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Afferent Fibres (afferent + fibre)
Selected AbstractsMechanical and neural stretch responses of the human soleus muscle at different walking speedsTHE JOURNAL OF PHYSIOLOGY, Issue 13 2009Neil J. Cronin During human walking, a sudden trip may elicit a Ia afferent fibre mediated short latency stretch reflex. The aim of this study was to investigate soleus (SOL) muscle mechanical behaviour in response to dorsiflexion perturbations, and to relate this behaviour to short latency stretch reflex responses. Twelve healthy subjects walked on a treadmill with the left leg attached to an actuator capable of rapidly dorsiflexing the ankle joint. Ultrasound was used to measure fascicle lengths in SOL during walking, and surface electromyography (EMG) was used to record muscle activation. Dorsiflexion perturbations of 6 deg were applied during mid-stance at walking speeds of 3, 4 and 5 km h,1. At each walking speed, perturbations were delivered at three different velocities (slow: ,170 deg s,1, mid: ,230 deg s,1, fast: ,280 deg s,1). At 5 km h,1, fascicle stretch amplitude was 34,40% smaller and fascicle stretch velocity 22,28% slower than at 3 km h,1 in response to a constant amplitude perturbation, whilst stretch reflex amplitudes were unchanged. Changes in fascicle stretch parameters can be attributed to an increase in muscle stiffness at faster walking speeds. As stretch velocity is a potent stimulus to muscle spindles, a decrease in the velocity of fascicle stretch at faster walking speeds would be expected to decrease spindle afferent feedback and thus stretch reflex amplitudes, which did not occur. It is therefore postulated that other mechanisms, such as altered fusimotor drive, reduced pre-synaptic inhibition and/or increased descending excitatory input, acted to maintain motoneurone output as walking speed increased, preventing a decrease in short latency reflex amplitudes. [source] Ultrastructural evidence for a pre- and postsynaptic localization of full-length trkB receptors in substantia gelatinosa (lamina II) of rat and mouse spinal cordEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2005Chiara Salio Abstract Brain-derived neurotrophic factor (BDNF) exerts its trophic effects by acting on the high-affinity specific receptor trkB. BDNF also modulates synaptic transmission in several areas of the CNS, including the spinal cord dorsal horn, where it acts as a pain modulator by yet incompletely understood mechanisms. Spinal neurons are the main source of trkB in lamina II (substantia gelatinosa). Expression of this receptor in dorsal root ganglion (DRG) cells has been a matter of debate, whereas a subpopulation of DRG neurons bears trkA receptors and contains BDNF. By the use of two different trkB antibodies we observed that 7.7% and 10.8% of DRG neurons co-expressed BDNF + trkB but not trkA, respectively, in rat and mouse. Ultrastructurally, full-length trkB (fl-trkB) receptors were present at somato-dendritic membranes of lamina II neurons (rat: 66.8%; mouse: 73.8%) and at axon terminals (rat: 33.2%; mouse: 26.2%). In both species, about 90% of these terminals were identified as primary afferent fibres (PAFs) considering their morphology and/or neuropeptide content. All fl-trkB-immunopositive C boutons in type Ib glomeruli were immunoreactive for BDNF and, at individual glomeruli and axo-dendritic synapses, fl-trkB receptors were located in a mutually exclusive fashion at pre- or postsynaptic membranes. Thus, only a small fraction of fl-trkB-immunoreactive dendrites were postsynaptic to BDNF-immunopositive PAFs. This is the first ultrastructural description of fl-trkB localization at synapses between first- and second-order sensory neurons in lamina II, and suggests that BDNF may be released by fl-trkB-immunopositive PAFs to modulate nociceptive input in this lamina of dorsal horn. [source] Presynaptic inhibition of Schaffer collateral synapses by stimulation of hippocampal cholinergic afferent fibresEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003David Fernández de Sevilla Abstract It has been known for decades that muscarinic agonists presynaptically inhibit Schaffer collateral synapses contacting hippocampal CA1 pyramidal neurons. However, a demonstration of the inhibition of Schaffer collateral synapses induced by acetylcholine released by cholinergic hippocampal afferents is lacking. We present original results showing that electrical stimulation at the stratum oriens/alveus with brief stimulus trains inhibited excitatory postsynaptic currents evoked by stimulation of Schaffer collaterals in CA1 pyramidal neurons of rat hippocampal slices. The increased paired-pulse facilitation and the changes in the variance of excitatory postsynaptic current amplitude that paralleled the inhibition suggest that it was mediated presynaptically. The effects of oriens/alveus stimulation were inhibited by atropine, and blocking nicotinic receptors with methyllycaconitine was ineffective, suggesting that the inhibition was mediated via the activation of presynaptic muscarinic receptors. The results provide a novel demonstration of the presynaptic inhibition of glutamatergic neurotransmission by cholinergic fibres in the hippocampus, implying that afferent cholinergic fibres regulate the strength of excitatory synaptic transmission. [source] Dual effects of NMDA receptor activation on polysialylated neural cell adhesion molecule expression during brainstem postnatal developmentEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2001Farima Bouzioukh Abstract Here we show a dual role of N -methyl- d -aspartate receptor (NMDAR) activation in controlling polysialylated neural cell adhesion molecule (PSA-NCAM) dynamic expression in the dorsal vagal complex (DVC), a gateway for many primary afferent fibres. In this structure the overall expression of PSA-NCAM decreases during the first 2 weeks after birth to persist only at synapses in the adult. Electrical stimulation of the vagal afferents causes a rapid increase of PSA-NCAM expression both in vivo and in acute slices before postnatal day (P) 14 whereas a similar stimulation induces a decrease after P15. Inhibition of NMDAR activity in vitro completely prevented these changes. These regulations depend on calmodulin activation and cGMP production at all stages. By contrast, blockade of neuronal nitric oxide synthase (nNOS) prevented these changes only after P10 in agreement with its late expression in the DVC. The pivotal role of NMDAR is also supported by the observation that chronic blockade induces a dramatic decrease in PSA-NCAM expression. [source] Plateau potential-dependent windup of the response to primary afferent stimuli in rat dorsal horn neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2000Valérie Morisset Abstract In the spinal cord, repetitive stimulation of nociceptive afferent fibres induces a progressive build-up of dorsal horn neuron (DHN) responses. This ,action potential windup' is used as a cellular model of central sensitization to pain. It partly relies on synaptic plasticity, being reduced after blocking NMDA and neurokinin receptors. Using intracellular recordings in a slice preparation of the rat spinal cord, we have analysed the implication of an additional non-synaptic component of windup. Primary afferent fibres were electrically stimulated in the dorsal root. Of 47 responding deep DHNs, 17 (36%) produced action potential windup and afterdischarge during consecutive periods of repeated stimuli (0.4,1 Hz) activating high- (n = 13 neurons) and low-threshold (n = 6 neurons) afferent fibres. When the NMDA receptors were blocked, the rate of windup did not change. In all neurons, there was an absolute correlation between expression of windup and the production of calcium-dependent plateau potentials. Sensitization of the DHN response, similar to the synaptically induced windup, was obtained by repetitive intracellular injection of depolarizing current pulses. This intracellularly induced windup had the same pharmacology as the plateau potential. Synaptically induced windup was also abolished by nifedipine, an L-type calcium-channel blocker. Expression of plateau properties in DHNs is therefore a critical component of windup, operating downstream of synaptic processes. Being associated with calcium influx, generation of plateau potentials could be a link between short-term plasticity and the long-term modification of DHN excitability associated with central sensitization. [source] Neurotransmitter and neuromodulatory mechanisms at peripheral arterial chemoreceptorsEXPERIMENTAL PHYSIOLOGY, Issue 6 2010Colin A. Nurse The control of breathing depends critically on sensory inputs to the central pattern generator of the brainstem, arising from peripheral arterial chemoreceptors located principally in the carotid bodies (CBs). The CB receptors, i.e. glomus or type I cells, are excited by chemical stimuli in arterial blood, particularly hypoxia, hypercapnia, acidosis and low glucose, which initiate corrective reflex cardiorespiratory and cardiovascular adjustments. Type I cells occur in clusters and are innervated by petrosal afferent fibres. Synaptic specializations (both chemical and electrical) occur between type I cells and petrosal terminals, and between neighbouring type I cells. This, together with the presence of a wide array of neurotransmitters and neuromodulators linked to both ionotropic and metabotropic receptors, allows for a complex modulation of CB sensory output. Studies in several laboratories over the last ,20 years have provided much insight into the transduction mechanisms. More recent studies, aided by the development of a co-culture model of the rat CB, have shed light on the role of neurotransmitters and neuromodulators in shaping the afferent response. This review highlights some of these developments, which have contributed to our current understanding of information processing at CB chemoreceptors. [source] Laser Doppler flowmetry in endodontics: a reviewINTERNATIONAL ENDODONTIC JOURNAL, Issue 6 2009H. Jafarzadeh Abstract Vascular supply is the most accurate marker of pulp vitality. Tests for assessing vascular supply that rely on the passage of light through a tooth have been considered as possible methods for detecting pulp vitality. Laser Doppler flowmetry (LDF), which is a noninvasive, objective, painless, semi-quantitative method, has been shown to be reliable for measuring pulpal blood flow. The relevant literature on LDF in the context of endodontics up to March 2008 was reviewed using PubMed and MEDLINE database searches. This search identified papers published between June 1983 and March 2008. Laser light is transmitted to the pulp by means of a fibre optic probe. Scattered light from moving red blood cells will be frequency-shifted whilst that from the static tissue remains unshifted. The reflected light, composed of Doppler-shifted and unshifted light, is returned by afferent fibres and a signal is produced. This technique has been successfully employed for estimating pulpal vitality in adults and children, differential diagnosis of apical radiolucencies (on the basis of pulp vitality), examining the reactions to pharmacological agents or electrical and thermal stimulation, and monitoring of pulpal responses to orthodontic procedures and traumatic injuries. Assessments may be highly susceptible to environmental and technique-related factors. Nonpulpal signals, principally from periodontal blood flow, may contaminate the signal. Because this test produces no noxious stimuli, apprehensive or distressed patients accept it more readily than current methods of pulp vitality assessment. A review of the literature and a discussion of the application of this system in endodontics are presented. [source] The Role of the Vagus Nerve in Mediating the Long-Term Anorectic Effects of LeptinJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2007C. Sachot Leptin, the product of the obese (ob) gene, is mainly known for its regulatory role of energy balance by direct activation of hypothalamic receptors. Recently, its function in the acute control of food intake was additionally attributed to activation of the vagus nerve to regulate meal termination. Whether vagal afferent neurones are involved in longer term effects of leptin on food intake, however, remains undetermined. Using vagotomised (VGX) rats, we sought to clarify the contributions of vagal afferents in mediating the long-lasting effect of leptin on appetite suppression. Intraperitoneal (i.p.) injection of leptin (3.5 mg/kg) attenuated food intake at 4, 6, 8 and 24 h and body weight at 24 h postinjection in SHAM-operated rats; however, this response was not abrogated by vagotomy. In a separate study using immunohistochemistry, we observed leptin-induced Fos expression in the nucleus tractus solitarii, a brain structure where vagal afferent fibres terminate. This signal was not attenuated in VGX animals compared to the SHAM group. Moreover, leptin treatment led to a similar level of nuclear STAT3 translocation, a marker of leptin signalling, in the hypothalami of SHAM and VGX animals. In addition to the effects of leptin, vagotomy surgery itself resulted in a decrease of 24 h food intake. Analyses of brains from saline-treated VGX animals revealed a significant induction of Fos in the nucleus tractus solitarii and changes in agouti-related peptide and pro-opiomelanocortin mRNA expression in the hypothalamus compared to their SHAM counterparts, indicating that the vagotomy surgery itself induced a modification of brain activity in areas involved in regulating appetite. Collectively, our data suggest that vagal afferents do not constitute a major route of mediating the regulatory effect of leptin on food intake over a period of several hours. [source] Activation of M2 muscarinic receptors leads to sustained suppression of hippocampal transmission in the medial prefrontal cortexTHE JOURNAL OF PHYSIOLOGY, Issue 21 2009Lang Wang Cholinergic innervation of the prefrontal cortex is critically involved in arousal, learning and memory. Dysfunction of muscarinic acetylcholine receptors and their downstream signalling pathways has been identified in mental retardation. To assess the role played by the muscarinic receptors at the hippocampal,frontal cortex synapses, an important relay in information storage, we used a newly developed frontal slice preparation in which hippocampal afferent fibres are preserved. Transient activation of muscarinic receptors by carbachol results in a long-lasting depression of synaptic efficacy at the hippocampal but not cortical pathways or local circuitry. On the basis of a combination of electrophysiological, pharmacological and anatomical results, this input-specific muscarinic modulation can be partially attributed to the M2 subtype of muscarinic receptors, possibly through a combination of pre- and postsynaptic mechanisms. [source] Substance P presynaptically depresses the transmission of sensory input to bronchopulmonary neurons in the guinea pig nucleus tractus solitariiTHE JOURNAL OF PHYSIOLOGY, Issue 2 2003Shin-ichi Sekizawa Substance P modulates the reflex regulation of respiratory function by its actions both peripherally and in the CNS, particularly in the nucleus tractus solitarii (NTS), the first central site for synaptic contact of the lung and airway afferent fibres. There is considerable evidence that the actions of substance P in the NTS augment respiratory reflex output, but the precise effects on synaptic transmission have not yet been determined. Therefore, we determined the effects of substance P on synaptic transmission at the first central synapses by using whole-cell voltage clamping in an NTS slice preparation. Studies were performed on second-order neurons in the slice anatomically identified as receiving monosynaptic input from sensory nerves in the lungs and airways. This was done by the fluorescent labelling of terminal boutons after 1,1,-dioctadecyl-3,3,3,,3,-tetra-methylindocarbo-cyanine perchlorate (DiI) was applied via tracheal instillation. Substance P (1.0, 0.3 and 0.1 ,M) significantly decreased the amplitude of excitatory postsynaptic currents (eEPSCs) evoked by stimulation of the tractus solitarius, in a concentration-dependent manner. The decrease was accompanied by an increase in the paired-pulse ratio of two consecutive eEPSCs, and a decrease in the frequency, but not the amplitude, of spontaneous EPSCs and miniature EPSCs, findings consistent with a presynaptic site of action. The effects were consistently and significantly attenuated by a neurokinin-1 (NK1) receptor antagonist (SR140333, 3 ,M). The data suggest a new site of action for substance P in the NTS (NK1 receptors on the central terminals of sensory fibres) and a new mechanism (depression of synaptic transmission) for regulating respiratory reflex function. [source] Reversal of acid-induced and inflammatory pain by the selective ASIC3 inhibitor, APETx2BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2010Jerzy Karczewski BACKGROUND AND PURPOSE Inflammatory pain is triggered by activation of pathways leading to the release of mediators such as bradykinin, prostaglandins, interleukins, ATP, growth factors and protons that sensitize peripheral nociceptors. The activation of acid-sensitive ion channels (ASICs) may have particular relevance in the development and maintenance of inflammatory pain. ASIC3 is of particular interest due to its restricted tissue distribution in the nociceptive primary afferent fibres and its high sensitivity to protons. EXPERIMENTAL APPROACH To examine the contribution of ASIC3 to the development and maintenance of muscle pain and inflammatory pain, we studied the in vivo efficacy of a selective ASIC3 inhibitor, APETx2, in rats. KEY RESULTS Administration of APETx2 into the gastrocnemius muscle prior to the administration of low pH saline prevented the development of mechanical hypersensitivity, whereas APETx2 administration following low-pH saline was ineffective in reversing hypersensitivity. The prevention of mechanical hypersensitivity produced by acid administration was observed whether APETx2 was applied via i.m. or i.t. routes. In the complete Freund's adjuvant (CFA) inflammatory pain model, local administration of APETx2 resulted in a potent and complete reversal of established mechanical hypersensitivity, whereas i.t. application of APETx2 was ineffective. CONCLUSIONS AND IMPLICATIONS ASIC3 contributed to the development of mechanical hypersensitivity in the acid-induced muscle pain model, whereas ASIC3 contributed to the maintenance of mechanical hypersensitivity in the CFA inflammatory pain model. The contribution of ASIC3 to established hypersensitivity associated with inflammation suggests that this channel may be an effective analgesic target for inflammatory pain states. [source] ELECTROPHYSIOLOGICAL EVIDENCE FOR THE INTERACTION OF SUBSTANCE P AND GLUTAMATE ON A, AND C AFFERENT FIBRE ACTIVITY IN RAT HAIRY SKINCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2006Qi Zhang SUMMARY 1The purpose of the present study was to investigate whether there was a cooperative interaction between substance P (SP) and glutamate (GLU) administered subcutaneously on A, and C primary afferent fibre activity in dorsal hairy skin of the rat in vivo. The single unit activities of A, and C afferent fibres were recorded by isolation of fibre filaments from the dorsal cutaneous nerve branches and the effects of subcutaneous injections of low doses of SP, GLU and SP + GLU on activity were determined. 2Sub-threshold doses of SP (1 µmol/L, 10 µL) administered subcutaneously into the dorsal hairy skin had no effect on the afferent discharges of either A, or C units. 3The afferent discharges of 35% (11/31) of A, fibres and 33% (6/18) of C fibres were increased by local injection of the submaximal doses of GLU (10 µmol/L, 10 µL) into the receptive fields. 4The GLU-induced excitatory response was significantly enhanced by coinjection of subthreshold doses of SP. The mean discharge rates of A, fibres and C fibres were increased from 5.84 ± 1.54 and 5.02 ± 2.65 impulses/min to 19.91 ± 4.35 and 17.58 ± 5.59 impulses/min, respectively, whereas the excitatory proportions of A, and C fibres were increased from 35 and 33% to 84 and 83%, respectively. The duration of the excitation for A, fibres and C fibres was also significantly increased after coinjection of SP + GLU compared with that observed when either substance was given alone. 5The present study provides electrophysiological evidence for an interaction between receptors for SP and GLU on the fine fibres activities in rat hairy skin, which may be involved in the mechanisms of hyperalgesia. [source] | |||||||||||||