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Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex.

ABSTRACT: Many cortical synapses exhibit spike timing-dependent plasticity (STDP) in which the precise timing of presynaptic and postsynaptic spikes induces synaptic strengthening [long-term potentiation (LTP)] or weakening [long-term depression (LTD)]. Standard models posit a single, postsynaptic, NMDA receptor-based coincidence detector for LTP and LTD components of STDP. We show instead that STDP at layer 4 to layer 2/3 synapses in somatosensory (S1) cortex involves separate calcium sources and coincidence detection mechanisms for LTP and LTD. LTP showed classical NMDA receptor dependence. LTD was independent of postsynaptic NMDA receptors and instead required group I metabotropic glutamate receptors and calcium from voltage-sensitive channels and IP3 receptor-gated stores. Downstream of postsynaptic calcium, LTD required retrograde endocannabinoid signaling, leading to presynaptic LTD expression, and also required activation of apparently presynaptic NMDA receptors. These LTP and LTD mechanisms detected firing coincidence on approximately 25 and approximately 125 ms time scales, respectively, and combined to implement the overall STDP rule. These findings indicate that STDP is not a unitary process and suggest that endocannabinoid-dependent LTD may be relevant to cortical map plasticity.

SUBMITTER: Bender VA

PROVIDER: S-EPMC3071735 | biostudies-literature | 2006 Apr

REPOSITORIES: biostudies-literature

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Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex.

Bender Vanessa A VA Bender Kevin J KJ Brasier Daniel J DJ Feldman Daniel E DE

The Journal of neuroscience : the official journal of the Society for Neuroscience 20060401 16

Many cortical synapses exhibit spike timing-dependent plasticity (STDP) in which the precise timing of presynaptic and postsynaptic spikes induces synaptic strengthening [long-term potentiation (LTP)] or weakening [long-term depression (LTD)]. Standard models posit a single, postsynaptic, NMDA receptor-based coincidence detector for LTP and LTD components of STDP. We show instead that STDP at layer 4 to layer 2/3 synapses in somatosensory (S1) cortex involves separate calcium sources and coincid ...[more]

PMID: 16624937

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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

Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex.

Publications

Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex.

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