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Results for “sensory function”

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At least 271 records · Page 15Linked to original sources

PubMed1988

The sensory-efferent function of capsaicin-sensitive sensory neurons.

Capsaicin-sensitive sensory neurons convey to the central nervous system signals (chemical and physical) arising from viscera and the skin which activate a variety of visceromotor and neuroendocrine reflexes integrated at various levels (intramurally in peripheral organs, at level of prevertebral ganglia, spinal and supraspinal level). Much evidence is now available that peripheral terminals of certain sensory neurons, widely distributed in skin and viscera have the ability to release, upon adequate stimulation, their transmitter content. In addition to the well-known "axon reflex" arrangement, the capsaicin-sensitive sensory neurons have the ability to release the stored transmitter also from the same terminal which is excited by the environmental stimulus. The efferent function of these sensory neurons is realized through the direct and indirect (i.e. mediated by activation of other cells) effects of released mediators. The action of released transmitters on postjunctional elements covers a wide range of effects which may have a physiological or pathological relevance. Development of drugs capable of controlling the sensory-efferent functions of the capsaicin-sensitive sensory neurons represent a new and very promising area of research for pharmacological treatment of various human diseases.

Animals↗

PubMed1987

The contribution of capsaicin-sensitive innervation to activation of the spinal vesico-vesical reflex in rats: relationship between substance P levels in the urinary bladder and the sensory-efferent function of capsaicin-sensitive sensory neurons.

In acute spinal rats (C2-C3) the transvesical infusion of saline activates a vesico-vesical excitatory reflex (Brain Res., 380 (1986) 83-93). In bladders containing a subthreshold amount of fluid the topical application of capsaicin on the outer surface of the bladder dome activated this spinal reflex and also produced a transient rise in blood pressure and heart rate. The effects of systemic capsaicin desensitization (50 mg/kg s.c. 5 min, 60 days before) on the sensory (activation of the spinal vesico-vesical reflex) and 'efferent' (tetrodotoxin-insensitive capsaicin-induced contraction) functions mediated by the capsaicin-sensitive sensory fibers were correlated to changes in substance P-like immunoreactivity (SP-LI) content of the urinary bladder in adult rats. Blockade of both sensory and efferent functions was observed at a time (60 min from capsaicin administration) when the SP-LI content of the urinary bladder was unaffected. Four days after capsaicin desensitization the SP-LI levels of the bladder are almost depleted indicating that the neuropeptide(s) are entirely stored in sensory structures. At this time the sensory-efferent functions mediated by these fibers are still blocked. At 15-60 days from systemic capsaicin desensitization there was a progressive, time-related recovery of SP-LI levels in the bladder as well as of the sensory-efferent functions. These findings indicate a role of the capsaicin-sensitive innervation of the urinary bladder in activating the spinal vesico-vesical reflex. The present findings suggest that measurement of SP-LI levels in the rat bladder may be a useful biochemical index for monitoring the function(s) of the capsaicin-sensitive, peptidergic sensory neurons.

Animals↗

PubMed1979

Sensory neglect after lesions of substantia nigra or lateral hypothalamus: differential severity and recovery of function.

Sensory neglect was studied in cats after unilateral lesions of: lateral hypothalamus (LH); internal capsule (IC) adjacent to the LH; substantia nigra (SN) or the ventromedial hypothalamus (VMH). Special behavioral tests were employed to yield quantifiable data and also to exclude any confounding due to simple movement deficits. Lesions of SN or IC produced severe and enduring contralateral visual and somesthetic deficits and a facilitation of ipsilateral visual responsiveness. In contrast, LH lesions sparing the adjacent IC produced only weak and transient deficits and VMH lesions had no effects on sensory function. This suggests that lesions of the SN or its forebrain connections are important for producing sensory neglect and that sensory deficits after LH lesions are due to infringement on fibers of passage to or from the SN. Lesions which produced neglect often suppressed the amplitude of flash evoked responses in the ipsilateral caudate nucleus and visual and association cortex. However, these evoked potential effects were transient. There was no effect on the spontaneous EEG and this fails to support the hypothesis of a lack of hemispheric arousal in sensory neglect. The results are discussed in relation to nigrotectal projections and the process of attention. This lesion-behavior model is suggested for studies of recovery of function.

Animals↗

PubMed1997

Preliminary evaluation of a sensory and psychomotor functional test battery for carpal tunnel syndrome: Part 2--Industrial subjects.

This study evaluated the Wisconsin functional sensory and psychomotor test battery for carpal tunnel syndrome (CTS). Subjects were 27 employees recruited from a food processing plant. Both hands of all subjects were examined and categorized by presence or absence of symptoms and nerve conduction study (NCS) findings (Symptom-/NCS-, Symptom+/NCS-, Symptom-/NCS+, and Symptom+/NCS+). Symptom-/NCS- category hands had significantly better performance (15-60%) for most of the functional test battery variables than Symptom+/NCS+ category hands. A significant gap detection threshold difference (32%) was observed between NCS+ and NCS- hands regardless of symptoms, with NCS- having impaired performance. No significant effect of CTS symptoms on performance was observed. Stepwise discriminant analysis was used to select the best variables to differentiate between groups. The ratio of the change in pinch rate with respect to required pinch force differentiated NCS+ from NCS- hands, with a sensitivity of 0.71 and a specificity of 0.68. The same variable had a sensitivity of 0.74 and specificity of 0.83 for distinguishing Symptom-/NCS- hands from all other categories. Pinch rate had a sensitivity of 0.82 and a specificity of 0.81 for separating Symptom+/NCS+ hands from all other categories. Use of both gap detection threshold and the ratio of the change in pinch rate with respect to required pinch force could best differentiate Symptom+/NCS+ from Symptom-/NCS- cases for a sensitivity of 0.91 and specificity of 0.87. Outcomes could not be generalized to a specific work population but demonstrate that the non-invasive test battery may be useful for providing objective measures of deficits associated with CTS symptoms and electrophysiological parameters.

Adult↗

PubMed2006

Considerations in evaluating new treatment alternatives following peripheral nerve injuries: a prospective clinical study of methods used to investigate sensory, motor and functional recovery.

The current problem finding reliable and objective methods for evaluating results after peripheral nerve repair is a challenge when introducing new clinical techniques. The aim of this study was to obtain reference material and to evaluate the applicability of different tests used for clinical assessment after peripheral nerve injuries. Fifteen patients with a history of complete median nerve transsection and repair, and 15 healthy volunteers were included. Each subject was investigated using a battery of conventional and new tests for functional, sensory and motor recovery including questionnaires, clinical evaluations, neurophysiological and physiological findings. The results were statistically analysed and comparisons were made within the patient group and between patients and healthy volunteers using a 'per protocol' and an 'intention to treat' approach. Criteria for success were stipulated in order to be able to judge the usefulness of each method. The results showed that 19 of 34 variables, representing six of 16 methods, were not able to fulfil the criteria and were thus questionable for the evaluations of nerve repair in a clinical trial setting. However, 2pd, sensory recovery according to the non-modified British Medical Research Council, sensory neurography, manual muscle test, electromyography, questionnaires (i.e. DASH and the 4 question form) and performance tests (i.e. AMPS and Sollerman's subtests 4 and 8) did fulfil the criteria defined for being useful.

Action Potentials↗

PubMed2001

Functional regeneration of chronically injured sensory afferents into adult spinal cord after neurotrophin gene therapy.

Lesioned axons within the dorsal roots fail to regenerate through the peripheral nerve transition zone and into the spinal cord. This regenerative failure leads to a persistent loss of sensory function. To induce axonal growth across this barrier, we used recombinant adenovirus to express fibroblast growth factor-2 (FGF2), nerve growth factor (NGF), L1 cell adhesion molecule (L1), or beta-galactosidase (LacZ) within the endogenous glia of the dorsal spinal cord 16 d after injury. Expression of either FGF2 or NGF, but not L1 or LacZ, induced robust axonal regeneration into normal as well as ectopic locations within the dorsal spinal cord. This regeneration led to near-normal recovery of thermal sensory function. Functional recovery and the majority of regenerating axons within the dorsal horn disappeared with recutting of the sensory roots. Injections of adenovirus encoding NGF, but not FGF2, also resulted in extensive sprouting of noninjured sensory axons, which we previously demonstrated could cause hyperalgesia and chronic pain. Thus, neurotrophic factor gene therapy administered as late as 16 d after injury may serve as a useful treatment to elicit recovery after dorsal root avulsion; however, the choice of neurotrophin is important to induce selective regeneration of damaged axons.

Adenoviridae↗

PubMedDate not supplied

Construct overlap in resource theories of memory aging. Commentary.

This article evaluates the conceptual status of working memory, processing speed, executive function and sensory function as mediational constructs to explain memory aging. The main difficulty for these mediational constructs is that they may not be independent. Mediational constructs may overlap with each other or with the dependent variable due to theoretical, substantive or methodological reasons. It is argued that sensory function has an advantage over processing speed, working memory and executive function as a mediational construct because it is non-cognitive. The problem of construct overlap is relevant to both cross-sectional and longitudinal studies. Further research is required to evaluate the relative importance of mediational constructs in theories of memory aging, general intellectual aging and dementia.

Aging↗

PubMedDate not supplied

Mitochondrial DNA deletions parallel age-linked decline in rat sensory nerve function.

In rats, the function of sensory nerves in the hind limb declines significantly with age. Normally aging rats and rats treated neonatally with capsaicin were studied here. Quantification of vascular response and substance P in young (3 months) and old (24 months) rats showed additive effects of age and capsaicin treatment. The levels in dorsal root ganglion of a particular deletion in mitochondrial DNA (mtDNA(4834)) were about 300-fold higher in old compared to young rats. Capsaicin treatment had no significant effect on mtDNA(4834) abundance. Dorsal root ganglia of old (but not young) rats were found to contain a spectrum of multiple deletions. The abundance of mtDNA(4834) in dorsal root ganglia from individual rats correlated strongly with their decline in vascular function, even where vascular responses were systematically depressed due to prior capsaicin treatment. One possibility is that mitochondrial DNA mutations directly lead to functional decline at mitochondrial and tissue levels. Alternatively, loss of mitochondrial DNA integrity and physiological decline may be consequences of the same factor, such as oxidative stress.

Aging↗

PubMed2004

Sensory processing and functional reorganization of sensory transmission under pathological conditions in the spinal dorsal horn.

The superficial dorsal horn, particularly substantia gelatinosa (SG) in the spinal cord, receives inputs from small-diameter primary afferents that predominantly convey noxious sensation. This sensory information via the high-threshold Adelta and C afferents is modified and integrated in SG, and consequently regulates the outputs of projection neurons located in lamina I and laminae IV-V. Recent studies using slice and in vivo patch-clamp recordings indicate that the sensory inputs to SG are functionally reorganized during post-natal development. Even in the mature state, the synaptic connectivity and receptor expression in SG can be altered easily following peripheral tissue damage. In addition, the descending pain inhibitory system to SG is also modified under certain pathological conditions. Considering that the pain system is phylogenetically primitive, it is, therefore, not surprising that the system easily exhibits a plastic change in response to inflammation or nerve damage. Because such plastic changes in the neuronal circuit or receptor expression in SG are now generally accepted to be one of the explanations for the induction of pathological pain, SG is thought to be a primary therapeutic target for chronic pain. We review here recent results demonstrating plastic changes in SG under pathological conditions.

Animals↗

PubMed1995

Recovery of function, peripheral sensitization and sensory neurone activation by novel pathways following axonal injury in Aplysia californica.

Recovery of behavioural and sensory function was examined following unilateral pedal nerve crush in Aplysia californica. Nerve crush that transected all axons connecting the tail to the central nervous system (CNS) eliminated the ipsilateral tail-evoked siphon reflex, whose sensory input travels in the crushed tail nerve (p9). The first reliable signs of recovery of this reflex were observed within 1 week, and most animals displayed tail-evoked siphon responses within 2 weeks. Wide-dynamic-range mechanosensory neurons with somata in the ventrocaudal (VC) cluster of the ipsilateral pleural ganglion exhibited a few receptive fields (RFs) on the tail 3 weeks after unilateral pedal nerve crush, indicating that the RFs had either regenerated or been reconnected to the central somata. These RFs were smaller and sensitized compared with corresponding RFs on the contralateral, uncrushed side. Centrally conducted axon responses of VC sensory neurones to electrical stimulation distal to the nerve crush site did not reappear until at least 10 days after the crush. Because the crush site was much closer to the CNS than to the tail, the failure of axon responses to be restored earlier than the behavioural responses indicates that early stages of reflex recovery are not due to regeneration of VC sensory neurone axons into the tail. Following nerve crush, VC sensory neurones often could be activated by stimulating central connectives or peripheral nerves that do not normally contain the sensory neurone's axons. These results suggest that recovery of behavioral function after nerve injury involves complex mechanisms, including regenerative growth of axotomized VC sensory neurones, sensitization of regenerating RFs and sprouting of VC sensory neurone fibres within the CNS. Furthermore, the rapidity of behavioural recovery indicates that its initial phases are mediated by additional mechanisms, perhaps centripetal regeneration of unidentified sensory neurones having peripheral somata, or transient reconnection of proximal and distal stumps of axotomized VC cells.

Animals↗

PubMed1988

Effects of chronic dietary restriction on sensory-motor function and susceptibility to stressor stimuli in the laboratory rat.

Two sets of experiments describing the effects of chronic undernutrition on sensory-motor function and susceptibility to environmental stressors are described. In the first, Fischer 344 rats between 10 and 12 months of age were placed on an every-other-day feeding regimen. Behavioral tests designed to assess sensory function (auditory and visual thresholds), somato-motor competence (hang time from a horizontal wire, balance on a narrow beam, descent of a wire mesh pole), and sensory-motor integrity (auditory startle) were then conducted every 3 to 6 months. Chronic undernutrition significantly increased life span and increased somato-motor competence but did not affect sensory function or sensory-motor integrity. In the second set of experiments both acute and chronic dietary restriction impaired the ability of young adult Sprague-Dawley rats to effectively thermoregulate in response to a cold environment. Body temperature dropped more rapidly and recovered at a slower rate in the dietarily restricted animals. Fischer 344 rats maintained on a restricted diet for 16 months were similarly impaired. The latter findings suggest that techniques for extending life span based on laboratory animal models may have little relevance to either animals or humans living in their natural habitats where a wide variety of environmental stressors are encountered.

Animals↗

PubMed1984

Behavioral evidence in rats for a peptidergic-noradrenergic interaction in cutaneous sensory and vascular function.

Cutaneous sensory and vascular function was examined following application of capsaicin to the sciatic nerve and systemic injection of guanethidine. Together the two drugs produced a reduction in sensitivity to heat-pain, inflammatory pain (formalin test), tactile stimulation and skin temperature of the foot that exceeded the effects of either drug alone. The inflammation produced by an injection of formalin to the plantar surface of the hind paw was reduced equally by capsaicin or capsaicin + guanethidine. Cold sensitivity and inflammation produced by yeast injection were unaffected by all treatments. The data imply a peripheral interaction between peptidergic and noradrenergic systems with significant functional implications that may be important in the pathology of familial dysautonomia.

Animals↗

PubMed1991

New autonomic and sensory neuropathy with loss of adrenergic sympathetic function and sensory neuropeptides.

A 30-year-old woman with longstanding dizziness was found to have a severe postural fall in blood pressure and a reduced skin axon-reflex flare response. Autonomic tests indicated selective impairment of adrenergic sympathetic function. Plasma noradrenaline, adrenaline, dopamine, and dopamine beta hydroxylase were undetectable. Skin biopsy specimens showed loss of tyrosine hydroxylase and neuropeptide Y (markers of adrenergic sympathetic fibres) and of substance P and calcitonin gene-related peptide (sensory neuropeptides). A sural nerve biopsy specimen showed severe depletion of unmyelinated fibres. The constellation of losses were compatible with nerve growth factor (NGF) deprivation, which was confirmed on assay. This new syndrome may be explained by loss of trophic action of NGF.

Adrenergic Fibers↗

PubMed1991

Autonomic and sensory nerve function in diabetic foot ulceration.

Peripheral sensory and autonomic nerve dysfunction are thought to be crucial factors in the pathogenesis of diabetic foot ulceration. However, their relative importance is not known. In this study we have compared peripheral sensory nerve function and cardiac autonomic reflexes in 51 diabetics with a history of foot ulceration and 480 diabetic control subjects. In the diabetics with ulceration ankle reflexes were absent or impaired and vibration perception threshold reduced in 96.1% and 82.4%, respectively, compared with 40.8% and 25.8%, respectively, in control subjects (P less than 0.001). Cardiac autonomic tests were abnormal more frequently in the diabetics with ulceration and an autonomic score derived from four tests was abnormal in 62.8% of those with ulceration compared with 13.5% of those without ulceration (P less than 0.001). Discriminant analysis of the two groups of diabetes showed that an abnormal autonomic score was the best predictor of foot ulceration in diabetic patients.

Diabetic Neuropathies↗

PubMed1981

Function of sensory input in insect motor systems.

The organization and function of sensory input has been examined in three insect motor systems: locust jumping, cockroach walking, and locust flight. In these three systems sensory input is primarily involved in the production of the normal patterns of motor activity rather than in the compensation for sudden changes in the external environment. At least two general functions for sensory input in the normal patterning of motor activity can be identified: (1) compensation for changes in the peripheral elements of the motor system which occur as a result of use and maturation and (2) regulation of switching from one phase of a movement to another following the attainment of a specific state by peripheral structures. Reflex pathways may exist for compensating for sudden environmental disturbances but these have not yet been clearly demonstrated.

Animals↗

PubMed2005

Strabismus and sensory-motor function of eye muscles.

Paul Bach-y-Rita and coworkers at the Smith-Kettlewell Institute of Visual Science of San Francisco were among the first to record activity in the muscle fibers of the eye muscles in animals. With their newly developed methods, they could describe fast and slow muscle fibers types and present possible patterns of recruitment of the fibers in different eye movements. These studies have been critical for continued animal research on eye muscle fibers and motor units in different species and in animals of different ages. Bach-y-Rita and coworkers also recorded from receptors in the muscles and demonstrated stretch reflexes different from those of skeletal muscles. Further research in animals revealed that it was difficult to delineate the functional role of the muscle receptors in oculomotor control. However, recent studies on sensory functions of human extra ocular muscles have suggested that proprioception participates in space localization, and the functions may differ in normal and strabismic subjects. The eye muscle studies initiated by Bach-y-Rita have enabled analysis of the sensory-motor components of strabismus or squint in greater detail than before.

Animals↗

PubMedDate not supplied

Nicotinic acetylcholine receptors in sensory cortex.

Acetylcholine release in sensory neocortex contributes to higher-order sensory function, in part by activating nicotinic acetylcholine receptors (nAChRs). Molecular studies have revealed a bewildering array of nAChR subtypes and cellular actions; however, there is some consensus emerging about the major nAChR subtypes and their functions in sensory cortex. This review first describes the systems-level effects of activating nAChRs in visual, somatosensory, and auditory cortex, and then describes, as far as possible, the underlying cellular and synaptic mechanisms. A related goal is to examine if sensory cortex can be considered a model system for cortex in general, because the use of sensory stimuli to activate neural circuits physiologically is helpful for understanding mechanisms of systems-level function and plasticity. A final goal is to highlight the emerging role of nAChRs in developing sensory cortex, and the adverse impact of early nicotine exposure on subsequent sensory-cognitive function.

Animals↗

PubMed2004

Experimentally induced ulcers and gastric sensory-motor function in rats.

Prior studies have demonstrated that inflammation can sensitize visceral afferent neurons, contributing to the development of hyperalgesia. We hypothesized that both afferent and efferent pathways are affected, resulting in changes in motor and sensory function. Kissing ulcers (KU) were induced in the distal stomach by injecting 60% acetic acid for 45 s into a clamped area of the stomach. In controls, saline was injected into the stomach. A balloon catheter was surgically placed into the stomach, and electromyographic responses to gastric distension were recorded from the acromiotrapezius muscle at various times after ulcer induction. The accommodation reflex was assessed by slowly infusing saline into the distally occluded stomach. Gastric pressure changes in response to vagal stimulation were measured in anesthetized rats. Contractile function of circular muscle strips was examined in vitro using force-displacement transducers. KU caused gastric hypersensitivity that persisted for at least 14 days. Fluid distension of the stomach led to a rapid pressure increase in KU but not in control animals, consistent with an impaired accommodation reflex. Gastric ulcers enhanced the contractile response to vagal stimulation, whereas the effect of cholinergic stimulation on smooth muscle in vitro was not changed. These data suggest that inflammation directly alters gastric sensory and motor function. Increased activation of afferents will trigger vagovagal reflexes, thereby further changing motility and indirectly activating sensory neurons. Thus afferent and efferent pathways both contribute to the development of dyspeptic symptoms.

Acetic Acid↗