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Spike-timing-dependent plasticity in primate corticospinal connections induced during free behavior.

ABSTRACT: Motor learning and functional recovery from brain damage involve changes in the strength of synaptic connections between neurons. Relevant in vivo evidence on the underlying cellular mechanisms remains limited and indirect. We found that the strength of neural connections between motor cortex and spinal cord in monkeys can be modified with an autonomous recurrent neural interface that delivers electrical stimuli in the spinal cord triggered by action potentials of corticospinal cells during free behavior. The activity-dependent stimulation modified the strength of the terminal connections of single corticomotoneuronal cells, consistent with a bidirectional spike-timing-dependent plasticity rule previously derived from in vitro experiments. For some cells, the changes lasted for days after the end of conditioning, but most effects eventually reverted to preconditioning levels. These results provide direct evidence of corticospinal synaptic plasticity in vivo at the level of single neurons induced by normal firing patterns during free behavior.

SUBMITTER: Nishimura Y

PROVIDER: S-EPMC4079851 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

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Spike-timing-dependent plasticity in primate corticospinal connections induced during free behavior.

Nishimura Yukio Y Perlmutter Steve I SI Eaton Ryan W RW Fetz Eberhard E EE

Neuron 20131107 5

Motor learning and functional recovery from brain damage involve changes in the strength of synaptic connections between neurons. Relevant in vivo evidence on the underlying cellular mechanisms remains limited and indirect. We found that the strength of neural connections between motor cortex and spinal cord in monkeys can be modified with an autonomous recurrent neural interface that delivers electrical stimuli in the spinal cord triggered by action potentials of corticospinal cells during free ...[more]

PMID: 24210907

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Project description:Classic in vitro studies have described spike-timing-dependent plasticity (STDP) at a synapse: the connection from neuron A to neuron B is strengthened (or weakened) when A fires before (or after) B within an optimal time window. Accordingly, more recent in vivo works have demonstrated behavioral effects consistent with an STDP mechanism; however, many relied on single-unit recordings. The ability to modify cortical connections becomes useful in the context of injury, when connectivity and associated behavior are compromised. To avoid the need for long-term, stable isolation of single units, one could control timed activation of two cortical sites with paired electrical stimulation. We tested the hypothesis that STDP could be induced via prolonged paired stimulation as quantified by cortical evoked potentials (EPs) in the sensorimotor cortex of awake, behaving monkeys. Paired simulation between two interconnected sites produced robust effects in EPs consistent with STDP, but only at 2/15 tested pairs. The stimulation protocol often produced increases in global network excitability or depression of the conditioned pair. Together, these results suggest that paired stimulation in vivo is a viable method to induce STDP between cortical populations, but that factors beyond activation timing must be considered to produce conditioning effects.SIGNIFICANCE STATEMENT Plasticity of neural connections is important for development, learning, memory, and recovery from injury. Cellular mechanisms underlying spike-timing-dependent plasticity have been studied extensively in vitro Recent in vivo work has demonstrated results consistent with the previously defined cellular mechanisms; however, the output measure in these studies was typically an indirect assessment of plasticity at the neural level. Here, we show direct plasticity in recordings of neuronal populations in awake, behaving nonhuman primates induced by paired electrical stimulation. In contrast to in vitro studies, we found that plastic effects were only produced between specific cortical areas. These findings suggest that similar mechanisms drive plasticity in vitro and in vivo, but that cortical architecture may contribute significantly to site-dependent effects.

Project description:Rhythmic activity has been associated with a wide range of cognitive processes including the encoding of sensory information, navigation, the transfer of information and others. Rhythmic activity in the brain has also been suggested to be used for multiplexing information. Multiplexing is the ability to transmit more than one signal via the same channel. Here we focus on frequency division multiplexing, in which different signals are transmitted in different frequency bands. Recent work showed that spike-timing-dependent plasticity (STDP) can facilitate the transfer of rhythmic activity downstream the information processing pathway. However, STDP has also been known to generate strong winner-take-all like competition between subgroups of correlated synaptic inputs. This competition between different rhythmicity channels, induced by STDP, may prevent the multiplexing of information. Thus, raising doubts whether STDP is consistent with the idea of multiplexing. This study explores whether STDP can facilitate the multiplexing of information across multiple frequency channels, and if so, under what conditions. We address this question in a modelling study, investigating the STDP dynamics of two populations synapsing downstream onto the same neuron in a feed-forward manner. Each population was assumed to exhibit rhythmic activity, albeit in a different frequency band. Our theory reveals that the winner-take-all like competitions between the two populations is limited, in the sense that different rhythmic populations will not necessarily fully suppress each other. Furthermore, we found that for a wide range of parameters, the network converged to a solution in which the downstream neuron responded to both rhythms. Yet, the synaptic weights themselves did not converge to a fixed point, rather remained dynamic. These findings imply that STDP can support the multiplexing of rhythmic information, and demonstrate how functionality (multiplexing of information) can be retained in the face of continuous remodeling of all the synaptic weights. The constraints on the types of STDP rules that can support multiplexing provide a natural test for our theory.

Dataset Information

Spike-timing-dependent plasticity in primate corticospinal connections induced during free behavior.

Publications

Spike-timing-dependent plasticity in primate corticospinal connections induced during free behavior.

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