Unmasking of the trigemino-accessory reflex in accessory facial anastomosis.
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OBJECTIVE: To evaluate the possible blink reflex responses in facial muscles reinnervated by the accessory nerve. METHOD: Eleven patients with a complete facial palsy were submitted to a surgical repair by an accessory facial nerve anastomosis (AFA). In this pathological group, blink reflex was studied by means of percutaneous electrical stimulation of the supraorbital nerve and recording from the orbicularis oculi muscle. A control group comprised seven normal people and seven patients with a complete Bell's facial palsy; in this group, responses on the sternocleidomastoideus (SCM) muscles were studied after supraorbital nerve stimulation. RESULTS: All the patients with AFA showed a consistent degree of facial reinnervation. Ten out of the 11 patients with AFA showed reflex responses; in six, responses were configured by a double component pattern, resembling the R1 and R2 components of the blink reflex; three patients had an R1-like response and one patient showed a unique R2 component. Mean values of latencies were 15.2 (SD 4.6) ms for the R1 and 85.3 (SD 9.6) ms for the R2. In the control group, eight out of 14 people had evidence of reflex responses in the SCM muscles; these were almost exclusively configured by a bilateral late component (mean latency 63.5 (SD15.9) ms) and only one of the subjects showed an early response at 11 ms. CONCLUSION: The trigemino-accessory reflex response in the pathological group was more complex and of a significantly higher incidence than in the control group. These differences could be tentatively explained by a mechanism of synaptic plasticity induced by the impairment of the efferent portion of the reflex. This could unmask the central linking between the trigeminal and the accessory limbs of the reflex. The findings described could be a demonstration of neurobionomic function in the repairing process of the nervous system. (+info)
Differential induction of long-term synaptic facilitation by spaced and massed applications of serotonin at sensory neuron synapses of Aplysia californica.
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Serotonin (5HT)-induced facilitation of synaptic transmission from tail sensory neurons (SNs) to motor neurons (MNs) in the marine mollusc Aplysia provides a cellular model of short- and long-term memory for behavioral sensitization of the tail withdrawal reflex. Synaptic facilitation at these synapses occurs in three temporal phases: short-term (STF, lasting minutes), intermediate-term (ITF, lasting more than an hour), and long-term (LTF, lasting >24 hr). STF, ITF, and LTF differ in their induction requirements: A single brief exposure of 5HT induces STF, whereas five applications are required for ITF and LTF. Moreover, STF and LTF can be induced independently. Different forms of memory often show differential sensitivity to the pattern of training trials. To begin to explore this effect at a cellular level, we examined ITF and LTF induced by one of two patterns of 5HT application: a spaced pattern (five 5-min exposures with an interval of 15 min) or a massed pattern (one continuous 25-min application). The spaced and massed patterns both induced ITF; however, spaced 5HT application was significantly more reliable at inducing LTF than was massed application. Thus, whereas induction of ITF and LTF require similar amounts of 5HT, the cellular mechanisms underlying the induction of LTF are more sensitive to the pattern of the induction trials. In the massed group, further analysis revealed a relationship between the expression of ITF and the subsequent expression of LTF, suggesting that these two processes may be mechanistically related. (+info)
Effect of several 5-hydroxytryptamine(1A) receptor ligands on the micturition reflex in rats: comparison with WAY 100635.
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Several novel N-arylpiperazine derivatives were synthesized and tested for their 1) affinity and functional activity on 5-hydroxytryptamine(1A) (5-HT(1A)) receptors in vitro; 2) activity in models predictive of antagonism at somatodendritic and postsynaptic 5-HT(1A) receptors; and 3) effects on the micturition reflex in anesthetized and conscious rats. These studies also included 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl] piperazine hydrobromide (NAN 190), 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4, 5]decane-7,9-dione dihydrochloride (BMY 7378), and N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl-N-(2-pyridinyl)cyclohex anecarboxamide (WAY 100635). Almost all compounds were found to be potent and selective for the human recombinant 5-HT(1A) receptor, with K(i) values in the nanomolar range. [(35)S]GTPgammaS binding in HeLa cells expressing the recombinant human 5-HT(1A) receptor allowed classification of the compounds into neutral antagonists and partial agonists. Almost all neutral antagonists were active in blocking 8-hydroxy-2-dipropylaminotetralin (8-OH-DPAT)-induced forepaw treading in rats (postsynaptic model) and hypothermia in mice (somatodendritic model) with the same potency, whereas compounds showing partial agonistic activity were active in the postsynaptic model but were inactive, or poorly active, in the somatodendritic model. Neutral antagonists potently inhibited volume-induced bladder-voiding contractions in anesthetized rats. Contractions were completely blocked, and the disappearance of bladder contractions lasted 7 to 13 min after the highest doses tested. Furthermore, neutral antagonists increased bladder volume capacity in conscious rats during continuous transvesical cystometry, whereas micturition pressure was only slightly, and not dose-dependently, reduced. Partial agonists were inactive or poorly active, inducing a disappearance time of bladder contractions that did not exceed 6 min in anesthetized rats, and failing to increase bladder volume capacity in conscious rats. These findings indicate that only neutral 5-HT(1A) receptor antagonists are endowed with inhibitory effects on the bladder. (+info)
Sympathetic inhibition of ascending and descending interneurones during the peristaltic reflex in the isolated guinea-pig distal colon.
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1. We investigated the effects of sympathetic nerve stimulation within ascending and descending reflex pathways underlying the peristaltic reflex in the guinea-pig distal colon. 2. A three-chambered partitioned bath was used to divide a segment of distal colon into stimulation, recording and intermediate regions. The effects of lumbar colonic nerves (LCN) could be localized to the intermediate region by surgical lesions of the mesentery and by application of guanethidine (3 microM) to the stimulation and recording chambers. 3. Brush stroking the mucosa in the anal and oral stimulation chambers elicited a synchronous contraction of the longitudinal muscle (LM) and circular muscle (CM) oral to, and transient relaxation of the LM and CM anal to, the stimulus, respectively. 4. After N omega-nitro-L-arginine (L-NA; 100 microM) in the oral and intermediate chambers, mucosal stimulation in the oral chamber elicited a prolonged descending inhibitory and excitatory complex in both the LM and CM in the anal recording chamber. This was blocked by hexamethonium (300 microM), which did not affect the transient relaxation response recorded in control conditions. 5. Stimulation of the LCN (1200 pulses, 20 Hz), delivered to the intermediate region, abolished the oral contraction and the L-NA-induced anal complex in both the LM and CM, but was without effect on the transient hexamethonium-resistant anal relaxation. These effects of LCN stimulation were reversed by phentolamine (3 microM) or yohimbine (100 nM), but not propranolol (10 microM), when added to the intermediate chamber. 6. LCN stimuli (2-20 Hz, 600 micros pulses) directed to the recording chamber elicited synchronous relaxations in the LM and CM that were unaffected by hexamethonium (300 microM), but were reduced by yohimbine and usually blocked by the further addition of propranolol (10 microM). 7. In conclusion, sympathetic nerve stimulation inhibits orally and anally projecting cholinergic interneurones underlying the peristaltic reflex in the distal colon. In addition, the LM and CM relax synchronously following release of sympathetic neurotransmitter, over a range of stimulus frequencies. (+info)
Contribution of the leg vasculature to hypotensive effects of an antiorthostatic posture change in humans.
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1. Previous results from our laboratory have shown that vasodilatation in the legs prevents mean arterial pressure (MAP) from increasing during water immersion. Therefore, we tested the hypothesis that vasodilatation in the legs is necessary for the hypotensive effects to occur during a moderate antiorthostatic posture change. 2. Ten healthy males underwent a 5 min posture change from upright seated to horizontal supine (SUP) and back to seated again with (OCCL-SUP) and without simultaneous total arterial (154 +/- 1 mmHg) thigh occlusion, and a control seated period, also with and without arterial occlusion. Cardiac output (CO) was measured by a non-invasive foreign (N2O) gas rebreathing technique. 3. MAP (brachial auscultation) decreased during SUP from 94 +/- 3 to 84 +/- 2 mmHg (P < 0.0001) and total peripheral vascular resistance (TPR = MAP/CO, n = 8) decreased by 15 +/- 4 % (P < 0.001). During OCCL-SUP, MAP decreased from 98 +/- 2 to 90 +/- 2 mmHg (P < 0.005) and TPR decreased by 14 +/- 3 % (P < 0.01). 4. In conclusion, vasodilatation in the legs is not necessary for the decrease in MAP to occur during a moderate antiorthostatic manoeuvre. Therefore, vasodilatation in more central vascular beds (e.g. abdomen) can alone account for the hypotensive effects. (+info)
Autonomic dysreflexia is a condition that develops after spinal cord injury in which potentially life-threatening episodic hypertension is triggered by stimulation of sensory nerves in the body below the site of injury. Central sprouting of small-diameter primary afferent fibers in the dorsal horn of the spinal cord occurs concurrently with the development of this condition. We propose a model for the development of autonomic dysreflexia in which increased nerve growth factor (NGF) in the injured cord stimulates small-diameter primary afferent fiber sprouting, thereby magnifying spinal sympathetic reflexes and promoting dysreflexia. We identified this population of afferent neurons using immunocytochemistry for calcitonin gene-related peptide. Blocking intraspinal NGF with an intrathecally-delivered neutralizing antibody to NGF prevented small-diameter afferent sprouting in rats 2 weeks after a high thoracic spinal cord transection. In the same rats, this anti-NGF antibody treatment significantly decreased (by 43%) the hypertension induced by colon stimulation. The extent of small-diameter afferent sprouting after cord transection correlated significantly with the magnitude of increases in arterial pressure during the autonomic dysreflexia. Neutralizing NGF in the spinal cord is a promising strategy to minimize the life-threatening autonomic dysreflexia that develops after spinal cord injury. (+info)
Thermal avoidance in Caenorhabditis elegans: an approach to the study of nociception.
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Upon perception of a noxious stimulus, an organism executes defense mechanisms, such as escape responses. The molecular basis of these mechanisms is poorly understood. In this paper we show that upon exposure to noxious temperature, Caenorhabditis elegans reacts by a withdrawal reflex. To analyze this thermal avoidance behavior, we developed a laser-based assay to quantify the response. The escape reflex can be observed in 98% of the adult animals, but is not executed in animals in diapause. The thermal avoidance response differs significantly from the thermotaxis behavior that is based on the perception of physiological temperature. It involves different neurons and is influenced by mutations in distinct genes. As in mammals, the strength of the thermal avoidance response is increased by application of capsaicin, the pungent ingredient in chili peppers. We find that thermal avoidance is strongly reduced in mutants affecting the neural transmission modulated by glutamate and neuropeptides as well as in mutants affecting the structure and function of sensory neurons. We suggest that the study of this nociceptive behavior in C. elegans can be used to understand the genetic and molecular basis of thermal nociception. (+info)
Reflex and muscular adaptations in rat soleus muscle after hindlimb suspension.
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Reflex, mechanical and histochemical adaptations of the soleus muscle following 3 weeks of hindlimb suspension (HS) were measured in the rat. HS transformed the soleus muscle fibre type composition from predominantly slow, type I, to approximately equal proportions of fast, type II and slow fibres. Consistent with this transformation was an increase in the maximum shortening velocity, V(max), and a decrease in the stiffness of the series elastic component. Disuse also produced muscle atrophy and a resultant decrease in twitch and tetanic force. Reflex responses of the ankle extensors were also obtained at 5 and 9 weeks of age for six control rats (C group) and six rats subjected to HS for 3 weeks (HS group). The soleus reflexes to a mechanical tap applied to the Achilles tendon (T reflex) and to an electrical stimulation of the sciatic nerve (H reflex) were measured. The maximal amplitude of these reflexes (T(max) and H(max)) were normalised to the maximal direct motor response (M(max)) and the T(max)/H(max) ratio was also calculated to give an index of the relative adaptations of the peripheral and central components of the reflex pathway. The HS group showed significantly higher H reflex gains than the C group, possibly due to changes in synaptic efficiency after HS. Conversely, the HS group presented strongly inhibited T reflexes and negative gains for the T(max)/H(max) ratios. This result indicated a reduced spindle solicitation after HS, which may reflect changes in the spindle sensitivity itself, but it could also be due to the decrease in stiffness of the musculo-tendinous elements in series with the muscle spindles. Such mechanical changes may play an important part in the decreased T reflex responses. (+info)