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Content available remote Intracortical mechanisms for the recruitment of motor cortex neurons
100%
EN
Neurons project out of motor cortex to the spinal cord and to other targets. Not all projection neurons recruit in the same way during behavior, but instead recruitment patterns depend on the projection target of the neurons. The problem is to understand how neurons projecting to different targets are recruited selectively. We have investigated possible mechanisms for the recruitment of motor cortex neurons with electrophysiological approaches in anesthetized cats. To determine if neurons projecting out of motor cortex to different targets have selective input connectivity from extrinsic sources we electrically stimulated corticocortical, callosal and thalamocortical pathways. Subthreshold effects of input pathways were detected by monitoring latency variations of antidromic responses. Itracortical connections to identified output neurons were evaluated by cross-correlation and a new variation of the antidromic latency method. Output neurons in different layers along single electrode tracks usually had different inputs from extrinsic sources. Neurons in close proximity were most likely to share the same inputs, especially when they projected axons to the same target. These results support the conclusion that combinations of inputs from extrinsic sources could selectively recruit efferent neurons from separate cortical layers or from within groups of nearby neurons, according to the target of their axonal projections. In contrast, the data on intracortical connectivity suggest that common drive causes a more synchronous activation of nearby cortical neurons.
EN
Horizontally-oriented intracortical connections have been proposed to serve as a substrate for plastic reorganizations of adult motor cortex. N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) of synaptic efficacy is a candidate mechanism of these reorganizations in mammalian species ranking from rats to humans. The acquisition of a motor skill is accompanied by increased strength of synaptic connections within adult rat primary motor cortex, most likely due to LTP-like mechanisms.
3
Content available remote Synaptic plasticity of local connections in rat motor cortex
80%
EN
This paper reviews studies that investigated mechanisms of the induction of long-term synaptic efficacy increase in local horizontal connections in slices of adult rat motor cortex. Long-term potentiation (LTP) could be induced by electrical stimulation of afferents using theta burst stimulation (TBS) conditionally, when synaptic inhibition was transiently blocked by focal application of GABAA receptor antagonist. Robust, long-lasting enhancement of synaptic transmission in horizontal connections was induced by brief application of the potassium channel blocker, tetraethylammonium (TEA, 25 mM), to the incubation medium. This TEA-LTP could be blocked by nifedipine, a voltage-dependent calcium channel blocker. A transient exposure of slices to elevated extracellular calcium (5 mM) resulted in a long-lasting enhancement of responses, termed Ca-LTP, which could be blocked by the antagonist of NMDA receptors, APV. The induction of both TEA-LTP and Ca-LTP, could be prevented by inhibitors of the extracellular signal regulated kinase (ERK) cascade U0126 and PD 98059. A transient activation of the ERK, 15 min after application of TEA or elevated [Ca2+], was demonstrated using immunofluorescence. Both forms of plasticity could also be prevented by the inhibitor of cAMP-dependent protein kinases (PKA), Rp-cAMPS. These studies indicate the involvement of the ERK and PKA signaling mechanisms in synaptic plasticity of the motor cortex in vitro. Since LTP in horizontal connections of the motor cortex has previously been shown to be related to the acquisition of a motor skill, it is suggested that the ERK and PKA signaling pathways may be involved in motor learning.
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