clearly reduced fat pad size. When coinfused with NPY, MT-II was able to cancel most of the NPY effects on feeding, but not those on the neuroendocrine axes. It appears therefore that, as expected, NPY and alpha-MSH closely interact in the control of feeding, whereas the neural pathways by which NPY affects growth and reproduction are distinct and not sensitive to MC peptide modulation.

Adipocytes↗

PubMed1999

Cognitive evoked potentials to anticipated oesophageal stimulus in humans: quantitative assessment of the cognitive aspects of visceral perception.

Evoked potential studies provide an objective measure of the neural pathways involved with perception. The effects of cognitive factors, such as anticipation or awareness, on evoked potentials are not known. The aim was to compare the evoked potential response to oesophageal stimulation with the cortical activity associated with anticipation of the same stimulus. In 12 healthy men (23.5 +/- 4 years), oesophageal electrical stimulation (15 mA, 0.2 Hz, 0.2 msec) was applied, and the evoked potentials recorded using scalp electrodes. A computerized model of randomly skipped stimuli (4:1 ratio) was used to separately record the evoked potentials associated with stimulation and those associated with an anticipated stimulus. The electrical stimulus represented the nontarget stimulus and the skipped impulse the target (anticipatory) stimulus. This anticipatory evoked potential was also compared to auditory P300 evoked potentials. Reproducible evoked potentials and auditory P300 responses were elicited in all subjects. Anticipatory evoked potentials (peak latency 282.1 +/- 7.9 msec, amplitude 8.2 +/- 0.7 microV, P < 0.05 vs auditory P300 evoked potential) were obtained with the skipped stimulus. This anticipatory evoked potential was located frontocentrally, while the auditory P300 potential was located in the centro-parietal cortex. The anticipatory evoked potential associated with expectation of an oesophageal stimulus, although of similar latency to that of the auditory P300 evoked response, originates from a different cortical location. The recording of cognitive evoked potentials to an expected oesophageal stimulus depends on attention to, and awareness of, the actual stimulus. Anticipatory evoked potentials to GI stimuli may provide an objective electrophysiological tool for the assessment of the cognitive factors associated with visceral perception.

Adult↗