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Effect of moxibustion stimulation of various skin areas on cortical cerebral blood flow in anesthetized rats.

The effect of moxibustion stimulation of various skin areas (cheek, forepaw, upper arm, chest, back, lower leg, hindpaw and perineum) on cerebral blood flow (CBF) of the parietal cortex was examined in anesthetized rats after eliminating emotional influences. Moxibustion stimulation was performed by burning a moxa cone of about 4 mg weight placed on the shaved skin. CBF of the parietal cortex was measured using a laser Doppler flowmeter. Stimulation of the cheek, forepaw, upper arm and hindpaw produced significant increases in CBF, but stimulation of the other areas did not produce significant responses. Moxibustion stimulation of the forepaw and hindpaw produced an increase in the mean arterial pressure (MAP), while stimulation of the other areas did not. After spinal transection at the 2nd thoracic level, the MAP response to stimulation of the forepaw was abolished, whereas the CBF response to stimulation of the forepaw remained. The CBF response in spinalized rats was not affected by cutting cervical sympathetic and facial parasympathetic nerves, while it was almost abolished by intravenous administration of muscarinic and nicotinic cholinergic blocking agents. The CBF response was abolished by crushing the brachial plexus ipsilateral to the stimulated side. It is suggested that the increase in CBF, independent of MAP and emotional responses, elicited by moxibustion stimulation is a reflex response whose afferent pathway is composed of somatic afferent nerves, and whose efferent pathway involves intracerebral cholinergic nerves. A contribution of endogenous opioids in the present CBF responses was neglected, because naloxone did not influence the CBF responses.

Animals↗

Thoracic cross-over pathways of the rat vagal trunks.

It is very difficult to study the independent contributions of the afferent and efferent pathways of the subdiaphragmatic vagus to physiology and behavior. Total subdiaphragmatic vagotomy can confound the interpretation of experimental results because it destroys both afferent and efferent vagal fibers. One approach to address this problem involves producing a total ablation of afferent (or efferent) vagal fibers while retaining half of the efferent (or afferent) vagal fibers by making a unilateral rhizotomy plus contralateral subdiaphragmatic vagotomy. However, the completeness of this afferent (or efferent) lesion is based on the assumption that there are no cross-over pathways within the thoracic cavity between the vagal trunks of the rat. To directly test for the presence of vagal cross-over pathways in the rat, we recorded the compound action potentials from the ventral and dorsal trunks of the subdiaphragmatic vagus following electrical stimulation of the left or right cervical vagi. C-fiber cross-over pathways comprised an average of 9% of the total nerve responses (range was 0 to 29%, n = 20). Direct application of the anesthetic bupivacaine to the vagus completely blocked the recorded signals. The vagal cross-over pathways were also demonstrated using capsaicin as a stimulus. These results indicate the presence of thoracic cross-over pathways between vagal trunks in the rat and demonstrate that for most animals it is not possible to produce a "complete" ablation of afferent (or efferent) components of the subdiaphragmatic vagus using unilateral rhizotomy combined with contralateral subdiaphragmatic vagotomy.

Action Potentials↗

Afferent and efferent connections of the dorsocentral telencephalon in an electrosensory teleost, Gymnotus carapo.

Biotinylated dextran amine was injected unilaterally into dorsal regions of the telencephalon of the weakly electric fish Gymnotus carapo in order to study the afferent and efferent connections of specific dorsal regions with ventral regions of the telencephalon and with other regions of the central nervous system. Efferent pathways from the dorsolateral area of the telencephalon project ipsilaterally to the anterior hypothalamic nucleus, the ventral thalamus and magnocellular tegmental nucleus, whose axons reach the spinal cord. Anterograde labeling showed that the central division of the dorsal telencephalon sends efferent projections through the lateral forebrain bundle towards the ipsilateral lateral and medial preglomerular nucleus, the pretectal nucleus, the optic tectum and the dorsal torus semicircularis, regions that are all involved in the processing of electrosensory and/or multisensory information. In addition, when biotinylated dextran amine was injected into the dorsal torus semicircularis, retrogradely labeled neurons were observed in the dorsocentral area of the telencephalon. The dorsocentral area is also a target of the extra-telencephalic afferents originating from rostral, lateral and medial regions of preglomerular complex. Within the telencephalon, neurons of many ventral subdivisions project ipsilaterally to the dorsocentral area. The dorsocentral, dorsolateral and dorsomedial areas are connected ipsilaterally and reciprocally. The dorsocentral area is reciprocally connected with its contralateral homologue through the anterior commissure.

Afferent Pathways↗

Centers involved in the autonomic reflex reactions originating from stretching of the atria.

Stretching the atria in anesthetized dogs produces reflex changes in heart rate, and in cardiac and renal sympathetic nerve activity. Anemic decerebration, cord transection at C4-C5, and severance of vagal or sympathetic cardiac nerves was done to identify the pathways and centers essential for these reflexes. Stretching the right atrium produced an aceleration of the heart and a definite increase in sympathetic nerve activity. Left atrial-stretch caused biphasic responses: an initial sympathetic nerve inhibition and slower heartbeat folowed by sympathetic excitation and heart acceleration. The afferents responsible were carried mainly by the vagi; efferent neural control of the heart was mostly sympathetic. The reflex inhibition observed was integrated chiefly at the medullary level, but supramedullary structures contributed to the augmentation in sympathetic activity and heart rate. When central connections between vagal afferent and sympathetic efferent pathways were separated by cord transection, atrial stretch caused a decrease in heart rate due to reflex action through the vagal loop. After the cord was sectioned, we found that some afferent impulses from the atria traveling in sympathetic nerves produced a slight reflex augmentation of sympathetic efferent activity, though insufficient to affect the heart rate. Somatosympathetic reflexes evoked in cardiac and renal sympathetic nerves by stimulation of various somatic afferent pathways were also affected by atrial stretch indicating central nervous system interactions. Reflex responses to right atrial stretch were superimposed on accelerations of myogenic origin.

Action Potentials↗

Abnormal ghrelin and pancreatic polypeptide responses in gastroparesis.

Vagal nerve dysfunction has been implicated in the pathogenesis of diabetic gastroparesis, but its role in idiopathic gastroparesis remains uncertain. The increase in pancreatic polypeptide with sham feeding is often used as a measure of vagal integrity. Ghrelin has been suggested to function as an appetite-stimulating hormone from the gut to the brain acting through vagal afferent pathways. Systemic ghrelin also rises in part due to vagal efferent pathways. Alterations in ghrelin and its effects on appetite could play a role in gastroparesis. In this study we aimed [1] to investigate the presence of vagal nerve dysfunction in patients with idiopathic and diabetic gastroparesis and [2] to determine if alterations in ghrelin concentrations occur in gastroparesis. Normal subjects and patients with diabetic, idiopathic, or postsurgical gastroparesis underwent a sham feeding protocol. Serial blood samples were obtained for plasma ghrelin and pancreatic polypeptide. Sham feeding was characterized by an increase in pancreatic polypeptide and ghrelin in normal controls and patients with idiopathic gastroparesis. The changes in pancreatic polypeptide and ghrelin levels in diabetic and postsurgical gastroparesis were significantly less than those in normal subjects. Vagal nerve dysfunction, as evidenced by an impaired pancreatic polypeptide response with sham feeding, is present in diabetic gastroparesis but not idiopathic gastroparesis. Systemic ghrelin concentrations increased with sham feeding in normal subjects and patients with idiopathic gastroparesis but not in diabetic or postsurgical gastroparesis. Vagal function and regulation of ghrelin levels are impaired in diabetic gastroparesis.

Adult↗

Impaired gastric motor activity after abdominal surgery in rats.

Postoperative ileus (POI) is a transient bowel dysmotility that occurs following abdominal surgery. Several mechanisms have been proposed such as neural reflex and inflammatory changes. We focused on gastric motility after abdominal surgery in rats. To investigate the time course of gastric motility after surgery, gastric motility was continuously recorded before, during and after surgery. After laparotomy, terminal ileum was manipulated for 10 min. Gastric motility was recorded by a strain gauge transducer implanted on the serosal surface of the stomach. To investigate whether peripheral sympathetic nerve is involved in the pathogenesis of POI, effects of guanethidine and celiac ganglionectomy were tested on the postoperative gastric motility. Although isoflurane anaesthesia reduced the gastric motility to 40%, the motility recovered immediately when isoflurane was withdrawn. Intestinal manipulation reduced the postoperative gastric motility for 3-24 h after surgery, compared with preoperative levels. Guanethidine administration and celiac ganglionectomy restored the impaired gastric motility. Feeding increased the gastric motility in each group. It is suggested that the pathogenesis of postoperative gastric ileus induced by intestinal manipulation involves viscero-sympathetic pathways. Intestinal manipulation causes impaired gastric motility via inhibitory sympathetic efferent pathway. Feeding may improve the postoperative gastric motility.

Adrenergic Agents↗

Responses of proximal tubule sodium transporters to acute injury-induced hypertension.

Renal injury-induced by phenol injection activates renal sympathetic afferent pathways, increases norepinephrine release from the posterior hypothalamus, activates renal efferent pathways, and provokes a rapid and persistent hypertension. This study aimed to determine whether phenol injury provoked a redistribution of proximal Na(+) transporters from internal stores to the apical cell surface mediated by sympathetic activation, a response that could contribute to generation or maintenance of hypertension. Anesthetized rats were cannulated for arterial blood pressure tracing and saline infusion and then 50 microl 10% phenol or saline was injected into one renal cortex (n = 7 each). Fifty minutes after injection, kidneys were removed and renal cortex membranes from injected kidneys were fractionated on sorbitol gradients and pooled into three windows (WI-WIII) that contained enriched apical brush border (WI); mixed apical, intermicrovillar cleft and dense apical tubules (WII); and intracellular membranes (WIII). Na(+) transporter distributions were determined by immunoblot and expressed as percentage of total in gradient. Acute phenol injury increased blood pressure 20-30 mmHg and led to redistribution of Na(+)/H(+) exchanger type 3 (NHE3) out of WIII (from 22.79 +/- 4.75 to 10.79 +/- 2.01% of total) to WI (13.07 +/- 1.97 to 27.15 +/- 4.08%), Na(+)-P(i) cotransporter 2 out of WII (68.72 +/- 1.95 to 59.76 +/- 2.21%) into WI (9.5 +/- 1.62 to 18.7 +/- 1.45%), and a similar realignment of dipeptidyl-peptidase IV immunoreactivity and alkaline phosphatase activity to WI. Renal denervation before phenol injection prevented the NHE3 redistribution. By confocal microscopy, NHE3 localized to the brush border after phenol injection. The results indicate that phenol injury provokes redistribution of Na(+) transporters from intermicrovillar cleft/intracellular membrane pools to apical membranes associated with sympathetic nervous system activation, which may contribute to phenol injury-induced hypertension.

Acute Disease↗

Efferent projection from the rostral ventrolateral medulla to the area postrema in rats.

The rostral ventrolateral medulla (RVLM) is a region of the brain primarily involved in cardiovascular control. It receives information from several areas of the brainstem, among which the area postrema (AP) and the nucleus of the solitary tract (NTS). The medial subnuclei of the solitary tract (TS) project towards the RVLM, providing cardiopulmonary information, and the AP serves information about circulatory hormones. Although the efferent pathways are well known, it is not the case for the connections from the RVLM towards the AP and the NTS. The present study was designed to examine the efferent connections from the RVLM onto the dorsal structures of the medulla: quantitatively by means of anatomical techniques, and functionally by means of electrophysiological techniques. Morphologically, Biocytin or Biotinylated dextran amine microinjections into the RVLM were followed by labelling of many fibres running towards the bulbar dorsomedial structures, with some pathways lying in the AP itself, or located in its caudal vicinity. Conversely, when microinjections of Fast Blue (FB) were made into the AP, FB-labelled cells could be observed within the RVLM. Electrophysiologically, single shock stimulation carried on AP allowed identification of axonal fibres issuing from somata located into the cardiovascular neuronal pool in the RVLM. From these results, we can assume: (1) the existence of dense efferent projection from RVLM to aspects of the dorsal vagal complex, including the AP and, among this dense projection, (2) the existence of some fibres terminating in, or crossing through the AP, and identified as conveying baroreceptor-related information, in the rat.

Amidines↗

Morphology of neurons and axon terminals associated with descending and ascending pathways of the lateral forebrain bundle in Rana esculenta.

The cells of origin of afferent and efferent pathways of the lateral forebrain bundle were studied with the aid of the cobalt-filling technique. Ascending afferents originated from the lateral thalamic nucleus, central thalamic nucleus, posterior tuberculum and the cerebellar nucleus. They terminated in the anterior entopeduncular nucleus, amygdala and the striatum. Telencephalic projection neurons, which are related to the lateral forebrain bundle, were located minaly in the ventral striatum and the anterior entopeduncular nucleus, but were not so numerous in the dorsal striatum. Irrespective of their location, most of the neurons projecting axons into the lateral forebrain bundle had piriform or pyramidal perikarya. Long apical dendrites usually arborized in a narrow space, whereas widely arborizing secondary dendrites originated from short dendritic trunks. The other neurons that contributed to the lateral forebrain bundle were fusiform or multipolar cells. Striatal efferents terminated in the pretectal area and in the anterodorsal, anteroventral and posteroventral tegmental nuclei.

Animals↗

Subcortical connections of the superior colliculus in the mustache bat, Pteronotus parnellii.

The mustache bat, Pteronotus parnellii, depends on echolocation to navigate and capture prey. This adaptation is reflected in the large size and elaboration of brainstem auditory structures and in the minimal development of visual structures. The superior colliculus, usually associated with orienting the eyes, is nevertheless large and well developed in Pteronotus. This observation raises the question of whether the superior colliculus in the echolocating bat has evolved to play a major role in auditory rather than visual orientation. The connections of the superior colliculus in Pteronotus were studied with the aid of anterograde and retrograde transport of wheat germ agglutinin conjugated to HRP. These results indicate that the superior colliculus of Pteronotus is composed almost entirely of the layers beneath stratum opticum. The retinal projection is restricted to a very thin zone just beneath the pial surface. Prominent afferent pathways originate in motor structures, particularly the substantia nigra and the deep nuclei of the cerebellum. Sensory input from the auditory system originates in three brainstem nuclei: the inferior colliculus, the anterolateral periolivary nucleus, and the dorsal nuclei of the lateral lemniscus. The projections from these auditory structures terminate mainly in the central tier of the deep layer. The most prominent efferent pathways are those to medial motor structures of the contralateral brainstem via the predorsal bundle and to the ipsilateral midbrain and pontine tegmentum via the lateral efferent bundle. Ascending projections to the diencephalon are mainly to the medial dorsal nucleus and zona incerta. Thus, the superior colliculus in Pteronotus possesses well-developed anatomical connections that could mediate reflexes for orienting its ears, head, or body toward objects detected by echolocation.

Afferent Pathways↗

Horseradish peroxidase labeling of the efferent and afferent pathways of the avian tangential vestibular nucleus.

The efferent and afferent pathways of the chick tangential nucleus were studied by using horseradish peroxidase (HRP: Sigma type VI) to label nerve cell bodies and fibers. Depositions of HRP into the tangential nucleus, as well as into the second cervical level of the spinal cord, show that the axons of tangential neurons on leaving the nucleus form an anteriorly coursing tract that passes through the ventrolateral vestibular nucleus without branching and then to the contralateral medial longitudinal fasciculus (MLF). Within the MLF, the tangential axons course posteriorly, forming collaterals that innervate the abducens nucleus, and then proceed to the cervical spinal cord. This pathway was demonstrated for the axons of the two main neurons, the principal and elongate cells, in 1-day, 1-week, and 7-week-old animals. In addition, we propose the existence of an unidentified, ipsilateral pathway to the spinal cord for the tangential axons, since HRP injections into one side of the spinal cord resulted in the bilateral labeling of tangential neurons. No labeled cells were found in the tangential nucleus following HRP depositions into the uvula, flocculus, pontine reticular formation, nucleus piriformis, nucleus jumeaux, vestibulocerebellar nucleus, retrotangential nucleus, or the dorsomedial part of the medial vestibular nucleus. The tangential nucleus receives afferents from the colossal vestibular fibers (spoon endings), small collaterals of fine vestibular ampullary fibers, flocculus, and high cervical levels of the spinal cord. From our small sample, it appears that the spinal cord fibers form most of the afferent terminals in the tangential nucleus in 1-day, 1-week, and 7-week-old animals.

Afferent Pathways↗

The upper esophageal sphincter in the cat: the role of central innervation assessed by transient vagal blockade.

Studies were performed on four cats to assess the role of extrinsic innervation via the cervical nerve trunks in the control of upper esophageal sphincter function. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks previously isolated in skin loops on each side of the neck. Upper esophageal sphincter pressure was measured using a multilumen oval manometry tube and a rapid pull-through technique. The upper esophageal sphincter response to cervical intraesophageal balloon distention and acid perfusion was assessed. The feline upper esophageal sphincter has a distinct asymmetric pressure profile, whereby anterior pressure greater than posterior pressure greater than left pressure greater than right pressure. Bilateral vagal nerve blockade lowered the mean upper esophageal sphincter pressure from 18.5 +/- 1.5 to 12.0 +/- 2.8 mmHg (1 mmHg = 133.3 Pa) (p less than 0.001), with a significant reduction in pressure in all four quadrants. Intraesophageal balloon distention and acid perfusion both produced a significant increase in upper esophageal sphincter pressure. Bilateral vagal nerve blockade completely abolished the response of the upper esophageal sphincter to balloon distention and acid perfusion. We conclude that normal upper esophageal sphincter tone in the cat is partially mediated by excitatory neural input via the cervical nerve trunks, presumably via the recurrent laryngeal nerves; and cervical intraesophageal balloon distention and acid perfusion produce reflex contraction of the upper esophageal sphincter, which is dependent on neural pathways via the cervical vagal nerve trunks, but the relative contribution of afferent and efferent pathways remains unknown.

Animals↗

Nervous regulation of insulin release by the intestinal vagal glucoreceptors.

In anesthetized cats and rats, it is demonstrated that glucose perfusion of the small intestine produces a rapid increase of insulin secretion (IRI) which precedes glycemia variation. This mechanism involves the autonomic nervous system and originates from intestinal glucoreceptors, the existence of which was recently reported. The nervous pathways are described in this study:(1) the afferent pathway is represented by vagal fibers coming from the intestinal glucoreceptors; (2) the efferent pathway involves both sympathetic fibers (splanchnic nerves) and chiefly parasympathetic fibers (vagal nerves). These results are established after surgical suppression of afferent and efferent vagal fibers, and pharmacological exclusion of parasympathetic or sympathetic fibers. The role of this nervous regulation of insulin secretion is discussed with special reference to other already known mechanisms.

Animals↗

Hind-limb vascular responses in anaesthetized dogs to aortic root injections of veratridine.

In dogs anaesthetized with chloralose we determined the reflex responses of the blood vessels in the vascularly isolated hind limb to injection of veratridine into the aortic root. The presence of a cannula tied in the ascending aorta ensured that responses were due to stimulation of nerves only in the region perfused by the coronary arteries. Injections of veratridine resulted in transient decreases in vascular resistance and in venous resistance in a perfused cutaneous vein. The responses were reduced when carotid perfusion pressure was elevated. The afferent pathway for the reflex lay in the vagus nerves and the efferent pathway to the limb was in the sciatic and femoral nerves, but the vasodilatation was shown to be predominantly non-cholinergic.

Anesthesia, General↗

Acceptable noise level, phoneme recognition in noise, and measures of auditory efferent activity.

Acceptable noise level (ANL) is unrelated to sentence recognition in noise but may be related to phoneme recognition in noise (PRN). Individual differences in efferent activity in medial olivocochlear bundle (MOCB) and acoustic reflex (AR) pathways may account for intersubject variability in ANL and PRN. Monotic and dichotic ANL, monotic PRN, contralateral suppression of transient evoked otoacoustic emissions, and ipsilateral and contralateral acoustic reflex thresholds were measured in 31 adults with normal hearing. Results indicate that monotic ANL and PRN are unrelated. Monotic and dichotic ANL are related, suggesting that nonperipheral factors mediate ANL. Intersubject variability in ANL cannot be accounted for by individual differences in MOCB or AR activation. Intersubject variability in PRN cannot be accounted for by individual differences in MOCB or contralateral AR activation. It may be influenced by the ipsilateral AR pathway. Efferent activity in the contralateral AR arc is correlated with efferent activity in the MOCB.

Adult↗

Efferent tracts and cochlear frequency selectivity.

The cochlear innervation of guinea pigs was sectioned medially in a rostrocaudal direction at the level of the floor of the fourth ventricle, to study the effects of efferent pathways on cochlear microphonic (CM) suppression, the compound action potential (CAP) masking phenomenon, the input-output CAP function, and cochlear frequency selectivity estimated with tuning curves of single auditory nerve fibers. Sectioning reduced CM suppression without having any effect on absolute CM amplitude; it also reduced CAP masking. The input-output CAP function was not changed at intensities below 75 dB, and the single-unit tuning curves recorded before and after nerve sectioning were unaffected. Thus, the crossed efferent tracts (i.e., mainly the medial system) seems to be involved in the masking function itself, rather than one of the mechanisms responsible for high frequency cochlear selectivity.

Acoustic Stimulation↗

Anaesthesia and cardiovascular regulation.

Cardiovascular homeostasis is dependent on the efficient performance of the effector organs, i.e. the vascular smooth muscle and the heart. Besides inherent activity and local control mechanisms, these effector organs are regulated by circulatory control centres within the central nervous system, which in turn receives information from receptors inside and outside the cardiovascular system. All these components of the circulatory systems, i.e. receptors, afferent and efferent pathways, control centres and effector organs, are possible sites for interactions by anaesthetics. Since different anaesthetics have different potencies and special predilections, there are a large variety of interaction patterns, as is discussed in the paper. Another way of evaluating circulatory effects of drugs used in anaesthesia is to analyse how these drugs may modify circulatory reflexes associated with surgery and trauma. For example, pain, hypoxia and/or hypovolaemia may evoke circulatory adjustments which correspond to and are functionally related to, from experimental physiology, well-known reflex patterns such as the somatosympathetic reflex, the chemoreceptor reflex and the baroreceptor reflex. These reflex adjustments are liable to modification by anaesthetics, as exemplified in the paper. Due to the complexity of circulatory control and the varying effects of different anaesthetic agents, it is difficult to draw general conclusions. It can, however, be stated that most general anaesthetics depress cardiovascular reflexes in proportion to the depth of anaesthesia, and that suprabulbar centres are more easily depressed than bulbar ones. Opiates seem to have a specific inhibitory effect on circulatory adjustments induced by noxious stimuli. Transmission in efferent and afferent pathways is liable to modification by local anaesthetics, ganglionic blockers or alpha- and beta-receptor antagonists.

Anesthesia↗

Periaqueductal gray matter input to cardiac-related sympathetic premotor neurons.

The periaqueductal gray matter (PAG) serves as the midbrain link between forebrain emotional processing systems and motor pathways used in the defense reaction. Part of this response depends upon PAG efferent pathways that modulate cardiovascular-related sympathetic outflow systems, including those that regulate the heart. While it is known that the PAG projects to vagal preganglionic neurons, including possibly cardiovagal motoneurons, no information exists on the PAG circuits that may affect sympathetically mediated cardiac functions and, thus, the purpose of this study was to use neuroanatomical methods to identify these pathways. First, viral transneuronal retrograde tracing experiments were performed in which pseudorabies virus (PRV) was injected into the stellate ganglion of rats. After 4 days survival, five PAG regions contained transynaptically infected neurons; these included the dorsomedial, lateral and ventrolateral PAG columns as well as the Edinger-Westphal and precommissural nuclei. Second, the descending efferent PAG projections were studied with the anterograde axonal marker Phaseolus vulgaris leuco-agglutinin (PHA-L) with a particular focus on determining whether the PAG projects to the intermediolateral cell column (IML). Almost no axonal labeling was found throughout the thoracic IML suggesting that the PAG modulates sympathetic functions by indirect pathways involving synaptic relays through sympathetic premotor cell groups, especially those found in the medulla oblongata. This possibility was examined by a double tracing study. PHA-L was first injected into either the lateral or ventrolateral PAG and after 6 days, PRV was injected into the ipsilateral stellate ganglion. After an additional 4 days survival, a double immunohistochemical procedure for co-visualization of PRV and PHA-L was used to identify the sympathetic premotor regions that receive an input from the PAG. The PAG innervated specific groups of sympathetic premotor neurons in the hypothalamus, pons, and medulla as well as providing reciprocal intercolumnar connections within the PAG itself (Jansen et al., Brain Res. 784 (1998) 329-336). The major route terminates in the ventral medulla, especially within the medial region which contains sympathetic premotor neurons lying within the raphe magnus and gigantocellular reticular nucleus, pars alpha. Both serotonergic and non-serotonergic sympathetic premotor neurons in these two regions receive inputs from the PAG. Weak PAG projections to sympathetic premotor neurons were found in the rostral ventrolateral medulla (including to C1 adrenergic neurons), locus coeruleus, A5 cell group, paraventricular and lateral hypothalamic nuclei. In summary, both the lateral and ventrolateral PAG columns appear to be capable of modulating cardiac sympathetic functions via a series of indirect pathways involving sympathetic premotor neurons found in selected sites in the hypothalamus, midbrain, pons, and medulla oblongata, with the major outflow terminating in bulbospinal regions of the rostral ventromedial medulla.

Animals↗