Between-hand coupling during response inhibition

Response inhibition reflects the process of terminating inappropriate preplanned or ongoing movements. When one hand is cued to stop after preparing a bimanual response (Partial trial), there is a substantial delay on the responding side. This delay is termed the interference effect and identifies a constraint that limits selective response inhibition. γ-Aminobutyric acid (GABA)-mediated networks within primary motor cortex (M1) may have distinct roles during response inhibition. In this study we examined whether the interference effect is the consequence of between-hand “coupling” into a unitary response and whether this is reflected in GABAergic intracortical inhibition within M1. Eighteen healthy right-handed participants performed a bimanual synchronous and asynchronous anticipatory response inhibition task. Electromyographic recordings were obtained from the first dorsal interosseous muscle bilaterally. Motor evoked potentials were elicited by single- and paired-pulse transcranial magnetic stimulation over right M1. As expected, Go trial performance was better with the synchronous compared with the asynchronous version of the task. Paradoxically, response delays during Partial trials were longer with the synchronous compared with the asynchronous task. Although task difficulty did not modulate GABAergic intracortical inhibition, there was a trend for between-hand coupling on asynchronous trials to be associated with greater GABAB receptor-mediated inhibition and lesser recruitment of GABAA receptor-mediated inhibition. The novel findings indicate that the interference effect is in part a consequence of between-hand coupling into a unitary response during movement preparation. The ability to respond independently with the two hands may rely on modulation of distinct inhibitory processes. NEW & NOTEWORTHY The temporal dynamics of an anticipated response task were manipulated to effect the difficulty of behavioral stopping and the underlying effects on motor neurophysiology. There were large response delays during trials where a subcomponent of an upcoming bimanual response was cued to stop in conditions where the anticipated action of the hands were synchronous, but not when asynchronous. Response delays reflected the integration of actions of both hands into a unitary response.

Mechanism for Increased Hippocampal Synaptic Strength Following Differential Experience

Exposure to novel environments or behavioral training is associated with increased strength at hippocampal synapses. The present study employed quantal analysis techniques to examine the mechanism supporting changes in synaptic transmission that occur following differential behavioral experience. Measures of CA1 synaptic strength were obtained from hippocampal slices of rats exposed to novel environments or maintained in individual cages. The input/output (I/O) curve of extracellularly recorded population excitatory postsynaptic potentials (EPSPs) increased for animals exposed to enrichment. The amplitude of the synaptic response of the field potential was related to the fiber potential amplitude and the paired-pulse ratio, however, these measures were not altered by differential experience. Estimates of biophysical parameters of transmission were determined for intracellularly recorded unitary responses of CA1 pyramidal cells. Enrichment was associated with an increase in the mean unitary synaptic response, an increase in quantal size, and a trend for decreased input resistance and reduction in the stimulation threshold to elicit a unitary response. Paired-pulse facilitation, the percent of response failures, coefficient of variance, and estimates of quantal content were not altered by experience but correlated well with the mean unitary response amplitude. The results suggest that baseline synaptic strength is determined, to a large extent, by presynaptic release mechanisms. However, increased synaptic transmission following environmental enrichment is likely due to an increase in the number or efficacy of receptors at some synapses and the emergence of functional synaptic contacts between previously unconnected CA3 and CA1 cells.