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PubMed1990

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↗
PubMed2001

GABA(B) receptors on vagal afferent pathways: peripheral and central inhibition.

To investigate GABA(B) receptors along vagal afferent pathways, we recorded from vagal afferents, medullary neurons, and vagal efferents in ferrets. Baclofen (7-14 micromol/kg i.v.) reduced gastric tension receptor and nucleus tractus solitarii neuronal responses to gastric distension but not gastroduodenal mucosal receptor responses to cholecystokinin (CCK). GABA(B) antagonists CGP-35348 or CGP-62349 reversed effects of baclofen. Vagal efferents showed excitatory and inhibitory responses to distension and CCK. Baclofen (3 nmol i.c.v. or 7-14 micromol/kg i.v.) reduced both distension response types but reduced only inhibitory responses to CCK. CGP-35348 (100 nmol i.c.v. or 100 micromol/kg i.v.) reversed baclofen's effect on distension responses, but inhibitory responses to CCK remained attenuated. They were, however, reversed by CGP-62349 (0.4 nmol i.c.v.). In conclusion, GABA(B) receptors inhibit mechanosensitivity, not chemosensitivity, of vagal afferents peripherally. Mechanosensory input to brain stem neurons is also reduced centrally by GABA(B) receptors, but excitatory chemosensory input is unaffected. Inhibitory mechano- and chemosensory inputs to brain stem neurons (via inhibitory interneurons) are both reduced, but the pathway taken by chemosensory input involves GABA(B) receptors that are insensitive to CGP-35348.

Afferent Pathways↗
PubMed1993

Secretin inhibits gastric emptying in rats via a capsaicin-sensitive vagal afferent pathway.

In awake rats, fitted with chronic gastric fistulas, secretin (30 and 300 pmol intraperitoneal, i.p.) inhibited gastric emptying of a non-nutrient liquid by 16% (NS) and 38% (P < 0.01) respectively. Functional ablation of vagal, but not spinal, capsaicin-sensitive afferents reversed the action of secretin by 61%. Inhibition of gastric emptying induced by cholecystokinin (CCK) (30 pmol i.p.) was reversed by around 50% by ablation of either the vagal or spinal capsaicin-sensitive afferent pathway. These results suggest that hormones released after a meal can inhibit gastric emptying via activation of visceral afferent pathways.

Afferent Pathways↗
PubMed1980

Afferent pathways of reflex hypotension and bradycardia during coronary occlusion.

Neural afferent pathways mediating reflex hypotension and bradycardia during coronary occlusion (CO) were determined mainly on the right side in anesthetized cats. Brief occlusion of the left anterior descending (LAD) or circumflex coronary artery (Cx) reuslted in significant hypotension and bradycardia, both of which could be attenuated by bilateral (BVB), unilateral right (RVB), or left vagal cold blockade (LVB) in the nec. The degree of attenuation in the responses was greater as follows: BVB greater than RVB greater than LVB for LAD occlusion, and BVB greater than RBV = LBV for Cx occlusion. Randomized section of cardiac nerves, i.e., the pericoronary nerve, vagal cardiac nerve trunk, and caudal vagal cardiac nerves on the right side produced significant attenuations in the circulatory responses to CO. These results indicate that vagal afferent activity transmitted via these cardiac nerves plays an important role in mediating the reflex responses to CO. This conclusion was further substantiated by electrical stimulation of afferent fibers in thee nerves or by recording increased afferent spontaneous activity form them during CO.

Afferent Pathways↗
PubMed1987

Neuropeptides in pelvic afferent pathways.

Neurochemical and pharmacological experiments have raised the possibility that several neuropeptides including, vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine amide (PHI), substance P, calcitonin gene-related peptide (CGRP), neurokinin A, cholecystokinin (CCK) and opioid peptides may be transmitters in afferent pathways to the pelvic viscera. These substances are widely distributed in: 1) nerve fibers in the pelvic organs, 2) visceral afferent neurons in the lumbosacral dorsal root ganglia and 3) at sites of afferent termination in the spinal cord. Double staining immunocytochemical techniques have shown that more than one peptide can be localized in individual visceral afferent neurons and that neuronal excitatory (VIP, substance P, CCK) and inhibitory peptides (leucine enkephalin) can coexist in the same afferent cell. Studies with the neurotoxin, capsaicin, indicate that peptidergic afferent pathways are involved in the initiation of central autonomic reflexes as well as peripheral axon reflexes which modulate smooth muscle activity, facilitate transmission in automatic ganglia and trigger local inflammatory responses.

Afferent Pathways↗
PubMed1987

In search of afferent pathways of a cardiogenic hypertensive chemoreflex.

Injection of serotonin (5-HT) into the left atrium or ventricle activates a hypertensive chemoreflex. The primary purpose of our study was to determine the afferent pathway(s) that mediates this response. A secondary goal was to localize the receptive sites of this reflex. We measured changes in arterial pressure, reflex vascular responses in skeletal muscle and paw, and changes in renal nerve traffic that occurred after the left atrial or left ventricular injection of 5-HT. Injection of 5-HT (100 to 600 micrograms) into left atrium or ventricle produced large reflex increases in vascular resistance and sympathetic outflow. These responses were not reduced after bilateral cervical vagotomy. In separate experiments, increases in renal nerve traffic with left ventricular injection of 5-HT were assessed before and after cardiac sympathetic deafferentation. Interruption of cardiac sympathetic afferent pathways did not significantly attenuate increases in renal nerve activity with 5-HT. Injection of 5-HT (300 micrograms) into the aortic root produced large increases in arterial pressure but this was not observed after injections into the vertebral or common carotid arteries or descending aorta. Injection of 5-HT (100 micrograms) into the left main coronary artery (perfused via a Gregg cannula from an external reservoir) resulted in a depressor reflex (Bezold-Jarisch). In contrast, injection of 5-HT (200 micrograms) into the left ventricle when the drug was prevented from reaching the left coronary artery produced a large pressor response.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1983

Functional elimination of afferent pathways and decreased safety factor during postembryonic development of cockroach giant interneurons.

The giant interneurons (GIN) from the cockroach CNS undergo two major physiological changes during the postembryonic developmental period: (A) a marked decrease in the number of afferent pathways innervating the GIN at the metathoracic ganglion (Ts); and (B) a gradual decrease in the safety factor for impulse propagation along the intraganglionic segment in T3. In 100% of the experiments (n greater than 100) performed on GIN from early developmental stages, spontaneous postsynaptic potentials (SPSPs) were recorded; in adults, on the other hand. SPSPs have been recorded in only 34% of the experiments (n = 74). Evoked synaptic potentials can be elicited in nymphal stages by stimulation of 8 nerves of T3, the contralateral connectives, ipsi- and contralateral nerve roots 2, 3, 5, and by stimulation of adjacent GINs. In adult, PSPs can be evoked by stimulation of adjacent GINs, and contralateral thoracic connectives, but not from nerves 2, 3 and 5. The functional disappearance of synaptic inputs to the GINs does not reflect a general phenomenon of reduction in synaptic transmission efficacy. In previous studies it was demonstrated that high frequency stimulation of adult GIN leads to blockage of impulse propagation in T3. In nymphal stages, the safety factor for propagation of impulses along T3 is higher. The reduction in safety factor appears gradually during the postembryonic developmental period. From analysis of the mechanisms underlying the elimination of functional afferent pathways and the appearance of low safety factor (see consecutive paper by Yarom and Spira) it is concluded that the functional elimination of afferents is a consequence of decreased transmission efficacy, while the appearance of low safety regions for impulse propagation is a consequence of morphological changes of the GIN segment within ganglion T3.

Afferent Pathways↗
PubMed2003

Afferent pathways and responses of T3-T4 spinal neurons to cervical and thoracic esophageal distensions in rats.

The purposes of this study were to (1) compare responses of T(3)-T(4) spinal neurons to thoracic and cervical esophageal distension (TED, CED) and (2) determine afferent pathways for esophageal input to these neurons. Extracellular potentials of single superficial and deeper T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Graded TED or CED was produced by water inflation (0.1-0.5 ml) of a latex balloon. TED changed activity of 121/432 (28%) neurons (114 were excited); CED activated 69/269 (26%) neurons (56 were excited). Of 151 neurons that were tested for responses to both TED and CED, 40 (26%) neurons responded to both TED and CED. Mean duration of excitatory responses in convergent neurons to TED was significantly longer than the duration of responses to CED (31.4+/-2.8 vs. 25.4+/-1.0 s, n=34, P<0.05). A total of 105 out of 121 (87%) and 66 out of 69 (96%) neurons responsive to TED and CED had somatic fields. Spinal transection at rostral C(1) and at C(7)-C(8) indicated that excitatory responses to TED resulted from activation of afferent input that entered thoracic spinal segments; whereas, excitatory responses to CED resulted from afferent inputs entering cervical or thoracic spinal segments. These data showed that the upper thoracic spinal cord received sensory information from the esophagus through cervical and/or thoracic spinal visceral afferent pathways.

Afferent Pathways↗
PubMed2001

Responses and afferent pathways of superficial and deeper c(1)-c(2) spinal cells to intrapericardial algogenic chemicals in rats.

Electrical stimulation of vagal afferents or cardiopulmonary sympathetic afferent fibers excites C(1)--C(2) spinal neurons. The purposes of this study were to compare the responses of superficial (depth <0.35 mm) and deeper C(1)--C(2) spinal neurons to noxious chemical stimulation of cardiac afferents and determine the relative contribution of vagal and sympathetic afferent pathways for transmission of noxious cardiac afferent input to C(1)--C(2) neurons. Extracellular potentials of single C(1)--C(2) neurons were recorded in pentobarbital anesthetized and paralyzed male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals (0.2 ml) that contained adenosine (10(-3) M), bradykinin, histamine, serotonin, and prostaglandin E(2) (10(-5) M each). Intrapericardial chemicals changed the activity of 20/106 (19%) C(1)--C(2) spinal neurons in the superficial laminae, whereas 76/147 (52%) deeper neurons responded to cardiac noxious input (P < 0.01). Of 96 neurons responsive to cardiac inputs, 48 (50%) were excited (E), 41 (43%) were inhibited (I), and 7 were excited/inhibited (E-I) by intrapericardial chemicals. E or I neurons responsive to intrapericardial chemicals were subdivided into two groups: short-lasting (SL) and long-lasting (LL) response patterns. In superficial gray matter, excitatory responses to cardiac inputs were more likely to be LL-E than SL-E neurons. Mechanical stimulation of the somatic field from the head, neck, and shoulder areas excited 85 of 95 (89%) C(1)--C(2) spinal neurons that responded to intrapericardial chemicals; 31 neurons were classified as wide dynamic range, 49 were high threshold, 5 responded only to joint movement, and no neuron was classified as low threshold. For superficial neurons, 53% had small somatic fields and 21% had bilateral fields. In contrast, 31% of the deeper neurons had small somatic fields and 46% had bilateral fields. Ipsilateral cervical vagotomy interrupted cardiac noxious input to 8/30 (6 E, 2 I) neurons; sequential transection of the contralateral cervical vagus nerve (bilateral vagotomy) eliminated the responses to intrapericardial chemicals in 4/22 (3 E, 1 I) neurons. Spinal transection at C(6)--C(7) segments to interrupt effects of sympathetic afferent input abolished responses to cardiac input in 10/10 (7 E, 3 I) neurons that still responded after bilateral vagotomy. Results of this study support the concept that C(1)-C(2) superficial and deeper spinal neurons play a role in integrating cardiac noxious inputs that travel in both the cervical vagal and/or thoracic sympathetic afferent nerves.

Afferent Pathways↗
PubMed1986

Identification of neuropeptides in pelvic and pudendal nerve afferent pathways to the sacral spinal cord of the cat.

The distribution of several neuropeptides, including vasoactive intestinal polypeptide (VIP), substance P, somatostatin, leucine enkephalin, methionine enkephalin, and cholecystokinin, in sacral afferent pathways of the cat was examined by immunohistochemical techniques. Certain peptides (substance P, somatostatin, and leucine enkephalin) could be demonstrated in normal dorsal root ganglion cells; however, topical administration or injections of colchicine solution into ganglia 36-56 hours prior to removal markedly increased the number of cells labeled and the intensity of staining. Other peptides (VIP, cholecystokinin, and methionine enkephalin) were only detected in significant numbers of cells following intraganglionic injections of colchicine. The distribution of peptides in dorsal root ganglion cells projecting to the pelvic nerve (visceral) and the pudendal nerve (somatic) was examined by retrograde dye labeling combined with immunohistochemistry. Fluorescent dyes were applied to the cut ends of the nerves 2 weeks prior to removal. A considerably higher percentage of pelvic nerve afferent neurons than pudendal nerve afferent neurons exhibited peptide immunoreactivity; e.g., VIP (42% vs. 10%), cholecystokinin (29% vs. 12%), substance P (24% vs. 21%), leucine enkephalin (30% vs. 24%), and methionine enkephalin (10% vs. 3%). Somatostatin was present in only a small percentage of either type of afferent neuron (0.3-2%). The total percentage of peptide-containing pelvic afferent neurons exceeded 100% (137%), suggesting that more than one peptide is present in some visceral afferent neurons. This has been confirmed in preliminary experiments. The peptide-containing cells were in general less than 40 micron in average diameter; however, a significant percentage of substance P and cholecystokinin neurons ranged from 40 to 60 micron in average diameter. VIP cells had the smallest average diameter (30 micron) whereas somatostatin cells had the largest average diameter (36 micron). Statistical analysis of cell sizes revealed that substance P cells projecting to the pelvic nerve were smaller than substance P cells sending axons into the pudendal nerve. On the other hand, VIP cells in the two afferent pathways were not significantly different in size. Sacral visceral and somatic afferent neurons contain a wide spectrum of neuropeptides, some of which (e.g., VIP and cholecystokinin) seem to be preferentially distributed in the visceral afferent systems.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Experimental colitis in mice and sensitization of converging visceral and somatic afferent pathways.

Chronic pain syndromes affecting different organs often coexist. We hypothesized that sensitization of one afferent pathway may affect converging input from other areas of the body. We induced colitis in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS); control animals were treated with equal volumes of vehicle (50% ethanol) only. Visceromotor responses to graded colorectal distension, cystometrograms, and response thresholds to mechanical and thermal stimulation of both hind paws were determined on days 7 and 14. Inflammation of colon and bladder was assessed with validated histological markers and scores. TNBS caused significant colitis on day 7 that resolved by day 14; there was no evidence of bladder inflammation. There was a significant hypersensitivity to colorectal distension on day 7, which returned to normal on day 14. This was associated with bladder overactivity, as demonstrated by early onset of micturition and more frequent micturition on day 7 after TNBS administration. Colitis also significantly altered responses to mechanical and thermal stimulation of both hind paws on day 7 but not day 14. We conclude that cross talk between afferent visceral and somatic pathways may contribute to the coexistence of pain syndromes.

Afferent Pathways↗
PubMed1977

[Effects of morphine on evoked potential recorded from pain-afferent pathways (author's transl)].

Effects of morphine (1 mg/kg i.v.) were examined on evoked potential of somatosensory afferent pathways elicited by tooth pulp stimulation in cats. Results were as follows: In central gray (CG) of the midbrain which has a triphasic evoked potential with a short latency, morphine decreased the amplitude. In nucl. lateralis posterior(LP) and nucl. medialis dorsalis(MD) of the thalamus, association relay nuclei, which have a late component followed by a fast component with a relatively short latency, morphine decreased the amplitude of the late component but not that of fast component of the evoked potential. In nucl. centralis lateralis(CL) of the thalamus, intralaminar nuclei, and pre-central association area(PCA) of the cortex, which have monophasic and triphasic evoked potentials with a long latency, respectively, morphine markedly decreased the amplitude of both evoked potentials. In nucl. ventralis posteromedialis(VPM) and somatic sensory area I (SI), lemniscal system, which has biphasic and mutiphasic evoked potentials with a short latency, respectively, morphine had no effect on these evoked potentials. As these depressant effects of morphine on evoked potentials were antagonized by naloxone (0.2mg/kg i.v.), a specific morphine action is suggested.

Afferent Pathways↗
PubMed2006

Afferent pathway and neuromodulation of superficial and deeper thoracic spinal neurons receiving noxious pulmonary inputs in rats.

The occurrence of vagally mediated afferent signaling by lung irritants is well known. However, spinal visceral afferent pathways also might be relevant to pulmonary irritation. In the present study, responses and modulation of superficial and deep T3 spinal neurons were examined using inhaled ammonia, and the peripheral afferent fibers were also characterized in part. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. Ammonia vapor (0.5, 1.0, 2.0 ml) was injected into the inspiratory line of the ventilator for 20 s. Inhaled ammonia (IA, 1.0 ml) excited 5/6 neurons and inhibited one spinal neuron recorded in superficial laminae, whereas deeper neurons responded with excitatory (E, n = 20), inhibitory (I, n = 4) or biphasic patterns (6 E-I, 3 I-E). Electrical and chemical stimulation of C1-C2 spinal neurons primarily suppressed T3 neuronal responses to IA. Resiniferatoxin (2 microg/kg, i.v.), which desensitizes afferent fibers containing transient receptor potential vanilloid receptor-1 (TRPV-1), abolished excitatory responses of 8/8 neurons to IA. Bilateral cervical vagotomy did not affect IA responses in 5 superficial neurons while 7 deeper neurons showed variable responses. 82% (32/39) of the spinal neurons responding to IA also received convergent noxious inputs from somatic fields in the chest and back areas. These results suggested that superficial and deeper spinal neuronal activation by inhaled ammonia mainly depended upon pulmonary sympathetic afferent fibers expressing TRPV-1. Additionally, C1-C2 spinal neurons, supraspinal sites and vagal afferents modulated the thoracic spinal neuronal responses to lower airway irritation.

Action Potentials↗
PubMed1984

Afferent pathways for hypoglossal and phrenic responses to changes in upper airway pressure.

Our purpose was to determine the afferent pathways underlying reflexes by which changes in upper airway pressure induced alterations in hypoglossal and phrenic nerve activities. An isolated upper airway was produced in decerebrate, vagotomized, paralyzed and ventilated cats. Efferent activities of the phrenic and hypoglossal nerves were monitored. Hypoglossal activity significantly increased following pressure changes in the upper airway of -4 to -21 cm H2O; phrenic discharge declined in most trials. Similar alterations of neural activities were induced by positive pressures though changes of +14 to +21 cm H2O were required for significant responses. These changes in hypoglossal and phrenic activities were greatly reduced following bilateral sectionings of the superior laryngeal nerves but were augmented after the pharyngeal branches of the glossopharyngeal nerves were sectioned. Additional bilateral destruction of the trigeminal nerves almost entirely eliminated responses to pressure changes. We conclude that upper airway receptors may serve to maintain patency of the upper airways. These receptors may play a crucial role in promoting release from upper airway obstructions, especially in sleep.

Afferent Pathways↗
PubMed1991

Electrical stimulation of visceral afferent pathways in the pelvic nerve increases c-fos in the rat lumbosacral spinal cord.

Electrical stimulation (20-35 Hz, 2-5 V, 1.5 h) of the pelvic nerve in urethane-anesthetized rats increased the expression of c-fos protein-immunoreactivity primarily in neurons in the L6-S1 segments of the spinal cord. The neurons were localized to areas receiving afferent input from the pelvic viscera including the superficial dorsal horn, the dorsal commissure, and lateral laminae V-VII in the region of the sacral parasympathetic nucleus. These experiments indicate that (1) electrical stimulation of abdominal nerves following surgical exposure is a useful method for tracing visceral afferent pathways and (2) afferent information from the pelvic viscera is received by neurons in specific areas of the dorsal horn.

Animals↗
PubMed1983

The effects of spinal cord injury on somatosensory evoked potentials produced by interactions between afferent pathways.

The purpose of the present study was to determine the utility of somatosensory evoked potentials (SEPs) produced by interaction between afferent pathways for spinal cord injury evaluation. Interaction was measured as alterations in SEP configuration compared to controls. Monkeys anesthetized with N2O were used. Stimulus intensities were sufficient to excite all nerve fibers. The conditioning stimulus (CS) was applied to the left peroneal nerve and test stimulus (TS) to the left radial nerve. CS-TS intervals were 100 msec in duration. SEPs were recorded from primary cortical receiving area for the forelimb. Different surgical lesions were made at spinal cord level T3-T4. Amplitudes of TS-produced-SEPs remained unchanged postlesion. CS-produced-SEPs were found to be dependent upon the integrity of anterolateral column pathways. Accentuated interaction was observed following dorsal column ablation. Interaction was slightly enhanced after left hemisection but diminished after right hemisection or central cord lesion. Interaction between spatially separate afferent inputs as measured by SEP alteration was determined to be a sensitive indicator of spinal cord injury.

Afferent Pathways↗