Journal of neurophysiology
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Randomized Controlled Trial Clinical Trial
Influence of instruction, prediction, and afferent sensory information on the postural organization of step initiation.
1. Our previous study showed that two distinct postural modifications occurred when subjects were instructed to step, rather than maintain stance, in response to a backward surface translation: 1) the automatic postural responses to the surfaces perturbation were reduced in magnitude and 2) the anticipatory postural adjustments promoting foot-off were shortened in duration. This study investigates the extent to which task instruction, prediction of perturbation velocity, and afferent sensory information related to perturbation velocity are responsible for these postural modification. 2. ⋯ We conclude that the CNS uses prediction of perturbation velocity to modify the excitability of early automatic postural responses when the postural goal changes. In contrast, actual afferent velocity information can be used to modify the duration of the anticipatory postural adjustments for a voluntary step in response to perturbation. Thus the CNS utilizes feed-forward prediction to modify peripherally triggered postural responses, and utilizes immediate afferent information to modify the centrally initiated postural adjustments associated with voluntary movement.
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1. One hundred twenty neurons were recorded in the central mesencephalic reticular formation (cMRF) of four rhesus monkeys, trained to make visually guided and targeted saccadic eye movements. Eye movements were recorded with the head fixed, using electrooculography (EOG) or subconjunctival scleral search coils. ⋯ These findings suggest that the buildup discharge of cMRF neurons occurs early enough before saccades to contribute to saccade triggering. The peak discharge, however, occurs with or after the burst in the SC, suggesting that this portion of the discharge serves a function other than saccade triggering. 7. The number of spikes in bursts associated with eye movement was correlated with saccade parameters.
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Comparative Study
Shared calcium signaling pathways in the induction of long-term potentiation and synaptic disinhibition in CA1 pyramidal cell dendrites.
1. Calcium signaling pathways were examined in the induction of long-term synaptic disinhibition following tetanization. Effects of tetanization on gamma-aminobutyric acid-A (GABAA receptor-mediated inhibitory responses were measured and compared with excitatory responses under experimental conditions previously used for examining induction mechanisms of N-methyl-D-aspartate (NMDA)-dependent long-term potentiation (LTP). ⋯ In recordings in which the intracellular pipette was preloaded with cypermethrin, a potent and selective inhibitor of phosphatase 2B, respective long-term changes of synaptic transmission (increases of excitation, decreases of synaptic inhibition) were prevented. At PT 40, EPSP peak amplitudes were 98 +/- 6%, EPSCs were 105 +/- 10%, IPSPs were 99 +/- 5%, IPSCs were 104 +/- 7%, synaptic GABAA conductances were 97 +/- 6% and iontophoretic GABAA conductances were 113 +/- 18% over pretetanus controls in cypermethrin-containing recordings. 6. In conclusion, the data presented demonstrate shared cellular pathways in the induction of both LTP and long-term synaptic disinhibition in apical dendrites of CA1 pyramidal cells after tetanization of the Schaffer collaterals.
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1. Spontaneous inhibitory synaptic currents (sIPSCs) were studied with whole cell voltage-clamp recordings from 131 pyramidal cells in adult rat somatosensory cortical slices. Neurons were intracellulary labeled with biocytin and classified as supragranular (SG, layers 2-3), layer IV (IV), or infragranular (IG, layer V) on the basis of the laminar localization of their somata. ⋯ Activation of AMPA receptors on inhibitory interneurons accounts for only a small proportion of the GABAA receptor-mediated events. Judging from the distribution of mIPSC frequencies in neurons of different laminae, there is a relatively uniform distribution of inhibitory synapses throughout the cortex. Tonic activation of GABAA receptors on neocortical pyramidal neurons generates an increase in resting membrane conductance that may play an important role in vivo by preventing the development of hyperexcitability, modulating excitatory synaptic events, and controlling the rate and patterns of spike discharge.