Inhibitory Plasticity Dictates the Sign of Plasticity at Excitatory Synapses

By Lang Wang, A. Maffei. 2014

84 citations recorded by the source corpus.

The broad connectivity of inhibitory interneurons and the capacity of inhibitory synapses to be plastic make them ideal regulators of the level of excitability of many neurons simultaneously. Whether inhibitory synaptic plasticity may also contribute to the selective regulation of single neurons and local microcircuits activity has not been investigated. Here we demonstrate that in rat primary visual cortex inhibitory synaptic plasticity is connection specific and depends on the activation of postsynaptic GABAB–Gi/o protein signaling. Through the activation of this intracellular signaling pathway, inhibitory plasticity can alter the state of a single postsynaptic neuron and directly affect the induction of plasticity at its glutamatergic inputs. This interaction is modulated by sensory experience. Our data demonstrate that in recurrent circuits, excitatory and inhibitory forms of synaptic plasticity are not integrated as independent events, but interact to cooperatively drive the activity-dependent rewiring of local microcircuits.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

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Citations in the corpus

The temporal paradox of Hebbian learning and homeostatic plasticity (2017, background): “For instance, there are cases in which induction of ISP alone can flip the sign of subsequent plasticity at excitatory synapses [89].”
Receptive field formation by interacting excitatory and inhibitory synaptic plasticity (2016, background): “This control of neuronal output by the interplay of excitation and inhibition suggests that through the establishment of E/I balance inhibitory synaptic plasticity can in turn exert an influence on excitatory plasticity (Wang & Maffei, 2014).”
A computational model of pattern separation efficiency in the dentate gyrus with implications in schizophrenia (2015, background): “Such improvement helps to explore the role of inhibitory synaptic plasticity and its role in disorders related to the DG dysfunctions (Flores and Méndez, 2014; Griﬀen and Maﬀei, 2014; Wang and Maﬀei, 2014).”