Hebbian and Anti-Hebbian Spike-Timing-Dependent Plasticity of Human Cortico-Cortical Connections

Information-Based Approaches of Noninvasive Transcranial Brain Stimulation

“…These studies overall demonstrate that ccPAS can induce LTP-(but also long-term depression (LTD)) -like effects [71] which are timing-, direction-and state-dependent. In addition, the recent use of ccPAS in combination with EEG [71,72] and neuroimaging techniques [73] has provided further evidence for induced STDP mechanisms, by showing causal and directional impact of the pre-synaptic over the post-synaptic target region, following the temporal profile of Hebbian plasticity [10]. Moreover, these studies have provided information about the impact of ccPAS on oscillatory coherence across the network [72] and on the spatial properties of the NTBS manipulation, confirming the specificity of enhanced connectivity between the stimulated nodes.…”

Applications of TMS to Study Brain Connectivity

“…Conversely, when PPC stimulation follows M1 by 5ms there is a trend toward a long-lasting decrease in M1 excitability (Koch et al 2013). Importantly, the direction of these plasticity aftereffects was also dependent on the coil orientation over M1.…”

“…However, there is also evidence in humans of STDP-like plasticity that elicits changes in corticospinal excitability that follows anti-Hebbian plasticity rules, where presynaptic stimulation before postsynaptic elicits inhibition, and the reverse elicits facilitation (Koch et al 2013).…”

Inefficient Neural Self-Stabilization: A theory of spontaneous resolutions and recurrent relapses in psychosis

“…Several studies of hallucinating individuals have reported an elevated level of neural activity involving sensory cortices 162,163 2. Disturbances in the normal constraints on associative plasticity: A cardinal feature of Hebbian plasticity is the dependence on the temporal order of coincidental neuronal activation 164 ; under certain circumstances, this temporal window can be prolonged, increasing the probability of formation of coincidences. For example, dopamine and substances inducing an excess release of dopamine could potentiate this mechanism 165 .…”