Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Afferent Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1981

[Activation response to photic stimulation in normal cats and after transection of the afferent pathways of the mesencephalic reticular formation].

In chronic experiments on waking unrestrained cats with implanted electrodes the reaction of EEG activation to light stimulation was recorded in two sets of experiments in normal cats and in animals with transsection of brachia colliculi superioris that separated mesencephalic reticular system. The intensity of the activating reaction in the intact cats increased ith a rise in the light stimulus intensity. In the cats with brachia-colliculi superioris transsected there was no definite dependence on the stimuli intensity and the intensity of the activating reaction changed randomly. It is suggested that this irregularity is accounted for by blocking of the excitating afferent flow usually coming to the mesencephalic reticular formation through brachia and colliculi both from the visual pathways (ascending flow) and from the cortex (descending activation regulating flow).

Animals↗
PubMed1976

[Effect of narcotic analgesics on impulse conduction along the afferent pathways of visceral nerves].

Experiments were conducted on chloralose-anesthetized cats. The action of morphine and promedol upon the potentials of the cortical and subcortical structures occurring after the visceral nerve stimulation was studied. Morphine proved to depress the potentials evoked by stimulation of the inferior cardiac and vagus nerves, in the specific, associative and nonspecific structures of the brain; promedol produced an analogous effect. Morphine also inhibited the potentials occurring after the stimulation of the splanchnic nerve in the associative and nonspecific structures; depression of the responses in the specific pathways was less pronounced.

Animals↗
PubMedDate not supplied

Simultaneous anterograde labelling of two afferent pathways to the same target area with Phaseolus vulgaris leucoagglutinin and Phaseolus vulgaris leucoagglutinin conjugated to biotin or dinitrophenol.

Anterograde transport of Phaseolus vulgaris leucoagglutinin (PHA-L) and PHA-L conjugated to either biotin or 2,4-dinitrophenol were used to simultaneously label two populations of axons converging onto the same target area. Using the rat hippocampus as a test system, the septohippocampal and contralateral hilar afferents were labelled with the tracers. Double immunohistochemical procedures and either nickel-enhanced 3,3'-diaminobenzidine (DAB) reaction (blue-black colour) or DAB alone (brown colour) were used to produce contrasting colours for the different tracers in the same section. Both the biotinylated PHA-L and PHA-L conjugated with dinitrophenol were used successfully as anterogradely transported axonal tracers. They produced extensive axonal labelling in the hippocampal formation. Excellent double labelling could be produced with the simultaneous application of PHA-L and biotinylated PHA-L. Biotinylated PHA-L was visualized by a sequence of avidin-biotinylated peroxidase complex (ABC), biotinylated goat antiavidin and ABC again using nickel-enhanced DAB as chromogen yielding a blue-black reaction endproduct. PHA-L alone was detected by the unlabelled antibody enzyme (PAP) method using goat antibodies to PHA-L, and DAB as chromogen for the peroxidase reaction, resulting in brown axons. The combination of biotinylated PHA-L and DNP-conjugated PHA-L gave similar results, although the sensitivity of detection by the latter procedure was inferior to that obtained with the other tracers. These protocols permitted visualization of axons of different origin, together with their terminals, either in a blue-black or brown colour, and also allowed the demonstration of overlapping inputs in strata radiatum and lacunosum moleculare of the hippocampus and stratum moleculare and hilus of the dentate gyrus.

Animals↗
PubMedDate not supplied

[Disorder and recovery of somatic sensitivity in cats with destruction of the afferent pathways of the spinal cord].

Somatic sensitivity was studied in intact cats and in the process of functions recovery after section of the posterior columns of the spinal cord and spino-cervical tracts. The state of somatic sensitivity was estimated by the change in the thresholds of food-procuring conditioned reflexes to electrocutaneous stimulation of the anterior limb. After section of the posterior columns or the spino-cervical tracts at the level of the 2nd cervical segment, the threshold rose. It gradually decreased in parallel to the recovery of motor activity, without reaching the initial level. The section of both tracts (simultaneous or in two stages) resulted in an intensive rise of the threshold which decreased in the course of recovery of disturbed functions. Evidently only partial recovery of somatic sensitivity takes place in the process of compensation of functions following the lesion of specific afferent ways of the spinal cord, and motor activity may be achieved with a consdierable deficit of somatic sensitivity.

Animals↗
PubMed2000

Afferent pathways in cardiovascular adjustments induced by volume expansion in anesthetized rats.

The role of baroreceptors, cardiopulmonary receptors, and renal nerves in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (Pharmacia; 1% body wt, 0.4 ml/min) were studied in urethan-anesthetized rats. In control animals, VE produced a transitory increase in mean arterial pressure (MAP), which peaked at 10 min (17 +/- 4 mmHg) and increases in renal (128 +/- 6 and 169 +/- 19% of baseline at 10 and 40 min, respectively) and hindlimb vascular conductance (143 +/- 6 and 150 +/- 10%). These cardiovascular adjustments to VE were unaffected by bilateral vagotomy. After sinoaortic denervation, the increase in MAP induced by VE was greater than in control rats (30 +/- 4 mmHg). However, renal vasodilation in response to VE was blocked, whereas hindlimb vasodilation was similar to that observed in control rats. After unilateral renal denervation (ipsilateral to flow recording), the initial renal vasodilation was blocked. However, 40 min after VE, a significant renal vasodilation (125 +/- 4%) appeared. The hindlimb vasodilation and MAP responses were unaffected by renal denervation. These results demonstrate that the baroreceptor afferents are an essential component of cardiovascular adjustments to VE, especially in the control of renal vascular conductance. They also suggest that renal vasodilation induced by VE is mediated by neural and hormonal mechanisms.

Anesthesia↗
PubMed1967

An afferent pathway for the selective release of vasopressin in response to carotid occlusion and haemorrhage in the cat.

1. The release of neurohypophysial hormones in response to carotid occlusion and haemorrhage has been studied in anaesthetized cats. Samples of jugular venous blood were extracted with alcohol and the extracts assayed for antidiuretic and milk-ejecting activity.2. The release of vasopressin in response to bilateral occlusion of the common carotid arteries has been confirmed in the cat; this effect was abolished when the sinus nerves were divided.3. Using a new sensitive preparation for the assay of milk-ejecting activity in blood extracts, it has been shown that no oxytocin accompanies the release of vasopressin during carotid occlusion.4. The independent release of vasopressin without oxytocin during haemorrhage has also been confirmed, and the role of the sinus nerves and vagi in this response investigated. Bilateral division of either nerve reduced the response, but the vagus appeared to be of greater importance than the sinus nerve.5. A reflex arc for the selective release of vasopressin has been proposed, of which the fibres of the sinus nerves and vagi form the afferent component and the neurones of the supraoptic nucleus the efferent component.

Animals↗
PubMed1995

Development of calretinin-immunoreactive unipolar brush-like cells and an afferent pathway to the embryonic and early postnatal mouse cerebellum.

In the developing mouse hindbrain, immunoreactivity for calretinin, a calcium-binding protein, was first observed at embryonic day 10, and was localized to neuronal cell bodies in the reticular formation. By embryonic day 12, fibers emanated rostrally from the calretinin-immunoreactive neurons, extended dorsally and then caudally in the uncinate fasciculus to reach the developing cerebellar plate. These fibers crossed the cerebellar midline and were distributed to the contralateral side of the cerebellum. The number and intensity of staining of cell bodies in the reticular formation was reduced in postnatal mice. After postnatal day 1, it was no longer possible to discern the calretinin-immunoreactive fiber bundle in the brainstem, although fibers were still visible at the level of the uncinate fasciculus and in the cerebellum. We also observed intensely calretinin-immunoreactive, smaller cells in the cerebellum (embryonic day 14) and dorsal cochlear nuclei (embryonic day 18), most of which we believe are destined to become the "unipolar brush", (also known as "pale" or "monodendritic") cells observed in the adult mammalian brain. An immature form of these cells exists in the developing mouse cerebellum. Thus, using calretinin antiserum as a marker, an afferent neuronal system was described which projects to the cerebellar primordium. It is suggested that the calretinin-containing hook bundle is an afferent projection which provides a feed-forward neuronal system to the cerebellum which, in turn, projects afferent fibers to the calretinin-containing and other cells of the reticular formation.

Animals↗
PubMed2000

Pathobiology of visceral pain: molecular mechanisms and therapeutic implications. III. Visceral afferent pathways: a source of new therapeutic targets for abdominal pain.

Visceral pain is the major cause of consulting in gastroenterology and the principal symptom of functional bowel disorders. This symptom is often associated with gut hypersensitivity to distension. The use of animal models has recently permitted the identification of some mediators supposed to play a pivotal role in the genesis of visceral hypersensitivity. Serotonin, through different receptor subtypes, as well as kinins and calcitonin gene-related peptide, are known to be involved, but other putative transmitters arise and are new potential targets for the development of efficacious treatments. This themes article addresses both physiological and preclinical issues of interest for the selection of active new drugs in regard to the clinical pharmacology of visceral pain.

Analgesics↗