PubMed · 7978611
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R O Bischof, G Buchalter. 1994. TAC Gel defined.. https://doi.org/10.1016/s0196-0644(94)70257-8
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1. The effects of perchlorate ions on intramembrane charge movements were examined under different conditions of ryanodine receptor (RyR) modification in intact voltage-clamped amphibian skeletal muscle fibres studied in the gluconate-containing solutions previously reported to emphasize the features of q gamma at the expense of those of the q beta charge. 2. The introduction of graded increases in perchlorate concentration to the experimental solutions selectively shifted the threshold of appearance of the q gamma 'hump' currents to more negative test potentials at which they actually appeared in the absence of prior q beta transients at perchlorate concentrations of 4.0-8.0 mM. Such findings suggested that the delayed (q gamma) transitions can take place independently of any previous exponential (q beta) decay. 3. These kinetic effects were accompanied by hyperpolarizing shifts in the transition potentials (V*) of the steady-state voltage dependences of either the overall or the isolated q gamma charge. These shifts were graded with concentration and reached their maximum effects at 4.0-8.0 mM perchlorate. However, both the total charge (Qmax) and the steepness factor (k) remained conserved at values consistent with a system that included significant contributions from the steeply voltage-sensitive q gamma component (overall charge: Qmax approximately 19-21 nC microF-1, k approximately 7-9 mV; q gamma component alone: Qmax approximately 10-12 nC microF-1, k approximately 4-6 mV). This contrasts with earlier reports on the effects of perchlorate in fibres that were studied in sulphate- or methanesulphonate-containing extracellular solutions. 4. Perchlorate (8.0 mM) restored the 'hump' waveform associated with q gamma charge movements that had previously been obliterated by the prior application of fully effective (0.1 mM) concentrations of either ryanodine or daunorubicin. 5. Perchlorate similarly reversed the positive shift in the transition potential of the q gamma component that was brought about by such RyR modification (from V* approximately -40 mV back to V* approximately -60 mV). In contrast, the values of either Qmax (overall charge, 19-21 nC microF-1; q gamma component, 10-13 nC microF-1) or k (overall charge, 7-9 mV; q gamma component, 4-6 mV) remained conserved through all these experimental manoeuvres. 6. The inclusion of perchlorate also reversed the action of 2 mM tetracaine and restored delayed q gamma transients to an extent that was graded with concentration (0.5-8.0 mM perchlorate). There was an accompanying recovery of the steeply voltage-dependent steady-state (q gamma) component consistent with a competitive interaction between these agents upon the q gamma intramembrane charge. 7. The present findings suggest that perchlorate exerts a specific action upon the q gamma charge in independent transitions that are driven by the tubular membrane field. Its interactions with the known RyR inhibitors that nevertheless conserve both the charge and its voltage sensitivity suggest a primary action upon the RyR that in turn exerts reciprocal actions upon the voltage sensor.
The striatum is involved in memory consolidation; also involved in this process is one of its two major efferent targets, namely, the substantia nigra. It is not clear, however, if the other target, the globus pallidus, participates in storage and/or performance of learned information. To examine this problem, male Wistar rats were trained in an inhibitory avoidance task and tested for retention 24 h afterward. Independent groups were infused, unilaterally, with 2% lidocaine in the pallidus either 2 min after training or 2 min before testing. No disturbances of memory were detected with posttraining infusion, but a significant deficit in retention was observed as a consequence of pretest infusion. Infusion of isotonic saline into the globus pallidus, or of lidocaine before testing into the parietal cortex, after training into the ventral thalamic nucleus, and both before training and testing into this thalamic nucleus were without effect. Taken together, the data indicate that unilateral inactivation of the GP interferes with retrieval of information derived from inhibitory avoidance training, but not with the early stages of memory consolidation of this task, and other work indicates that the pallidus may be involved in a late phase of this process.
The effect of intravenous administration of the local anaesthetic lidocaine (1, 3 or 5 mg/kg) on the responsiveness and size of the cutaneous receptive fields of 18 lumbar dorsal horn neurons was examined in intact urethane-anaesthetized rats. Lidocaine induced expansion of the receptive field in the majority of neurons examined, particularly after the two higher doses. The expansion occurred usually within 10 min after lidocaine injection and the effect was reversible. Lidocaine also altered the responsiveness of dorsal horn neurons to peripheral mechanical stimulation. The responses of wide-dynamic-range neurons to noxious pinch were usually inhibited by lidocaine. However, some low-threshold neurons started to react to noxious mechanical stimulation and some high-threshold neurons started to respond to innocuous brushing after lidocaine injection. The present results show that moderate doses of systemic lidocaine induce complex changes in the excitability of dorsal horn neurons, including an increase in the size of the receptive field and altered response characteristics to mechanical stimulation.