正常运动模式训练偏瘫患者疗效观察

应用神经促通技术为主综合治疗中风偏瘫病人５６例。治疗前功能Ｉ－Ⅲ阶段，上肢３８例（６７．９％）、下肢３５例（６２．５％）；出院时Ⅳ－Ⅵ阶段，上肢４４例（７８．６％）、下肢５４例（９６．４％），有显著上升＜Ｐ＜０．０１。在后９个月更加强调心理、平衡和协调运动，使正常步态由前９个月的３８．５％上升到９０．６％，偏瘫下态则减少４６．９％，Ｐ均＜０．０１     

Paired pulse facilitation of GABAergic IPSCs in ventral horn neurons in neonatal rat spinal cord

Whole-cell patch-clamp recording of GABAergic inhibitory postsynaptic currents (IPSCs) were made in ventral horn neurons of neonatal rat lumbar spinal cord in slice. In contrast to the hippocampus where paired pulse depression is reported to be observed for GABAergic IPSCs, double pulse stimulation of GABAergic inputs resulted in enhancement in the amplitude of the second IPSC in the spinal ventral horn. The facilitation ratio was decreased during enhanced synaptic transmission by increasing Ca²⁺ concentration in the external recording solution. Baclofen and adenosine, which are reported to depress synaptic transmission by presynaptic mechanisms, depressed IPSCs and increased the facilitation ratio. A postsynaptic manipulation such as application of bicuculline or changing the driving force did not affect the facilitation ratio. These results suggest that paired pulse facilitation of GABAergic IPSCs observed in neonatal rat spinal ventral horn appears to be based upon a mechanism similar to that underlying frequency-dependent facilitation of excitatory synaptic transmission, and is sensitive to presynaptic changes in synaptic strength.     

Mechanisms of tumor necrosis factor-α (TNF-α) hyperalgesia

Activation of immune cells by pathogens induces the release of a variety of proinflammatory cytokines, including IL-1β and TNF-α. Previous studies using IL-1β have demonstrated that this cytokine can alter brain function, resulting in a variety of ‘illness responses’ including increased sleep, decreased food intake, fever, etc. We have recently demonstrated that i.p. IL-1β also produces hyperalgesia and that this hyperalgesia (as well as most illness responses) is mediated via activation of subdiaphragmatic vagal afferents. The present series of studies were designed to provide an initial examination of the generality of proinflammatory cytokine-induced hyperalgesia by examining the effects of i.p. TNF-α on pain responsivity. These studies demonstrate that: (a) i.p. TNF-α produces dose-dependent hyperalgesia as measured by the tailflick test, (b) this hyperalgesia is mediated via the induced release of IL-1β, (c) hyperalgesia is mediated via activation of subdiaphragmatic vagal afferents, and (d) the effects of subdiaphragmatic vagotomy cannot be explained by a generalized depression of neural excitability.     

Waveform analysis suggests that LTP alters the kinetics of synaptic receptor channels

The waveform of an isolated excitatory monosynaptic response reflects the kinetics of transmitter release, the kinetics of synaptic receptor channels and the filtering properties of neurons. Results reported here indicate that long-term potentiation (LTP) causes correlated decreases in the rise time and decay time constant of synaptic potentials recorded in hippocampal slices in which inhibitory currents and post-synaptic spiking were suppressed. Statistical comparisons of waveforms revealed that the distortions introduced by LTP could be corrected by stretching the time-scale of potentiated responses according to the percent change in the decay time constant. The LTP associated decrease in the decay time constant also obtained in slices from immature hippocampus which contain spines and dendrites greatly simplified from those of the adult. Hence, filtering properties of spines are not likely involved in the effect. Paired-pulse facilitation (PPF), a transient increase in transmitter release, did not reproduce the waveform effects of LTP but did cause a slight leftward shift of the response. These results suggest that LTP modifies the kinetics of receptor channels, and that PPF accelerates release.     

Facilitation and disruption of the long-term store of memory with neural excitants

Male hybrid mice (C57BL/6J × DBA/2J) were trained for 2 days in a 6-unit brightness discrimination maze. Beginning 24 hr after training, mice were administered daily injections of strychnine sulphate, Metrazol, d-amphetamine sulphate, caffeine citrate, nicotine alkaloid, or saline for 5 days. Forty-eight hr after the injection series was completed, mice were trained to criterion in the maze. Mice administered strychnine sulphate or Metrazol showed significantly better retention than those administered saline while mice administered d-amphetamine sulphate were significantly poorer. Nicotine alkaloid produced a trend toward facilitation, while caffeine citrate had no effect. The observed facilitation and disruption were not due to enhancement or impairment of learning ability and could not be attributed to effects upon the consolidation process.     

GABA-Induced Synaptic Facilitation at Type B to A Photoreceptor Connections in Hermissenda

Gamma-aminobutyric acid (GABA) is a prevalent neurotransmitter in both vertebrate and invertebrate systems. Here we report that, in addition to its usual inhibitory actions, GABA induced synaptic facilitation at type B to A photoreceptor connections of the marine mollusk Hermissenda when applied transiently to the isolated nervous system. Synaptic facilitation also occurred in response to mechanical stimulation of the GABAergic hair cells, which are normally activated by rotational unconditioned stimuli during behavioral training of the intact animal. This synaptic facilitation represents a novel form of GABA-induced neuromodulation which may contribute to learning-dependent suppression of phototaxis in Hermissenda.     

Effect of short-term intraocular pressure increase on cat retinal ganglion cell activity

By means of microelectrode recordings receptive field properties and flicker responses of cat retinal ganglion cells were studied during elevated intraocular pressure (IOP). At moderate IOP elevation (perfusion pressure, PP, approx. 50 mm Hg), a slight increase in the maintained activity and the neuronal activation obtained from the receptive field (RF)-center or RF-periphery occurred in some of the neurons. At critical perfusion pressure (PP 30-10 mm Hg), the RF-periphery mechanisms were less sensitive to ischemia than the RF-center mechanisms. The spontaneous activity was completely suppressed at an average PP of 36.6 +/- 9.0 mm Hg, the flicker-evoked responses at 17.7 +/- 9.6 mm Hg. At critical perfusion pressures, the stimulus-response latency increased by 20 ms at stimulation frequencies of 10-20 Hz. The critical flicker frequency was already slightly reduced at a PP of 50 mm Hg and decreased further with a further decrease in PP. The threshold values of the intensity function shifted to higher luminance levels when PP was reduced to less than 40 mm Hg, but the slope remained constant. A close interneuronal correlation was found in simultaneous recordings of pairs of ganglion cells during different levels of increased IOP. This finding indicates that the interneuronal response variability to IOP increase appearing in successively recorded neurons was predominantly caused by experimental factors. The main impairment in retinal neuronal function during increased IOP seems to occur proximal to the receptors but distal to the retinal ganglion cell somata.     

d-Amphetamine: disruptive effects on the long-term store of memory and proactive facilitatory effects on learning in inbred mice.

Male, C57BL/6J mice were given two daily trials on an appetitively-motivated successive brightness discrimination maze problem; they then received daily intraperitoneal injections of saline or d-amphetamine for 5 days. When trained again in the maze, mice in all d-amphetamine groups tended to display impaired retention: retention was significantly impaired in the 2.0 mg/kg group. Naive mice were treated exactly as were the pretrained mice except that they received no initial maze training prior to drug treatments. Mice in all naive d-amphetamine groups tended to display enhanced acquisition of the maze problem: acquisition was significantly enhanced in the 1.0 mg/kg groups. These results could not be explained as effects of d-amphetamine on attentional, motivational or other performance factors.     

Relationship Between Different Recovery Curves Representing Rate-Dependent AV Nodal Function in Rabbit Heart

Nodal Function and Recovery Measures. Introduction: The rate-dependent changes in atrioventricular (AV) nodal conduction time show different characteristics depending upon whether the conduction times are plotted against the atrial interval (AA-recovery curve) or His-atrial interval (HA-recovery curve). This study characterizes these differences in the context of controlled changes of nodal functional properties, determines their functional significance, and tests the hypothesis that they are related solely to the nodal conduction time of the last beat (last conduction time) before the premature beat.
Methods and Results; Premature nodal conduction times obtained in isolated rabbit heart preparations under various steady-state and transient conditions were plotted as a function of the corresponding HA and AA intervals, as well as the AA interval corrected for the last conduction time. Under all conditions, the corrected AA-recovery curve was indistinguishable in shape from the HA-recovery curve, and as such reflected similar underlying nodal functional properties. Moreover, a selective increase in the last conduction time, induced in the absence of time-dependent effects associated with the functional property of fatigue, shifted the AA-recovery but not the HA-recovery curve upward with respect to the control curve.
Conclusion: The last conduction time accounts entirely for differences between AA-recovery and HA-recovery curves that otherwise reflect the same underlying nodal functional state. Thus, a consistent assessment of rate-dependent changes in nodal function can be achieved with either measure of recovery time.     

Reversal potential of the end-plate currents and potassium feedback at the neuromuscular synapse

The experiments were carried out at the neuromuscular junction of the frog. E_rev of epc was estimated by two methods—extrapolation and interpolation. In K⁺- enriched solution E_rev obtained by linear extrapolation from high-mp region changed according to the Takeuchi equation. The behavior of E_rev obtained by interpolation was better described by the Goldman-Hodgkin-Katz equation. Under the change of the nerve stimulation frequency from 0.5 to 50/sec, the positive shift of E_rev estimated by both methods was observed. This indicates K⁺ accumulation in active synaptic segments during activity. The elimination of the potassium current of epc by clamping of mp at the ? 130 mV level resulted in the lowering of facilitation under paired nerve stimulation (20 msec interval) and in the decrease of the rate of facilitation under 50/sec frequency stimulation. The data support the presence of antidromic K⁺ action in the neuromuscular synapse.