Afferent Signals (afferent + signal)

Distribution by Scientific Domains


Selected Abstracts


Muscle afferent contributions to the cardiovascular response to isometric exercise

EXPERIMENTAL PHYSIOLOGY, Issue 6 2004
James P. Fisher
The cardiovascular response to isometric exercise is governed by both central and peripheral mechanisms. Both metabolic and mechanical stresses on the exercising skeletal muscle produce cardiovascular change, yet it is often overlooked that the afferent signal arising from the muscle can be modified by factors other than exercise intensity. This review discusses research revealing that muscle fibre type, muscle mass and training status are important factors in modifying this peripheral feedback from the active muscles. Studies in both animals and humans have shown that the pressor response resulting from exercise of muscle with a faster contractile character and isomyosin content is greater than that from a muscle of slower contractile character. Athletic groups participating in training programmes that place a high anaerobic load on skeletal muscle groups show attenuated muscle afferent feedback. Similarly, longitudinal studies have shown that specific local muscle training also blunts the pressor response to isometric exercise. Thus it appears that training may decrease the metabolic stimulation of muscle afferents and in some instances chronic exposure to the products of anaerobic metabolism may blunt the sensitivity of the muscle metaboreflex. There may be surprising parallels between the local muscle conditions induced in athletes training for longer sprint events (e.g. 400 m) and by the low-flow conditions in, for example, the muscles of chronic heart failure patients. Whether their similar attenuations in muscle afferent feedback during exercise are due to decreased metabolite accumulation or to a desensitization of the muscle afferents is not yet known. [source]


Central control of thermogenesis in mammals

EXPERIMENTAL PHYSIOLOGY, Issue 7 2008
Shaun F. Morrison
Thermogenesis, the production of heat energy, is an essential component of the homeostatic repertoire to maintain body temperature in mammals and birds during the challenge of low environmental temperature and plays a key role in elevating body temperature during the febrile response to infection. The primary sources of neurally regulated metabolic heat production are mitochondrial oxidation in brown adipose tissue, increases in heart rate and shivering in skeletal muscle. Thermogenesis is regulated in each of these tissues by parallel networks in the central nervous system, which respond to feedforward afferent signals from cutaneous and core body thermoreceptors and to feedback signals from brain thermosensitive neurons to activate the appropriate sympathetic and somatic efferents. This review summarizes the research leading to a model of the feedforward reflex pathway through which environmental cold stimulates thermogenesis and discusses the influence on this thermoregulatory network of the pyrogenic mediator, prostaglandin E2, to increase body temperature. The cold thermal afferent circuit from cutaneous thermal receptors ascends via second-order thermosensory neurons in the dorsal horn of the spinal cord to activate neurons in the lateral parabrachial nucleus, which drive GABAergic interneurons in the preoptic area to inhibit warm-sensitive, inhibitory output neurons of the preoptic area. The resulting disinhibition of thermogenesis-promoting neurons in the dorsomedial hypothalamus and possibly of sympathetic and somatic premotor neurons in the rostral ventromedial medulla, including the raphe pallidus, activates excitatory inputs to spinal sympathetic and somatic motor circuits to drive thermogenesis. [source]


Influences of dopaminergic lesion on epidermal growth factor-ErbB signals in Parkinson's disease and its model: neurotrophic implication in nigrostriatal neurons

JOURNAL OF NEUROCHEMISTRY, Issue 4 2005
Yuriko Iwakura
Abstract Epidermal growth factor (EGF) is a member of a structurally related family containing heparin-binding EGF-like growth factor (HB-EGF) and transforming growth factor alpha (TGF,) that exerts neurotrophic activity on midbrain dopaminergic neurons. To examine neurotrophic abnormality in Parkinson's disease (PD), we measured the protein content of EGF, TGF,, and HB-EGF in post-mortem brains of patients with Parkinson's disease and age-matched control subjects. Protein levels of EGF and tyrosine hydroxylase were decreased in the prefrontal cortex and the striatum of patients. In contrast, HB-EGF and TGF, levels were not significantly altered in either region. The expression of EGF receptors (ErbB1 and ErbB2, but not ErbB3 or ErbB4) was down-regulated significantly in the same forebrain regions. The same phenomenon was mimicked in rats by dopaminergic lesions induced by nigral 6-hydroxydopamine infusion. EGF and ErbB1 levels in the striatum of the PD model were markedly reduced on the lesioned side, compared with the control hemisphere. Subchronic supplement of EGF in the striatum of the PD model locally prevented the dopaminergic neurodegeration as measured by tyrosine hydroxylase immunoreactivity. These findings suggest that the neurotrophic activity of EGF is maintained by afferent signals of midbrain dopaminergic neurons and is impaired in patients with Parkinson's disease. [source]


Sensor Mechanism and Afferent Signal Transduction of the Urinary Bladder: Special Focus on transient receptor potential Ion Channels

LUTS, Issue 2 2010
Masayuki TAKEDA
In the urine storage phase, mechanical stretch stimulates bladder afferents. These urinary bladder afferent sensory nerves consist of small diameter A, - and C-fibers running in the hypogastic and pelvic nerves. Neuroanatomical studies have revealed a complex neuronal network within the bladder wall. The exact mechanisms that underline mechano-sensory transduction in bladder afferent terminals remain ambiguous; however, a wide range of ion channels (e.g. TTX-resistant Na+ channels, Kv channels and hyperpolarization-activated cyclic nucleotidegated cation channels, degenerin/epithelial Na+ channel), and receptors (e.g. TRPV1, TRPM8, TRPA1, P2X2/3, etc.) have been identified at bladder afferent terminals and have implicated in the generation and modulation of afferent signals, which are elcited by a wide range of bladder stimulations including physiological bladder filling, noxious distension, cold, chemical irritation and inflammation. The mammalian transient receptor potential (TRP) family consists of 28 channels that can be subdivided into six different classes: TRPV (Vanilloid), TRPC (Canonical), TRPM (Melastatin), TRPP (Polycystin), TRPML (Mucolipin), and TRPA (Ankyrin). TRP channels are activated by a diversity of physical (voltage, heat, cold, mechanical stress) or chemical (pH, osmolality) stimuli and by binding of specific ligands, enabling them to act as multifunctional sensors at the cellular level. TRPV1, TRPV2, TRPV4, TRPM8, and TRPA1 have been described in different parts of the urogenital tract. Although only TRPV1 among TRPs has been extensively studied so far, more evidence is slowly accumulating about the role of other TRP channels, ion channels, and receptors in the pathophysiology of the urogenital tract, and may provide a new strategy for the treatment of bladder dysfunction. [source]


Bladder control, urgency, and urge incontinence: Evidence from functional brain imaging,

NEUROUROLOGY AND URODYNAMICS, Issue 6 2008
Derek Griffiths
Abstract Aim To review brain imaging studies of bladder control in subjects with normal control and urge incontinence; to define a simple model of supraspinal bladder control; and to propose a neural correlate of urgency and possible origins of urge incontinence. Methods Review of published reports of brain imaging relevant to urine storage, and secondary analyses of our own recent observations. Results In a simple model of normal urine storage, bladder and urethral afferents received in the periaqueductal gray (PAG) are mapped in the insula, forming the basis of sensation; the anterior cingulate gyrus (ACG) provides monitoring and control; the prefrontal cortex makes voiding decisions. The net result, as the bladder fills, is inhibition of the pontine micturition center (PMC) and of voiding, together with gradual increase in insular response, corresponding to increasing desire to void. In urge-incontinent subjects, brain responses differ. At large bladder volumes and strong sensation, but without detrusor overactivity (DO), most cortical responses become exaggerated, especially in ACG. This may be both a learned reaction to previous incontinence episodes and the neural correlate of urgency. The neural signature of DO itself seems to be prefrontal deactivation. Possible causes of urge incontinence include dysfunction of prefrontal cortex or limbic system, suggested by weak responses and/or deactivation, as well as abnormal afferent signals or re-emergence of infantile reflexes. Conclusions Bladder control depends on an extensive network of brain regions. Dysfunction in various parts may contribute to urge incontinence, suggesting that there are different phenotypes requiring different treatments. Neurourol. Urodynam. 27:466,474, 2008. © 2007 Wiley-Liss, Inc. [source]


Diagnosis and Management of the Painful Ankle/Foot.

PAIN PRACTICE, Issue 4 2003
Interpretation, Management, Part 2: Examination
,,Abstract: Diagnosis, interpretation, and subsequent management of ankle/foot pathology can be challenging to clinicians. A sensitive and specific physical examination is the strategy of choice for diagnosing selected ankle/foot injuries and additional diagnostic procedures, at considerable cost, may not provide additional information for clinical diagnosis and management. Because of a distal location in the sclerotome and the reduced convergence of afferent signals from this region to the dorsal horn of the spinal cord, pain reference patterns are low and the localization of symptoms is trustworthy. Effective management of the painful ankle/foot is closely linked to a tissue-specific clinical examination. The examination of the ankle/foot should include passive and resistive tests that provide information regarding movement limitations and pain provocation. Special tests can augment the findings from the examination, suggesting compromises in the structural and functional integrity of the ankle/foot complex. The weight bearing function of the ankle/foot compounds the clinician's diagnostic picture, as limits and pain provocation are frequently produced only when the patient attempts to function in weight bearing. As a consequence, clinicians should consider this feature by implementing numerous weightbearing components in the diagnosis and management of ankle/foot afflictions. Limits in passive motion can be classified as either capsular or non-capsular patterns. Conversely, patients can present with ankle/foot pain that demonstrates no limitation of motion. Bursitis, tendopathy, compression neuropathy, and instability can produce ankle/foot pain that is challenging to diagnose, especially when they are the consequence of functional weight bearing. Numerous non-surgical measures can be implemented in treating the painful ankle/foot, reserving surgical interventions for those patients who are resistant to conservative care.,, [source]


A simple two-stage model predicts response time distributions

THE JOURNAL OF PHYSIOLOGY, Issue 16 2009
R. H. S. Carpenter
The neural mechanisms underlying reaction times have previously been modelled in two distinct ways. When stimuli are hard to detect, response time tends to follow a random-walk model that integrates noisy sensory signals. But studies investigating the influence of higher-level factors such as prior probability and response urgency typically use highly detectable targets, and response times then usually correspond to a linear rise-to-threshold mechanism. Here we show that a model incorporating both types of element in series , a detector integrating noisy afferent signals, followed by a linear rise-to-threshold performing decision , successfully predicts not only mean response times but, much more stringently, the observed distribution of these times and the rate of decision errors over a wide range of stimulus detectability. By reconciling what previously may have seemed to be conflicting theories, we are now closer to having a complete description of reaction time and the decision processes that underlie it. [source]


Interaction of pre-programmed control and natural stretch reflexes in human landing movements

THE JOURNAL OF PHYSIOLOGY, Issue 3 2002
Martin J. N. McDonagh
Pre-programmed mechanisms of motor control are known to influence the gain of artificially evoked stretch reflexes. However, their interaction with stretch reflexes evoked in the context of unimpeded natural movement is not understood. We used a landing movement, for which a stretch reflex is an integral part of the natural action, to test the hypothesis that unpredicted motor events increase stretch reflex gain. The unpredicted event occurred when a false floor, perceived to be solid, collapsed easily on impact, allowing the subjects to descend for a further 85 ms to a solid floor below. Spinal stretch reflexes were measured following solid floor contact. When subjects passed through the false floor en route to the solid floor, the amplitude of the EMG reflex activity was double that found in direct falls. This was not due to differences in joint rotations between these conditions. Descending pathways can modify H- and stretch-reflex gain in man. We therefore manipulated the time between the false and real floor contacts and hence the time available for transmission along these pathways. With 30 ms between floors, the enhancement of the reflex was extinguished, whereas with 50 ms between floors it reappeared. This excluded several mechanisms from being responsible for the doubling of the reflex EMG amplitude. It is argued that the enhanced response is due to the modulation of reflex gain at the spinal level by signals in descending pathways triggered by the false platform. The results suggest the future hypothesis that this trigger could be the absence of afferent signals expected at the time of false floor impact and that salient error signals produced from a comparison of expected and actual sensory events may be used to reset reflex gains. [source]


Sensory and motor function of teeth and dental implants: A basis for osseoperception

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2005
Mats Trulsson
SUMMARY 1.,When dental implants are loaded mechanically, a sensation, often referred to as osseoperception, is evoked. The sensory signals underlying this phenomenon are qualitatively different from the signals evoked when loading a natural tooth. In contrast with osseointegrated dental implants, natural teeth are equipped with periodontal mechanoreceptors that signal information about tooth loads. In the present review, the functional properties of human periodontal mechanoreceptors will be presented, along with a discussion about their likely functional role in the control of human jaw actions. 2.,Microneurographic experiments reveal that human periodontal mechanoreceptors adapt slowly to maintained tooth loads. Populations of periodontal receptors encode information about both which teeth are loaded and the direction of forces applied to individual teeth. 3.,Most receptors exhibit a markedly curved relationship between discharge rate and force amplitude, featuring the highest sensitivity to changes in tooth load at surprisingly low forces (below 1 N for anterior teeth and 4 N for posterior teeth). Accordingly, periodontal receptors efficiently encode tooth load when subjects first contact, hold and gently manipulate food by the teeth. In contrast, only a minority of receptors encodes the rapid and strong increase in force generated when biting through food. 4.,It is concluded that humans use periodontal afferent signals to control jaw actions associated with intra-oral manipulation of food rather than exertion of jaw power actions. Consequently, patients who lack information from periodontal receptors show an impaired fine motor control of the mandible. [source]