Fast and slow synaptic potentials produced in a mammalian sympathetic ganglion by colon distension.

Radial distension of the large intestine produced a slow depolarization in a population of neurons in the inferior mesenteric ganglion of the guinea pig. The slow potentials often occurred simultaneously with cholinergic fast potentials [( excitatory postsynaptic potentials (EPSPs]) yet persisted in the presence of nicotinic and muscarinic cholinergic antagonists when all fast EPSPs were absent. The amplitude of the distension-induced noncholinergic slow depolarization increased with increasing distension pressure. For distensions of 1-min duration at pressures of 10-20 cm of water, the mean depolarization amplitude was 3.4 mV. The slow depolarization was associated with an increase in membrane resistance, and prolonged periods of colon distension resulted in a tachyphylaxis of the depolarization. Desensitization of ganglion cells to the peptide substance P attenuated the distension-induced slow potential by an average of 49% +/- 17%. Thus, two colonic mechanosensory afferent pathways converge on principal ganglion cells in the inferior mesenteric ganglion: one was previously described to be mediated by acetylcholine, and the other is described here, whose transmitter remains to be determined but which preliminary evidence suggests is mediated in part by substance P. The noncholinergic afferent pathway may enhance the intestinal inhibitory reflex mediated by cholinergic mechanosensory afferent input to the abdominal prevertebral sympathetic ganglia.     

How many kinds of visceral afferents?

Most afferent signals from the viscera do not give rise to conscious experience and yet they participate in the complex neural control of visceral functions. Surprisingly little information is available on the origin, morphology, and receptor functional characteristics of the nerve endings of most primary afferent neurones to the digestive tract. This review deals with the morphological nature of the afferent neurones that supply the gastrointestinal tract specifically.     

Role of P(1) purinergic receptors in myocardial ischemia sensory transduction

OBJECTIVES: To characterize the role that cardiac sensory P(1) purinergic (adenosine A(1) or A(2)) receptors play in transducing myocardial ischemia. METHODS: Porcine nodose ganglion cardiac sensory neuron adenosine A(1) or A(2) receptor function was studied in situ during control states as well as in the presence of the peptides bradykinin and substance P or focal ventricular ischemia. The responses of porcine nodose ganglion cardiac and non-cardiac afferent neuronal somata to adenosine were also studied in vitro. RESULTS: Local application of A(1) or A(2) adenosine receptor agonists modified the activity generated by ventricular sensory neurites associated with 70 and 74% of identified nodose ganglion cardiac afferent somata in situ, respectively, exciting most neurons. In contrast, adenosine reduced the excitability of nodose ganglion cardiac afferent neuronal somata in vitro. Bradykinin and substance P affected 56 and 63%, respectively, of tested afferent neurons. The capacity of ventricular sensory neurites to transduce signals relating to these peptides was virtually eliminated by the presence of P(1) purinergic receptor antagonists. So was their capacity to transduce focal ventricular ischemia. Since most cardiac sensory neurites responded differently to adenosine in vivo than did cardiac afferent neuronal somata in vitro, it appears that the transduction properties of cardiac afferent neurons need to be characterized in situ. CONCLUSIONS: Most ventricular sensory neurites associated with nodose ganglion afferent neurons possess adenosine A(1) and/or A(2) receptors that play a primary role in transducing myocardial ischemic events to central neurons. These data support clinical observations implicating cardiac sensory purinoceptors in transducing myocardial ischemic events.     

Myocardial ischaemia and the cardiac nervous system.

The intrinsic cardiac nervous system has been classically considered to contain only parasympathetic efferent postganglionic neurones which receive inputs from medullary parasympathetic efferent preganglionic neurones. In such a view, intrinsic cardiac ganglia act as simple relay stations of parasympathetic efferent neuronal input to the heart, the major autonomic control of the heart purported to reside solely in the brainstem and spinal cord. Data collected over the past two decades indicate that processing occurs within the mammalian intrinsic cardiac nervous system which involves afferent neurones, local circuit neurones (interconnecting neurones) as well as both sympathetic and parasympathetic efferent postganglionic neurones. As such, intrinsic cardiac ganglionic interactions represent the organ component of the hierarchy of intrathoracic nested feedback control loops which provide rapid and appropriate reflex coordination of efferent autonomic neuronal outflow to the heart. In such a concept, the intrinsic cardiac nervous system acts as a distributive processor, integrating parasympathetic and sympathetic efferent centrifugal information to the heart in addition to centripetal information arising from cardiac sensory neurites. A number of neurochemicals have been shown to influence the interneuronal interactions which occur within the intrathoracic cardiac nervous system. For instance, pharmacological interventions that modify beta-adrenergic or angiotensin II receptors affect cardiomyocyte function not only directly, but indirectly by influencing the capacity of intrathoracic neurones to regulate cardiomyocytes. Thus, current pharmacological management of heart disease may influence cardiomyocyte function directly as well as indirectly secondary to modifying the cardiac nervous system. This review presents a brief summary of developing concepts about the role of the cardiac nervous system in regulating the normal heart. In addition, it provides some tentative ideas concerning the importance of this nervous system in cardiac disease states with a view to stimulating further interest in neural control of the heart so that appropriate neurocardiological strategies can be devised for the management of heart disease.     

Bag cell peptide acts directly on ovotestis of Aplysia californica: Basis for an in vitro bioassay

Extracts of the parietovisceral ganglion (PVG) of Aplysia californica cause release of eggs from isolated fragments of ovotestis. Spontaneous release of eggs by ovotestis in vitro is similar in artificial sea water (ASW) and hemolymph; PVG extracts increase egg release in ASW and hemolymph similarly. PVG-induced egg release is dose dependent in vitro. The number of eggs released in vitro by PVG extract or by ASW alone increases with time after oviposition. Extracts of genital or pleural ganglia or of branchial nerve do not increase egg release above control levels in ASW; isolated bag cell clusters are most effective at inducing egg release. PVG-induced egg release persists after the extract is boiled but not after incubation with trypsin or protease. These in vitro results are consistent with previous in vivo studies on egg-laying and provide evidence that a bag cell peptide acts directly on the ovotestis. Therefore, egg release in vitro appears to be a function of peptide concentration and oviposition history. The logarithmic relation between PVG concentration and relative egg release provides an in vitro bioassay for the bag cell peptide(s).     

Visceral perception: sensory transduction in visceral afferents and nutrients

The possible mechanisms that may be involved in nutrient detection in the wall of the gastrointestinal tract are reviewed. There is strong functional and electrophysiological evidence that both intrinsic and extrinsic primary afferent neurones mediate mechano- and chemosensitive responses in the gastrointestinal tract. This review focuses on the extrinsic afferent pathways as these are the ones that convey information to the central nervous system which is clearly necessary for perception to occur.     

Cardiac sympathetic afferent cell bodies are located in the peripheral nervous system of the cat

Studies of the stellate ganglion and middle cervical ganglion indicate that sympathetic efferent nerve activity can be modified by peripheral excitatory inputs and that these neural connections may function as pathways for a peripheral reflex at the level of the thoracic sympathetic ganglia. This excitatory synaptic input could have a soma in either the central or the peripheral nervous system. A study was designed to determine whether chronic decentralization (3 weeks) of the stellate ganglion in cats would 1) abolish sympathetic cardiac afferent nerve activity recorded at the stellate cardiac nerve and 2) abolish local thoracic reflexes that are generated by stimulation of peripheral nerves. The ansae subclaviae, T3 and T4 rami, and stellate ganglion were also examined by electron microscopy for the extent of Wallerian degeneration. Afferent cardiac activation of the axon collaterals arising from cell bodies located in the dorsal root ganglia was abolished due to degeneration. However, sympathetic afferent nerve activity from the left ventricular receptors was still present and was recorded from the stellate cardiac nerve in all cats. Cardiac receptors were sensitive to mechanical distortion, increases in the left ventricular pressure, and epicardial application of veratrine hydrochloride. These data imply that 1) cardiovascular afferent input to the stellate ganglion persists following chronic decentralization and 2) the sensory neurons are located in the peripheral sympathetic nervous system. Thus, we find that regulation of the heart occurs in part via thoracic ganglia, independently of the central nervous system.     

Splanchnic and pelvic mechanosensory afferents signal different qualities of colonic stimuli in mice

BACKGROUND&AIMS: Mechanosensory information from the colon is conducted via lumbar splanchnic nerves (LSN) and sacral pelvic nerves (PN) to the spinal cord. The precise nature of mechanosensory information encoded by each pathway has remained elusive. Here, we characterize and directly compare the properties of mechanosensitive primary afferents from these 2 pathways. METHODS: Using a novel in vitro mouse colon preparation, mechanosensitive primary afferents were recorded from the LSN and PN and distinguished based on their response to receptive field stimulation with 3 distinct mechanical stimuli: probing (70 mg-4 g), circular stretch (1-5 g), and mucosal stroking (10-1000 mg). RESULTS: Five different classes of afferent were recorded from the LSN and PN. Three of these classes of afferent (serosal, muscular, and mucosal) were conserved between both pathways; however, their respective proportions, receptive field distributions, and response properties differed greatly. In general, these 3 classes of afferent recorded from the PN responded to lower stimulation intensities, displayed greater response magnitudes, and adapted less completely to mechanical stimulation compared with their LSN counterparts. In addition, the LSN and PN each contain a specialized class of afferent (mesenteric and muscular/mucosal), which is unique to their respective pathway. CONCLUSIONS: The splanchnic and pelvic pathways contain distinct populations of mechanosensitive afferents. These afferents are capable of detecting an array of mechanical stimuli and are individually tuned to detect the type, magnitude, and duration of the stimulus. This knowledge contributes to our understanding of the role that these 2 pathways play in conveying mechanical information from the colon.     

Plasticity of vagal afferent fibres mediating cough

Increased sensitivity of cough pathways has been demonstrated in numerous studies. The underlying mechanisms of this sensitization are largely unknown; however, a burgeoning body of evidence suggests that vagal primary afferent neurones that innervate the airways are likely to be involved. This plasticity includes changes in anatomy, neurochemistry and function. PGE2 is an example of an inflammatory mediator that increases responsiveness to tussive stimuli. Electrophysiological studies of neurone cell bodies isolated from afferent ganglia have revealed that prostanoids modulate the function of a variety of distinct ion channels including those that carry TTX-insensitive voltage-gated sodium currents, slow post-spike hyperpolarizations and a hyperpolarization-activated cation current. Mediator-induced modulation of the function of various voltage-gated currents operating at the peripheral terminals of airway afferent neurons would probably influence input from the airways into the central nervous system and contribute to the urge to cough and increased responsiveness to tussive stimuli.     

Physiology of esophageal motor function

The esophagus is a region with three functional zones: (1) the upper esophageal sphincter; (2) the esophageal body; and (3) the lower esophageal sphincter. Control mechanisms within the central nervous system and peripherally serve to integrate these functional zones in a region where voluntary and involuntary control mechanisms and the activity of two different types of muscle are intimately coordinated. The distal 50 to 60 per cent of the esophagus in humans is entirely smooth muscle. Extrinsic control for esophageal motor function resides in a brainstem swallowing center with an afferent reception system, an efferent system of motor neurones, and a complex organizing or internuncial system of neurones. Sensory information from the esophagus is carried in the vagus nerves, but sensory pathways are also present in sympathetics entering the spinal cord. The vagus nerve receiving fibers both from the nucleus ambiguus and the dorsal motor nucleus innervates the striated and smooth muscle esophagus, respectively, including the sphincters. There is a myenteric nerve plexus in both the striated and smooth muscle segments. In the smooth muscle esophagus, there are two important effector neurones, an excitatory cholinergic neurone, and a nonadrenergic, noncholinergic (NANC) inhibitory neurone. The striated muscle contraction is directed and coordinated by sequential excitation through vagal fibers programmed by the central control mechanism. There are at least four potential control mechanisms for peristalsis in the smooth muscle esophagus: efferent motor fibers programmed by the swallowing center fire sequentially during peristalsis; the intramural neural mechanism can be excited to produce peristalsis near the onset of stimulation or with a delay after termination of stimulation; there is evidence for myogenic propagation of a peristaltic contraction. In humans, swallow-induced peristalsis is cholinergic and appears to result primarily from sequencing and activation of the intramural excitatory cholinergic neurones. Both central and peripheral levels of control are highly integrated to focus on the excitatory cholinergic neurones. It is likely that under normal circumstances, the central control mechanism exerts the dominant influence on these neurones for initiation and coordination of peristalsis in the smooth muscle esophagus. In humans, resting tone in the lower esophageal sphincter is predominantly cholinergic, but this tone is regulated by a balance between many excitatory and inhibitory influences. The relaxation on swallowing is caused by active inhibition of the muscle through NANC inhibitory neurones and cessation of tonic neural excitation to the     

Dietary sodium loading increases arterial pressure in afferent renal-denervated rats

In rats fed high sodium diet, increasing renal pelvic pressure > or =3 mm Hg activates renal mechanosensory nerves, resulting in a renorenal reflex-induced increase in urinary sodium excretion. The low activation threshold of the renal mechanosensory nerves suggests a role for natriuretic renorenal reflexes in the regulation of arterial pressure and sodium balance. If so, interruption of the afferent renal innervation by dorsal rhizotomy (DRX) at T9-L1 would impair urinary sodium excretion and/or increase arterial pressure during high dietary sodium intake. DRX and sham-DRX rats were fed either a high or a normal sodium diet for 3 weeks. Mean arterial pressure measured in conscious rats was higher in DRX than in sham-DRX rats fed a high sodium diet, 130+/-2 vs 100+/-3 mm Hg (P<0.01). However, mean arterial pressure was similar in DRX and sham-DRX rats fed a normal sodium diet, 115+/-1 and 113+/-1 mm Hg, respectively. Steady-state urinary sodium excretion was similar in DRX and sham-DRX rats on high (17.9+/-2.2 and 16.4+/-1.8 mmol/24 h, respectively) and normal (4.8+/-0.3 and 5.0+/-0.4 mmol/24 h, respectively) sodium diets. Studies in anesthetized rats showed a lack of an increase in afferent renal nerve activity in response to increased renal pelvic pressure and impaired prostaglandin E2-mediated release of substance P from the renal pelvic nerves in DRX rats fed either a high or a normal sodium diet, suggesting that DRX resulted in decreased responsiveness of peripheral renal sensory nerves. In conclusion, when the afferent limb of the renorenal reflex is interrupted, a high sodium diet results in increased arterial pressure to facilitate the natriuresis and maintenance of sodium balance.     

Ablation of capsaicin sensitive afferent nerves impairs defence but not rapid repair of rat gastric mucosa.

Capsaicin sensitive afferent neurones have previously been reported to play a part in gastric mucosal protection. The aim of this study was to investigate whether these nociceptive neurones strengthen mucosal defence against injury or promote rapid repair of the damaged mucosa, or both. This hypothesis was examined in anaesthetised rats whose stomachs were perfused with ethanol (25 or 50% in saline, wt/wt) for 30 minutes. The gastric mucosa was inspected 0 and 180 minutes after ethanol had been given at the macroscopic, light, and scanning electron microscopic level. Rapid repair of the ethanol injured gastric mucosa (reduction of deep injury, partial re-epithelialisation of the denuded surface) took place in rats anaesthetised with phenobarbital, but not in those anaesthetised with urethane. Afferent nerve ablation as a result of treating rats with a neurotoxic dose of capsaicin before the experiment significantly aggravated ethanol induced damage as shown by an increase in the area and depth of mucosal erosions. Rapid repair of the injured mucosa, however, as seen in rats anesthetised with phenobarbital 180 minutes after ethanol was given, was similar in capsaicin and vehicle pretreated animals. Ablation of capsaicin sensitive afferent neurones was verified by a depletion of calcitonin gene related peptide from the gastric corpus wall. These findings indicate that nociceptive neurones control mechanisms of defence against acute injury but are not required for rapid repair of injured mucosa.     

Cardiac Pain, Sympathetic Afferents, and Life-Threatening Arrhythmias

Cardiac Pain, Sympathetic Afferents, and Life-Threatening Arrhythmias. Myocardial ischemia activates receptors of sympathetic and vagal afferent fibers. Although both afferent pathways are excited, this article primarily focuses on the sympathetic pathways. Increased sympathetic afferent activity to cells of the spinal cord can lead to cardiac pain and reflex sympathetic hyperactivity that can be quite arrhythmogenic. Complicating factors that affect the relationship arises from activation of vagal afferent fibers. Sympathetic afferent fibers in the ventricle appear to be composed of mechanosensitive and chemosensitive receptors. Sympathetic afferent fibers excite cells of origin of the spinothalamic tract, the classical pain pathway that transmits information about noxious somatic and visceral episodes to areas of the brain involved with pain perception. Activation of selected brainstem nuclei, the vagus, and the dorsal columns can suppress afferent information from the heart that excites spinothalamic tract cells. Excitation of sympathetic afferent fibers initiates a series of cardiovascular reflexes, some of which may affect cardiac electrical stability significantly. Increased arrhythmogenesis can be reduced when C₈-T₅ dorsal roots are transected. Stimulation of cardiac nerves that involve the left stellate ganglion can produce life-threatening arrhythmias, particularly if combined with myocardial ischemia or infarction. Through reflex mechanisms, activation of sympathetic afferent fibers can suppress activity of vagal efferent fibers. If prevention of cardiac pain through reduced firing or inhibition of cells in the spinothalamic tract reduces afferent sympathetic activity that occurs during acute myocardial ischemia, it would be logical to surmise that another significant benefit would follow, namely reduced risk for malignant arrhythmias.     

The role of the vagal nerve in peripheral PYY3-36-induced feeding reduction in rats

Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY(3-36), the major form of circulating PYY, binds to the hypothalamic neuropeptide Y Y2 receptor (Y2-R) with a high-affinity, reducing food intake in rodents and humans. Additional gastrointestinal hormones involved in feeding, including cholecystokinin, glucagon-like peptide 1, and ghrelin, transmit satiety or hunger signals to the brain via the vagal afferent nerve and/or the blood stream. Here we determined the role of the afferent vagus nerve in PYY function. Abdominal vagotomy abolished the anorectic effect of PYY(3-36) in rats. Peripheral administration of PYY(3-36) induced Fos expression in the arcuate nucleus of sham-operated rats but not vagotomized rats. We showed that Y2-R is synthesized in the rat nodose ganglion and transported to the vagal afferent terminals. PYY(3-36) stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY(3-36) could directly alter the firing rate of the vagal afferent nerve via Y2-R. We also investigated the effect of ascending fibers from the nucleus of the solitary tract on the transmission of PYY(3-36)-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY(3-36)-induced reductions in feeding. This study indicates that peripheral PYY(3-36) may transmit satiety signals to the brain in part via the vagal afferent pathway.     

Cardiovascular reflexes mediated by capsaicin sensitive cardiac afferent neurones in the dog

Reflex circulatory changes mediated by capsaicin sensitive cardiac afferent neurones were studied in anaesthetised, open chest dogs. Application of capsaicin to the epicardium of the left ventricle, either in single doses (0.01-100 micrograms) or by superfusion (20 micrograms X min-1), consistently resulted in dose related increases in blood pressure and heart rate. These responses were not affected by bilateral vagotomy but were abolished or reversed by bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy. Injection of capsaicin (0.3-1 microgram X kg-1) into the left circumflex coronary artery caused either systemic hypotension and bradycardia (70.3% of experiments), a pressor response associated with tachycardia (13.5%), or a biphasic effect with an initial rise and then fall in blood pressure and heart rate (16.2%). With intravenous injections of capsaicin (3-5 micrograms X kg-1) the response was invariably cardioinhibitory and depressor. The reflex bradycardia and hypotension evoked with either intracoronary or intravenous injections of capsaicin were reversed after bilateral vagotomy to increases in cardiac rate and blood pressure. The post-vagotomy tachycardia occurring with intracoronary capsaicin could be abolished by beta adrenoceptor blockade with propranolol (0.5 mg X kg-1 iv), whereas ganglionic transmission blockade with pentolinium (0.5 mg X kg-1 iv) eliminated both the tachycardia and pressor effects. The results indicate that in the dog's heart capsaicin sensitive afferent neurones capable of affecting the circulatory system have both vagal and spinal sympathetic origin. It is suggested that capsaicin induced excitatory cardiogenic reflex is nociceptive in nature and may involve activation of substance P containing afferent fibres incorporated in cardiac sympathetic nerves.     

Activation of endothelin-a receptors contributes to angiotensin-induced suppression of renal sensory nerve activation

Activation of renal mechanosensory nerves is enhanced by a high-sodium diet and suppressed by a low-sodium diet. Angiotensin (Ang) II and endothelin (ET)-1 each contributes to the impaired responsiveness of renal mechanosensory nerves in a low-sodium diet. We examined whether stimulation of ETA receptors (Rs) contributes to Ang II-induced suppression of the responsiveness of renal mechanosensory nerves. In anesthetized rats fed a low-sodium diet, renal pelvic administration of the Ang type I receptor (AT1-R) antagonist losartan enhanced the afferent renal nerve activity (ARNA) response to increasing renal pelvic pressure 7.5 mm Hg from 7+/-2% to 15+/-2% and the prostaglandin (PG) E(2)-mediated substance P release from 0+/-1 to 8+/-1 pg/min. Adding the ETA-R antagonist BQ123 to the renal pelvic perfusate containing losartan did not produce any further enhancement of the ARNA response or PGE(2)-mediated release of substance P (17+/-3% and 8+/-1 pg/min). Likewise, renal pelvic administration of BQ123 and BQ123+losartan resulted in similar enhancements of the ARNA responses to increased renal pelvic pressure and PGE(2)-mediated substance P release. In high-sodium-diet rats, pelvic administration of Ang II reduced the ARNA response to increased renal pelvic pressure from 27+/-4% to 8+/-3% and the PGE(2)-mediated substance P release from 9+/-0 to 1+/-1 pg/min. Adding BQ123 to the renal pelvic perfusate containing Ang II restored the increases in ARNA and the PGE(2)-mediated substance P release toward control (27+/-6% and 7+/-1 pg/min). In conclusion, stimulation of ETA-R plays an important contributory role to the Ang II-mediated suppression of the activation of renal mechanosensory nerves in conditions of low-sodium diet.     

Integration of gut function by sympathetic reflexes

1. The spinal sympathetic outflow that innervates the gastrointestinal tract, including its blood vessels, has an impressive representation quantitatively, yet little is known about the functions of this system and its peripheral or central organization. Electrical stimulation or section of the splanchnic nerves have variable effects on the GI tract and does not, therefore, lead to a deeper understanding of the system. 2. The targets of the sympathetic supply of the GI tract are blood vessels, nonvascular (sphincteric) smooth musculature, myenteric neurones, submucous neurones and gut associated lymphoid tissues. The corresponding functions associated with these targets are regulation of blood flow (particularly through the mucosa) and resistance to flow, of motility, of secretion and absorption and of immune responses. Little is known about the effects of the sympathetic nervous system on the latter function. 3. The sympathetic postganglionic neurones are (at least in the guinea-pig) neurochemically characterized with respect to the targets. Neurones projecting to blood vessels contain neuropeptide Y in addition to noradrenaline, while neurones projecting to the submucous plexus contain somatostatin. No neuropeptide has been detected to date in neurones projecting to the myenteric plexus. 4. Transmission through guinea-pig prevertebral ganglia in vitro have been studied electrophysiologically. The following functions have been demonstrated: (a) transmission and distribution of preganglionic impulse activity to the targets in a relay-like fashion; (b) mediation of peripheral intestinointestinal reflexes between different sections of the GI tract; (c) integration of activity from the spinal cord and from various peripheral sources. The first function may apply particularly to the sympathetic pathway innervating blood vessels. Whether the second function occurs in vivo is questionable. The third function is the most important one for pathways involved in the regulation of motility and probably secretion and absorption. 5. Only limited information is available on preganglionic neurones projecting to prevertebral ganglia. Neurones regulating blood vessels are probably located in the intermediolateral cell column, and non-vascular visceral preganglionic neurones are situated medial to this cell column in the intermediate zone of the spinal cord. Vascular (vasoconstrictor) neurones exhibit a reflex pattern which is largely dependent on the brain stem. Spinal cord transection rostral to the sympathetic outflow causes an immediate abolition of basal and reflex activity in these neurones.(ABSTRACT TRUNCATED AT 400 WORDS)     

Intrahepatic and portal venous gas detected by ultrasonography.

During a 3-year period, sonographic evidence of portal venous gas (PVG) was found in 11 patients. Of these, 10 patients were examined for clinically suspected necrotizing enterocolitis (NEC). In the 11th patient, suffering from nephroblastoma, PVG was detected by routine sonography. Radiographic examination, performed in nine of 11 patients did not show any PVG. Intestinal pneumatosis was radiographically identifiable in only four of these children, whereas eight of 11 patients with sonographically detectable PVG also had sonographic evidence of intramural gas. Follow-up examinations in five patients showed cessation of PVG soon after onset of adequate therapy, indicating that ultrasonography is also a reliable method for monitoring NEC. Sonographic evidence of PVG, however, may be limited to the time before onset of therapy.     

Regulation of GH secretagogue receptor gene expression in the rat nodose ganglion

It has been shown that the ghrelin receptor, GH secretagogue receptor (GHS-R), is synthesized in neurons of the nodose ganglion and then transmitted to axon terminals, where it binds to ghrelin. The orexigenic signal of ghrelin secreted from the stomach is transmitted to the brain via the vagal afferent nerve. To explore the regulation of GHS-R synthesis in the nodose ganglion, we examined whether or not GHS-R type a mRNA expression shows circadian rhythm, and is affected by starvation, vagotomy, or i.v. administration of gastrointestinal peptides. Nodose ganglion GHS-R mRNA levels showed a diurnal rhythm, being high during periods of light and low during darkness. Although starvation tended to increase the level of GHS-R mRNA, a more significant increase was observed upon re-feeding. Vagotomy decreased the level of GHS-R mRNA significantly in comparison with animals that underwent a sham procedure. Cholecystokinin and gastrin increased the level of GHS-R mRNA after 2 h, but after 4 h, the level decreased. These results suggest that GHS-R synthesis in the nodose ganglion is regulated centrally and peripherally by neuronal and humoral information, and that these dynamic changes of GHS-R mRNA expression may be involved in the regulation of feeding by ghrelin.