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The renal afferent pathways in the rat: a pseudorabies virus study.

Retrograde tract tracing studies have indicated that dorsal root ganglion cells from T8 to L2 innervate the rat's left kidney. Electrophysiology studies have indicated that putative second-order sympathetic afferents are found in the dorsal horn at spinal segments T10 to L1 in laminae V-VII. Here, the spread of pseudorabies virus through renal sensory pathways was examined following 2-5 days post-infection (PI) and the virus was located immunocytochemically using a rabbit polyclonal antibody. Two days PI, dorsal root ganglion neurons (first-order sympathetic afferents) were infected with PRV. An average of 1.2, 0.8, 2.1 and 4.4% of the infected dorsal root ganglion neurons were contralateral to the injected kidney at spinal segments T10, T11, T12 and T13, respectively. Four days PI, infected neurons were detected within laminae I and II of the dorsal horn of the caudal thoracic and upper lumbar spinal cord segments. The labeling patterns in the spinal cord are consistent with previous work indicating the location of renal sympathetic sensory pathways. The nodose ganglia were labeled starting 4 days PI, suggesting the involvement of parasympathetic sensory pathways. Five days PI, infected neurons were found in the nucleus tractus solitarius. In the present study, it was unclear whether the infected neurons in the nucleus tractus solitarius are part of sympathetic or parasympathetic afferent pathways or represent a convergence of sensory information. Renal denervation prevented the spread of the virus into the dorsal root ganglia and spinal cord. Sectioning the dorsal roots from T10-L3 blocked viral spread into the spinal cord dorsal horn, but did not prevent infection of neurons in dorsal root ganglion nor did it prevent infection of putative preganglionic neurons in the intermediolateral cell column. The present results indicated that renal afferent pathways can be identified after pseudorabies virus infection of the kidney. Our results suggest that renal afferents travel in sympathetic and parasympathetic nerves and that this information may converge at the NTS.

Animals↗

The role of bladder afferent pathways in bladder hyperactivity induced by the intravesical administration of nerve growth factor.

PURPOSE: Interstitial cystitis, a chronic disease of the bladder, is characterized by urinary frequency, urgency and suprapubic pain. Nerve growth factor is a substance that may sensitize afferent nerves and induce bladder hyperactivity. It is often increased in the urine of patients with interstitial cystitis. We evaluated the role of Adelta and C fiber afferents in the type of bladder hyperactivity induced by the intravesical administration of nerve growth factor. MATERIALS AND METHODS: A total of 22 Wistar and 8 Sprague-Dawley adult female rats were anesthetized with 1.2 gm/kg urethane given subcutaneously. A transurethral catheter was inserted into the bladder. Some animals were pretreated with 125 mg/kg capsaicin injected subcutaneously 4 days before nerve growth factor administration. Cystometry was performed by slowly filling the bladder at a rate of 0.04 ml per minute for 15 minutes with a volume of up to 0.6 ml. Parameters measured included volume threshold and pressure threshold for inducing the micturition reflex, compliance, bladder contraction amplitude, number of contractions and the inter-contraction interval. Nerve growth factor (0.5 ml of 20 microg/ml in 10% dimethyl sulfoxide) or a vehicle solution (0.5 ml of 10% dimethyl sulfoxide) was infused into the bladder through a transurethral catheter and retained for 1 hour. RESULTS: In Wistar rats nerve growth factor increased the mean number of contractions by 111% versus controls (5.7 versus 2.7, p <0.05), and decreased the mean volume threshold by 41% (0.244 versus 0.412 ml, p <0.05). This effect of nerve growth factor was not detected in Sprague-Dawley rats. Capsaicin pretreatment increased the volume threshold by 59% but did not change nerve growth factor induced bladder hyperactivity. CONCLUSIONS: The intravesical application of nerve growth factor acutely induced bladder hyperactivity in Wistar but not in Sprague-Dawley rats. Because the C fiber afferent neurotoxin capsaicin did not change the effect of nerve growth factor, we believe that Adelta afferent neurons have a major role in nerve growth factor induced bladder hyperactivity.

Administration, Intravesical↗

[The role of vestibular and proprioceptive afferent pathways in the reaction to pushing (author's transl)].

The reaction to pushing was studied in 6 normal subjects and 3 patients with bilateral peripheral vestibular lesions. The reaction to pushing was tested on the anterior tibial and soleus, by modifying the proprioceptive afferent impulses. The respective parts of the vestibular, proprioceptive, visual components, and of a sudden, start are analyzed; the afferent impulses obtain information from the initial posture and modulate the relative importance of these different factors at a supra-segmentary level.

Afferent Pathways↗

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

The effects of endotoxin on gastric emptying of a solid nutrient meal and the neural mechanisms involved in such a response were investigated in conscious rats. The intraperitoneal (i.p.) administration of E. coli endotoxin (40 microg/kg) significantly reduced the 4-h rate of gastric emptying of a standard solid nutrient meal. Ablation of primary afferent neurons by systemic administration of high doses of capsaicin (20+30+50 mg/kg s.c.) to adult rats did not modify the rate of gastric emptying in control animals but prevented the delay in gastric transit induced by endotoxin. Local application of capsaicin to the vagus nerve rather than application of capsaicin to the celiac ganglion significantly repressed endotoxin-induced delay in gastric emptying. Neither treatment modified the rate of gastric emptying in vehicle-treated animals. Blockade of CGRP receptors (CGRP 8-37, 100 microg/kg i.v.) did not alter gastric emptying in control animals but significantly prevented endotoxin-induced inhibition of gastric emptying. In contrast, a tachykinin receptor antagonist ([D-Pro2, D-Trp7.9]-substance P, 2 mg/kg i.p.) significantly reduced the rate of gastric emptying in control animals and did not modify the inhibitory effects of endotoxin. Adrenergic blockade with phentolamine (3 mg/kg i.p.) +/- propranolol (5 mg/kg i.p.) or muscarinic antagonism with atropine (0.1 mg/kg i.p.) failed to reverse the delay in gastric emptying induced by endotoxin. These observations indicate that endotoxin-induced delay in gastric emptying of a solid nutrient meal is mediated by capsaicin-sensitive afferent neurons.

Adrenergic alpha-Antagonists↗

Afferent pathways for cardiac-somatic motor reflexes in rats.

The present study used a rat model in which algogenic chemicals were infused into the pericardial sac to evoke spasmlike contractions in paraspinal muscles. The following techniques were used to study the roles of sympathetic (SCA) and vagal cardiac afferents (VCA) in electromyographic (EMG) responses to pericardial algogenic chemicals: chemical stimulation, electrical stimulation, and nerve transection. Activation with bradykinin (n = 46) produced a significantly higher peak response than infusion of an algogenic mixture (n = 53) containing chemicals that also activate VCA. Electrical stimulation of SCA produced bilateral EMG activities (7 of 7). Electrical stimulation of VCA did not evoke EMG activity but inhibited the chemically evoked EMG response (12 of 12). The chemically evoked response was decreased after transection of the left sympathetic chain (n = 22) and was increased after bilateral vagotomy (n = 19). These results suggest an excitatory and inhibitory role for SCA and VCA, respectively. Therefore, in addition to spinothalamic convergence of somatic and visceral afferents, activation of SCA to generate spasmlike muscle contractions could account in part for anginal pain, and VCA activation could attenuate this effect.

Afferent Pathways↗

[Afferent pathways arising from the lower urinary tract. Physiology, pathophysiology, and clinical implications].

Voluntary control of bladder function is mainly influenced by sensations arising from the lower urinary tract. Conscious perception of these sensations is imperative for appropriate urine storage and voiding at a socially accepted time and place and depends on the integrity of the afferent axis urothelium -- peripheral nerves -- spinal cord -- pons -- mesencephalon -- sensory cortex. This review considers the current knowledge about normal and impaired sensations arising from the bladder and the sphincter and addresses their clinical significance.

Afferent Pathways↗

A critical review of the afferent pathways and the potential chemical mediators involved in cardiac pain.

There is considerable evidence that on the anterior surface of the heart (which is usually supplied by the left anterior descending and the proximal part of the left circumflex coronary arteries), sympathetic efferent reflexes characterized by tachycardia and/or hypertension predominate following experimental or pathological perturbations. These cardiovascular reflexes are accompanied by an increase in presumed nociceptive afferent traffic and, in pathological condition, by pain. In these experiments, there is generally no effect of vagotomy on afferent nerve traffic, and lower cervical and upper thoracic sympathectomies help provide relief from angina. On the other hand, experimental or pathological perturbations involving the inferior-posterior surface of the heart (supplied by the right and distal parts of the left circumflex coronary arteries), are characterized by vagal efferent reflexes, resulting in bradycardia and/or hypotension. These reflexes are accompanied by an increase in vagal afferent nerve traffic and, in pathological conditions, by pain. In these experiments, vagotomy generally abolishes such cardiovascular reflexes, and lower cervical and upper thoracic sympathectomies are not effective in the relief from angina. Although cardiac sympathetic afferents are unquestionably involved in the central transmission of nociceptive information from the heart, it is also likely that there is a contributing role from the vagus in cardiac pain. It is important experimentally to understand the natural stimulus that gives rise to angina. In the clinical situation, a decrease in coronary blood flow or an increase in the metabolic demands of the myocardium due to increased work are obvious precipitating factors which lead to myocardial ischemia. In the experimental situation, occlusion of the coronary arteries is often used as a stimulus which mimics myocardial ischemia. As people who frequently experience angina have varying degrees of coronary artery disease, it is difficult to accept that the state of the coronary arteries of the normal experimental animal bear any resemblance to the state of the coronary arteries under pathological conditions. That is, the gain of homeostatic reflexes, the basal concentrations of neuroactive substances in the plasma, the myocardium and the afferent terminals, the excitability of the afferents, access of chemical mediators (e.g. bradykinin, 5-HT, adenosine, histamine, prostaglandins, potassium, lactate), to afferents, and the overall function of the animal are all significantly different. We have no idea how control mechanisms have been altered in the person with severe coronary artery disease compared to the normal patient or the "normal" experimental animal.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

Morphological evidence for the activation of descending modulatory control by nociceptive afferent pathways: an immunocytochemical study.

Immunocytochemical technique was used to compare the content of substance P (SP), Met-enkephalin (Met-Enk) and neurotensin (NT) on two sides of the lumbar dorsal horn of rats in which the unilateral dorsolateral funiculus was transected while formalin (0.2 ml, 5%) was injected equally into two hindpaws. The results showed that the SP-like immunoreactivity (SP-LI) and Met-Enk-LI were significantly higher and the NT-LI was significantly lower in the superficial laminae of dorsal horn on the side ipsilateral to the intact DLF than that on the opposite side, implying that peripheral noxious inputs can activate the supraspinal descending inhibitory systems which in turn modulate the transmission of noxious message at the spinal level by changing the activities of related peptidergic neurons.

Afferent Pathways↗

Intestinal lipid inhibits gastric emptying via CCK and a vagal capsaicin-sensitive afferent pathway in rats.

The mechanism by which lipid in the duodenum inhibits gastric emptying was investigated in awake rats fitted with chronic gastric and duodenal cannulas. Perfusion of the duodenum with lipid (Intralipid, 5 and 10%; total amount 50 and 100 mg) caused a significant inhibition (26 and 78%, respectively) of gastric emptying of a nonnutrient liquid (0.9% saline). Functional ablation of the capsaicin-sensitive vagal, but not the spinal, sensory innervation to the upper gastrointestinal tract significantly attenuated by 57% lipid-induced inhibition of gastric emptying. In intact rats, administration of a specific cholecystokinin (CCK)-A receptor antagonist, devazepide, significantly attenuated by 66% the response to lipid. Administration of devazepide in perivagal capsaicin-treated rats did not further reduce the response to lipid. These results suggest that lipid in the duodenum inhibits gastric emptying via a mechanism involving an action of CCK at type A receptors and capsaicin-sensitive vagal afferents.

Afferent Pathways↗

Nitric oxide synthase in the glossopharyngeal and vagal afferent pathway of a teleost, Takifugu niphobles. The branchial vascular innervation.

To examine the presence of nitric oxide synthase (NOS) in the sensory system of the glossopharyngeal and vagus nerves of teleosts, nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) activity and immunoreactivity for NOS were examined in the puffer fish Takifugu niphobles. The nitrergic sensory neurons were located in the ganglia of both the glossopharyngeal and the vagal nerves. In the vagal ganglion, positive neurons were found in the subpopulations for the branchial rami and the coelomic visceral ramus, but not for the posterior ramus or the lateral line ramus. In the medulla, nitrergic afferent terminals were found in the glossopharyngeal lobe, the vagal lobe, and the commissural nucleus. In the gill structure, the nitrergic nerve fibers were seen in the nerve bundles running along the efferent branchial artery of all three gill arches. These fibers appeared to terminate in the proximal portion of the efferent filament arteries of three gill arches. On the other hand, autonomic neurons innervating the gill arches were unstained. These results suggest that nitrergic sensory neurons in the glossopharyngeal and vagal ganglia project their peripheral processes through the branchial rami to a specific portion of the branchial arteries, and they might play a role in baroreception of this fish. A possible role for nitric oxide (NO) in baroreception is also discussed.

Afferent Pathways↗

Intracortical spread of neuronal activities induced by stimulation of recurrent and thalamic afferent pathways compared with epicortical activation.

In the encéphale isolé cat preparation the cerebral peduncle (CP) and the nucleus ventralis lateralis (VL) of the thalamus were stimulated. Short-latency responses recorded from precruciate cortical neurons consisted of excitatory (EPSP) and inhibitory postsynaptic potentials (IPSP). Laminar distributions of these responses and their latencies wee viewed as the spatiotemporal pattern of spread of excitation and inhibition within the cortex in comparison with those obtained by epicortical stimulation (EPICS). In contrast with activities by EPICS spreading downwards from superficial to deep layers, CP recurrent activities spread upwards from deep to middle or superficial layers, and those by VL afferents spread from middle to both superficial and deep layers bidirectionally. These three intracortical routes shared common cell assemblies in that they received convergent EPSPs or IPSPs to various extents from different inputs. The routes for EPICS and VL inputs were overlapped particularly with abundant supply of convergence in spite of their functional difference. Relevant potentiality of the cerebral network in forming plural patterns was discussed.

Afferent Pathways↗

[Restoration of instrumental movements in cats after section of spinal cord afferent pathways].

Instrumental fore-leg movements (pedal pressing) were studied in the course of recovery of motor functions after section of the posterior columns and the spino-cervical tract at the cervical level. Recovery of supporting-locomotor functions reached a high level. Instrumental reactions connected with inborn forms of motor activity (running etc.) were being restored parallel to the locomotion restoration. Complex instrumental movements were restored slower and didn't reach a high degree of accuracy. A more simple instrumental movement (pressing on the open pedal) had a more rapid and more complete recovery. It is concluded that the possibilities of substitution of different channels, transmitting afferent somatic impulses to the sensorimotor cortex, are very limited for elaborated instrumental movements.

Afferent Pathways↗