The knowledge that excitatory synapses on aspiny hippocampal interneurons can develop genuine forms of activity-dependent remodeling, independently from the surrounding network of principal cells, is a relatively new concept. Cumulative evidence has now unequivocally demonstrated that, despite the absence of specialized postsynaptic spines that serve as compartmentalized structure for intracellular signaling in principal cell plasticity, excitatory inputs onto interneurons can undergo forms of synaptic plasticity that are induced and expressed autonomously from principal cells. Yet, the rules for induction and expression of interneuron plasticity are much more heterogeneous than in principal neurons. Long-term plasticity in interneurons is not necessarily dependent upon postsynaptic activation of NMDA receptors nor relies on the same postsynaptic membrane potential requirements as principal cells. Plasticity in interneurons rather requires activation of Ca2+-permeable AMPA receptors and/or metabotropic glutamate receptors and is triggered by postsynaptic hyperpolarization. In this review we will outline these distinct features of interneuron plasticity and identify potential critical candidate molecules that might be important for sustaining long-lasting changes in synaptic strength at excitatory inputs onto interneurons. This article is part of a Special Issue entitled 'Synaptic Plasticity & Interneurons'.
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience