Computer-generated stimulus patterns were used to study the response of cat skeletal muscle to nerve signals of changing impulse rates. Isometric tension responses were recorded. This method of testing demonstrated that muscle introduces alterations into dynamic nerve signals which are not obvious when tested with only a single pulse or even with uniform tetanic trains of stimuli. Within the range of physiological response characteristics, muscle introduces large lags in the response. The importance of such lags in the stretch reflex and other feedback systems is emphasized. Muscle also shows less isometric response amplitude for rapid cyclic inputs than for inputs of nerve impulses which change slowly in rate. Graphs are presented which illustrate the differences in amplitude and lag effects introduced by muscle when dealing with pulse rate signals varying at different cyclic frequencies. feedback analysis; pulse rate modulation; lag; reflex; isometric response; muscle dynamics; movement Submitted on January 9, 1964

SUMMARY1. Spike frequency adaptation was studied in large neurones of the marine molluscs Archidoris montereyensis and Anisodoris nobilis. These cells respond to a current step with a rapid rise in spike frequency followed by a gradual decline to a new steady level.2. An exponentially declining current, I., was measured when the cell was voltage clamped following an adapting spike train. The initial amplitude of this current depended on the preceding number of spikes and on the voltage to which the cell was clamped. A reversal potential (V.) for this current was obtained by clamping to various potentials following a spike train. The time constant (Tj) of decay of the current was dependent upon the clamping potential.3. Clamping the membrane potential to a constant test level from various initial levels initiates an exponentially decaying current of similar time constant. The voltage dependence of the steady-state conductance (g5a5(V, co)) associated with this current was determined using this technique.4. Equations for neural repetitive firing (Connor & Stevens, 1971c) were modified by the addition of a term describing these slow membrane currents:id(=gt a)(V t)( -Vs),The solution to the modified equation was in good agreement with the spike frequency adaptation observed in these cells.

The sections in this article are: Representation of Muscle Properties Dimensions Used Models Real Motor Systems Summary Properties of the Contractile Unit Passive Mechanical Contributions Response to Neural Signals Interaction Between Neural and Other Inputs Functional Variations Summary Multiple Units of Muscle The Unit of Muscle Function Relationships in Multiunit Function Summary Some Measures of Muscle Function Summary Motor Functions of Muscles Final Summary Epilogue Appendix Units for Measure of Motor Function

SummaryExposure to ethanol during development triggers neuronal cell death and this is thought to play a central role in the pathophysiology of fetal alcohol spectrum disorder (FASD). Studies suggest that ethanol-induced neurodegeneration during the period of synaptogenesis results from widespread potentiation of GABA A receptors and inhibition of NMDA receptors throughout the brain, with neocortical layer II being particularly sensitive. Here, we tested whether ethanol modulates the function of these receptors during this developmental period using patch-clamp electrophysiological and Ca 2+ imaging techniques in acute slices from postnatal day 7-9 rats. We focused on pyramidal neurons in layer II of the parietal cortex (with layer III as a control). Ethanol (70 mM) increased spontaneous action potential-dependent GABA release in layer II (but not layer III) neurons without affecting postsynaptic GABA A receptors. Protein and mRNA expression for both the Cl − importer, NKCC1, and the Cl − exporter KCC2, were detected in layer II/III neurons. Perforated-patch experiments demonstrated that E Cl − is shifted to the right of E m ; activation of GABA A receptors with muscimol depolarized E m , decreased action potential firing, and minimally increased [Ca 2+ ] i . However, the ethanol-induced increase of GABAergic transmission did not affect neuronal excitability. Ethanol had no effect on currents exogenously evoked by NMDA or AMPA receptor-mediated spontaneous excitatory postsynaptic currents. Acute application of ethanol in the absence of receptor antagonists minimally increased [Ca 2+ ] i . These findings are inconsistent with the excessive inhibition model of ethanol-induced neurodegeneration, supporting the view that ethanol damages developing neurons via more complex mechanisms that vary among specific neuronal populations.

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