Sacral dorsal horn neurone activity during micturition in the cat.
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The excitability of two groups of neurones located in different parts of the sacral spinal cord were examined during micturition in decerebrate adult cats. One group of cells, characterized by their activation by pudendal cutaneous afferents, was located in the dorsal commissure of the first and second sacral spinal segments. The second group, located in the dorsal horn of the first sacral spinal segment, was excited by group II muscle and cutaneous afferents. Micturition was evoked by distension of the urinary bladder or by electrical stimulation of the pontine micturition centre. Tonic firing was induced in the neurones by ejection of DL-homocysteic acid from the recording extracellular micropipette. The instantaneous firing frequency of 11/17 sacral dorsal grey commissure neurones was decreased from 7 to 100 % during micturition, and on average was about half of the prevoid firing frequency. It is hypothesized that these sacral neurones are interposed in polysynaptic excitatory pathways from sacral perineal afferents to sphincter motoneurones and that they are subject to direct postsynaptic inhibition during micturition. One other cell showed no change in firing during micturition, two displayed complex patterns of modulation, while 3/17 of the dorsal grey commissure neurones increased their firing rate 30 to 1000 % during micturition. It is hypothesized that the excited neurones may be part of the inhibitory pathways mediating postsynaptic inhibition of sphincter motoneurones or sacral primary afferent depolarization during micturition. Alternatively, they may be part of the excitatory urethral-bladder reflex circuitry. A small (5-15 %) but significant decrease in firing was observed in 4/5 of the group II rostral sacral neurones examined; the firing of a fifth neurone was unchanged. The depression of group II neurones may serve to suppress unwanted hindlimb reflexes that could disrupt micturition. (+info)
Mechanisms of H+ modulation of glycinergic response in rat sacral dorsal commissural neurons.
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Many ionotropic receptors are modulated by extracellular H+. So far, few studies have directly addressed the role of such modulation at synapses. In the present study, we investigated the effects of changes in extracellular pH on glycinergic miniature inhibitory postsynaptic currents (mIPSCs) as well as glycine-evoked currents (IGly) in mechanically dissociated spinal neurons with native synaptic boutons preserved. H+ modulated both the mIPSCs and IGly biphasically, although it activated an amiloride-sensitive inward current by itself. Decreasing extracellular pH reversibly inhibited the amplitude of the mIPSCs and IGly, while increasing external pH reversibly potentiated these parameters. Blockade of acid-sensing ion channels (ASICs) with amiloride, the selective antagonist of ASICs, or decreasing intracellular pH did not alter the modulatory effect of H+ on either mIPSCs or IGly. H+ shifted the EC50 of the glycine concentration-response curve from 49.3 +/- 5.7 microM at external pH 7.4 to 131.5 +/- 8.1 microM at pH 5.5, without altering the Cl- selectivity of the glycine receptor (GlyR), the Hill coefficient and the maximal IGly, suggesting a competitive inhibition of IGly by H+. Both Zn2+ and H+ inhibited IGly. However, H+ induced no further inhibition of IGly in the presence of a saturating concentration of Zn2+. In addition, H+ significantly affected the kinetics of glycinergic mIPSCs and IGly. It is proposed that H+ and/or Zn2+ compete with glycine binding and inhibit the amplitude of glycinergic mIPSCs and IGly. Moreover, binding of H+ induces a global conformational change in GlyR, which closes the GlyR Cl- channel and results in the acceleration of the seeming desensitization of IGly as well as speeding up the decay time constant of glycinergic mIPSCs. However, the deprotonation rate is faster than the unbinding rate of glycine from the GlyR, leading to reactivation of the undesensitized GlyR after washout of agonist and the appearance of a rebound IGly. H+ also modulated the glycine cotransmitter, GABA-activated current (IGABA). Taken together, the results support a "conformational coupling" model for H+ modulation of the GlyR and suggest that H+ may act as a novel modulator for inhibitory neurotransmission in the mammalian spinal cord. (+info)
A 62-year-old female presented with multiple sacral nerve root cysts manifesting as localized unilateral perineal pain. Myelography just after contrast material injection revealed multiple cysts at the sacral level. However, perioperative dye injection showed hardly any flow in the reverse direction. Only the S3 nerve was constricted by hyperplasia of the dura mater, and adhered to the cyst wall. Other nerves were not constricted, nor adhered to cyst walls. The S3 nerve constriction and tight adhesion was the cause of the pain. The one-way flow of spinal fluid from the spinal subarachnoid space to the cysts is probably closely correlated with cyst formation. (+info)
Enhanced noradrenergic transmission in the spontaneously hypertensive rat anococcygeus muscle.
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There is a long-known hyper-responsiveness of vascular adrenergic transmission in the spontaneously hypertensive rat (SHR) that is uncovered specifically in the presence of cocaine and attributed to blockade of the neuronal monoamine transporter. We have now used the rat anococcygeus muscle to investigate whether this phenomenon is generic to sympathetic transmission to smooth muscle rather than a purely vascular phenomenon. We sought the origin of the effect by successively blocking the buffering effects of the neuronal monoamine transporter, prejunctional alpha2-adrenoceptors and NO from nitrergic nerves with desipramine (0.1 microm), rauwolscine (0.01 microm) and l-NG-nitro-arginine (100 microm). In the presence of desipramine, contractile responses to electrical field stimulation but not to noradrenaline (1 nm-100 microm) were greater in SHR than in Wistar-Kyoto (WKY). Neither inhibition of prejunctional alpha2-adrenoceptors nor the blockade of neuronal nitric oxide synthase (nNOS) accounted for the differential enhancement of response in SHR. The enhanced effectiveness of motor neurotransmission in SHR becomes most apparent when all known major buffering mechanisms are removed. When nitrergic responses were isolated pharmacologically (phentolamine 1 microm and guanethidine 30 microm; tone raised with carbachol 50 microm), they were not different between SHR and WKY. Western blots showed that both nNOS and tyrosine hydroxylase are expressed to a similar extent in anococcygeus muscle from SHR and WKY, suggesting similar adrenergic and nitrergic innervations in the two strains. This suggests that enhanced motor transmission is due to increased transmitter release per varicosity rather than there being normal transmission from a greater number of sites. We conclude that there is a generic enhancement of sympathetic transmission in SHR rather than this being a vascular phenomenon. (+info)
The vacuum assisted closure of complex wounds: report of 3 cases.
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Treatment of wounds using conventional methods is frequently limited by inadequate local wound conditions, or by a poor systemic clinical situation. Vacuum system may promote faster granulation tissue formation, remove excessive exudate, increase blood flow in the wound, and attract the borders of the wound to the center, reducing its dimension. We present 3 cases of patients with difficult wounds, due to bad local conditions, or poor clinical situation, in whom we used a vacuum system to prepare the wound for the surgical closure. One patient had a pressure ulcer, another had a diabetic foot ulcer, and the third one had an open foot stump. In the 3 cases a significant improvement of the wound conditions was achieved after 7 to 8 days, allowing successful surgical treatment with flap or skin grafts. (+info)
Sacrococcygeal extraspinal ependymoma: a case report.
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Ependymomas, the common glial tumors of the spinal cord, occur occasionally outside the central nervous system and are called extraspinal ependymomas (ESE). ESE, which are clinically confused with other sacrococcygeal tumors, are rarely seen and found primarily in the sacrococcygeal region during childhood. We report a case of a seven-year-old boy presenting with a midline mass (6 cm diameter) over his coccyx. The solid mass was diagnosed as maxillopapillary type of ependymoma. Clinical and histopathological features of the case are described and literature reviewed. (+info)
Role of persistent sodium and calcium currents in motoneuron firing and spasticity in chronic spinal rats.
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After chronic spinal injury, motoneurons spontaneously develop two persistent inward currents (PICs): a TTX-sensitive persistent sodium current (sodium PIC) and a nimodipine-sensitive persistent calcium current (calcium PIC). In the present paper, we examined how these PICs contributed to motoneuron firing. Adult rats were spinalized at the S(2) sacral level, and after 2 months intracellular recordings were made from sacrocaudal motoneurons in vitro. The PICs and repetitive firing were measured with slow triangular voltage and current ramps, respectively. The sodium PIC was examined after blocking the calcium PIC with nimodipine (20 microM; n = 12). It was always activated subthreshold, and during current ramps in nimodipine, it produced a sodium plateau that assisted in initiating and maintaining firing (self-sustained firing). The sodium PIC oscillated off and on during firing and helped initiate each spike, and near threshold this caused abnormally slow firing (2.82 +/- 1.21 Hz). A low dose of TTX (0.5 microM) blocked the sodium PIC, sodium plateau, and very slow firing prior to affecting the spike itself. The calcium PIC was estimated as the current blocked by nimodipine or current remaining in TTX (2 microM; n = 13). In 59% of motoneurons, the calcium PIC was activated subthreshold to firing and produced a plateau that assisted in initiating and sustaining firing because nimodipine significantly increased the firing threshold current and decreased the self-sustained firing. In the remaining motoneurons (41%), the calcium PIC was activated suprathreshold to firing and during current ramps did not initially affect firing but eventually was activated and caused an acceleration in firing followed by self-sustained firing, which were blocked by nimodipine. The frequency-current (F-I) slope was 3.0 +/- 1.0 Hz/nA before the calcium PIC activation (primary range), 6.3 +/- 3.6 Hz/nA during the calcium PIC onset (secondary range; acceleration), and 2.1 +/- 1.3 Hz/nA with the calcium PIC steadily activated (tertiary range). Nimodipine eliminated the secondary and tertiary ranges, leaving a linear F-I slope of 3.7 +/- 1.0 Hz/nA. A single low-threshold shock to the dorsal root evoked a many-second-long discharge, the counterpart of a muscle spasm in the awake chronic spinal rat. This long-lasting reflex was caused by the motoneuron PICs because when the activation of the voltage-dependent PICs was prevented by hyperpolarization, the same dorsal root stimulation only produced a brief excitatory postsynaptic potential (<1 s). Both the calcium and sodium PIC were involved because nimodipine only partly reduced the reflex and there remained very slow firing mediated by the sodium PIC. (+info)
The superior gluteal artery perforator flap for the closure of sacral sores.
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The purpose of this paper is to report the use of the superior gluteal artery perforator (SGAP) flap in the closure of sacral pressure sores here in Singapore. This fasciocutaneous flap is a refinement of the musculocutaneous flap which is popularly used for the closure of sacral sores. There were minimal complications. This is a reliable flap and gives the option of further reconstructive possibilities should a recurrence occur. (+info)