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At least 433 records · Page 24Linked to original sources
PubMed2005

Flexor reflex responses triggered by imposed knee extension in chronic human spinal cord injury.

Hypersensitivity of the flexor reflex pathways to input from force-sensitive muscle afferents may contribute to the prevalence and severity of muscle spasms in patients with spinal cord injury (SCI). In this study, we triggered flexor reflexes with constant velocity knee movements in 15 subjects with SCI. Ramp and hold knee extension perturbations were imposed on one leg while the hip and ankle were held in an isometric position using an instrumented leg brace. Knee, ankle and hip torque responses and electromyograms from six muscles of the leg were recorded following controlled knee extension at four different velocities. Tests were conducted with the hip in both flexed and extended positions. During the movement into knee extension, a velocity-dependent stretch reflex, represented by a progressively increasing knee flexion torque, was observed. In addition, another type of reflex that resembled a flexor reflex (flexion of the hip and ankle) was also triggered by the imposed knee extension. The magnitude of the ankle dorsiflexion torque responses was significantly correlated to the stretch reflex torque at the knee in 9 of the 15 subjects. We concluded that stretch reflexes initiate a muscle contraction that then can contribute to a flexor reflex response, possibly through muscle group III/IV afferent pathways. These results suggest that spasticity in SCI consists of a myriad of complex reflex responses that extend beyond stretch reflexes.

Adult↗
PubMed1998

Effects of two anticholinergic drugs, trospium chloride and biperiden, on motility and evoked potentials of the oesophagus.

BACKGROUND: Anticholinergic drugs are known to impair the motor function of the oesophagus but their effects on the oesophageal afferent pathways are unknown. AIM: To determine the effects of a peripherally-acting (trospium chloride) and a centrally-acting (biperiden) anticholinergic drug on the motility and the evoked potentials of the oesophagus. METHODS: Nine healthy volunteers were randomized to receive 1.2 mg trospium chloride (TC), 5 mg biperiden (BIP) or saline i.v. Primary peristalsis was elicited by swallowing a 5 mL water bolus and secondary peristalsis by insufflation of 20 mL air, 10 times each. Oesophageal potentials were evoked by electrical stimulation in the distal and proximal oesophagus (30 stimulations at 0.4 Hz, two runs). RESULTS: Both anticholinergic drugs reduced by a similiar amount the contraction amplitudes (TC 17 mmHg, BIP 25 mmHg, saline 67 mmHg; P < 0.01) and the rate of secondary contractions (TC 60%, BIP 70%, saline 95%; P < 0.01). In contrast, only biperiden prolonged the latencies of the evoked potentials (N1 peak, distal oesophagus: BIP 191 ms, TC 102 ms, saline 101 ms; P < 0.01; P1 peak: BIP 322 ms, TC 161 ms, saline 144 ms; P < 0.01). CONCLUSIONS: Both anticholinergic drugs depress oesophageal motility, but only the centrally-acting anticholinergic drug biperiden modifies the oesophageal evoked potentials, suggesting a central cholinergic transmission of the oesophageal afferent pathways.

Adult↗
PubMed1984

The exercise pressor reflex: evidence for an afferent pressor pathway outside the dorsolateral sulcus region.

Pressor reflexes evoked by muscle contraction following stimulation of the cut distal portions of the L7 and S1 ventral roots were studied in decerebrate unanesthetized cats. Reflex responses evoked by this simulated exercise persisted after lesions were made in the dorsolateral sulcus region of the T13-L1 spinal cord, indicating that this area is not essential for mediation of these reflexes. Additional evidence suggested that the pathway responsible for the exercise pressor reflex located in the surviving spinal cord is most likely bilateral.

Animals↗
PubMed1979

Changes in body temperature after administration of amino acids, peptides, dopamine, neuroleptics and related agents.

Drugs may alter body temperature by acting on any component of the thermoregulatory system. These components include heat production, heat conservation and heat loss effectors and their efferent pathways, thermosensors and their afferent pathways and neurons within the central nervous system that coordinate thermoregulatory effector activities. A thermostat is often thought to be involved although thermoregulation can be explained by models that do not incorporate a thermostat. An action on a particular component can be assessed by determining the effect of a drug on body temperature over a range of environmental temperatures and by observation and measurement of associated changes in effector activities. A scheme for such assessment is presented along with examples of its use. The study of drug-induced changes in body temperature has expanded greatly within the past decade. The primary purpose of this review is to provide a readily available source of information on interactions between certain drugs and the thermoregulatory system. Extensive tables are presented of body temperature changes after administration of amino acids, peptides, dopamine and related agents, phenothiazine neuroleptics and also phenothiazines that lack neuroleptic activity, butyrophenones, diphenylbutylpiperidines such as pimozide and miscellaneous neuroleptics. The information tabulated includes the species used, route of administration and dose of drugs, the environmental temperature at which the experiments were performed, the number of tests, the direction and magnitude of body temperature change and remarks on the presence of special conditions, such as age or lesions, or on the influence of other drugs, such as antagonists, on the response to the primary drug. Most of the cited literature was published since 1965.

Amino Acids↗
PubMed1980

Afferent visual pathways and receptive field properties of superior colliculus neurons in stroboscopically reared cats.

Unit recordings were made in the superior colliculus of strobe-reared cats. Receptive field properties were studied and electrical stimulation in the chiasma and optic tract made it possible to characterize the visual input. The retinal Y-cell input and the cortical input were found to be deficient. The principal response deficit was the decrease of selective response to direction of movement, also shown to be largely absent in the corticotectal pathway. These results are compared to similar findings in dark-reared animals and discussed in connection with the importance of visual movement to the developing visual system.

Animals↗
PubMed1989

Analysis of human long-latency reflexes by cooling the peripheral conduction pathway; which afferents are involved?

This chapter first outlines current views on the afferents of origin of human "long-latency stretch reflexes", and especially whether they are fast or slow. Attention is concentrated on methodology; other approaches can be found elsewhere with appropriate bibliography (Marsden et al., 1983; Matthews, 1985, 1986a; Wiesendanger, 1986). Recent experiments involving cooling of the human arm are then described. They were performed on the abductor digiti minimi and first dorsal interosseus muscles. The arm was cooled from wrist to axilla by circulating cold water through a tube wrapped round it. Cooling slows conduction by a constant proportion, hence the conduction delay introduced by cooling a segment of nerve is greater for small slow axons than for large fast ones. On this basis it was concluded that group I muscle afferents (presumably Ia) can elicit a long-latency reflex with a long central delay, as also can fast cutaneous afferents. No evidence was found for a long-latency reflex with the delay introduced peripherally by conduction along slow axons (i.e. spindle group II afferents). However, the co-existence of such a mechanism has yet to be excluded.

Cold Temperature↗
PubMed2002

Sensory neurone responses to mucosal noxae in the upper gut: relevance to mucosal integrity and gastrointestinal pain.

The digestive tract is supplied by extrinsic and intrinsic sensory neurones that, together with endocrine and immune cells, form a surveillance network that is essential to gut function. This article focuses on the responses of extrinsic afferent neurones to chemical insults of the gastrointestinal mucosa and their pathophysiological relevance to mucosal integrity and abdominal pain. Within the gastroduodenal region, spinal afferents subserve an emergency function because, in case of alarm by influxing acid, they stimulate mechanisms of mucosal protection via an efferent-like release of transmitters. Other sensory neurones signal chemical noxae to the brain, a task that is not confined to spinal afferents because vagal afferents communicate gastric acid and peripheral immune challenges to the brainstem and in this way elicit autonomic, endocrine, affective and behavioural reactions. Emerging evidence indicates that hypersensitivity of extrinsic afferent pathways to mechanical and chemical stimuli makes an important contribution to the abdominal hyperalgesia seen in functional dyspepsia and irritable bowel syndrome. Sensitization may be brought about by inflammatory processes that lead to up-regulation and functional alterations of receptors and ion channels on sensory neurones. Such sensory neurone-specific molecules, which include vanilloid (capsaicin) receptors, may represent important targets for novel drugs to treat abdominal pain.

Animals↗
PubMed2002

Baroreceptor reflex pathways and neurotransmitters: 10 years on.

The central nervous system plays a critical role in the management of blood flow to the tissues and its return to the heart and lungs. This is achieved by a complex interplay of neural efferent pathways, humoral mechanisms and afferent pathways. In this review, we focus on recent progress (within the past 10 years) that has been made in the sympathetic control of arterial blood pressure with a special emphasis on the role of baroreceptor mechanisms and central neurotransmitters. In particular, we focus on new features since 1991, such as neurotransmission in the nucleus tractus solitarius, the role of neurons in the most caudal part of the ventrolateral medulla oblongata and the increasing understanding of the exquisite control of different sympathetic pathways by different neurotransmitter systems.

Animals↗
PubMed2003

Effect of moxibustion stimulation of various skin areas on cortical cerebral blood flow in anesthetized rats.

The effect of moxibustion stimulation of various skin areas (cheek, forepaw, upper arm, chest, back, lower leg, hindpaw and perineum) on cerebral blood flow (CBF) of the parietal cortex was examined in anesthetized rats after eliminating emotional influences. Moxibustion stimulation was performed by burning a moxa cone of about 4 mg weight placed on the shaved skin. CBF of the parietal cortex was measured using a laser Doppler flowmeter. Stimulation of the cheek, forepaw, upper arm and hindpaw produced significant increases in CBF, but stimulation of the other areas did not produce significant responses. Moxibustion stimulation of the forepaw and hindpaw produced an increase in the mean arterial pressure (MAP), while stimulation of the other areas did not. After spinal transection at the 2nd thoracic level, the MAP response to stimulation of the forepaw was abolished, whereas the CBF response to stimulation of the forepaw remained. The CBF response in spinalized rats was not affected by cutting cervical sympathetic and facial parasympathetic nerves, while it was almost abolished by intravenous administration of muscarinic and nicotinic cholinergic blocking agents. The CBF response was abolished by crushing the brachial plexus ipsilateral to the stimulated side. It is suggested that the increase in CBF, independent of MAP and emotional responses, elicited by moxibustion stimulation is a reflex response whose afferent pathway is composed of somatic afferent nerves, and whose efferent pathway involves intracerebral cholinergic nerves. A contribution of endogenous opioids in the present CBF responses was neglected, because naloxone did not influence the CBF responses.

Animals↗
PubMed2001

Norepinephrine-induced calcium signaling pathways in afferent arterioles of genetically hypertensive rats.

This study provides new information about the relative importance of calcium mobilization and entry in the renal vascular response to adrenoceptor activation in afferent arterioles isolated from 7- to 8-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Intracellular free calcium concentration ([Ca(2+)](i)) was measured in microdissected arterioles utilizing ratiometric photometry of fura 2 fluorescence. There was no significant strain difference in baseline [Ca(2+)](i). Norepinephrine (NE; 10(-6) and 10(-7) M) elicited immediate, sustained increases in [Ca(2+)](i). The general temporal pattern of response to 10(-6) M NE consisted of an initial peak and a maintained plateau phase. The response to NE was partially blocked by nifedipine (10(-6) M) or 8-(N,N-diethylamino) octyl-3,4,5-trimetoxybenzoate (TMB-8; 10(-5) M). A calcium-free external solution abolished the sustained [Ca(2+)](i) plateau response to NE, with less influence on the peak response. In the absence of calcium entry, TMB-8 (10(-5) M) completely blocked the calcium response to NE in WKY but not SHR, suggesting strain differences in mobilization. A higher concentration of TMB-8 (10(-4) M), however, blocked all discernible mobilization in both strains. We conclude that there are differences in Ca(2+) handling in renal resistance vessels between young WKY and SHR with respect to mobilization stimulated by alpha-adrenoceptors. Afferent arterioles of young SHR appear to have a larger inositol-1,4,5-trisphosphate-sensitive pool or release from a site less accessible to TMB-8.

Adrenergic alpha-Agonists↗