, 1998), which is a key kinase downstream of NMDA receptor-mediated Ca2+ influx in pyramidal neurons. However, the evidence that spines are essential for LTP is purely circumstantial, and the dendrites of many interneurons are not completely smooth. As for the essential role of CaMKIIα, this does not rule out closely related kinases or alternative biochemical cascades, which sustain LTP induction in pyramidal neurons in early postnatal

hippocampus (Yasuda et al., 2003) and in dentate granule cells of mice in which CaMKIIα autophosphorylation is prevented (Cooke et al., 2006). More direct evidence see more that excitatory synapses on interneurons could be persistently altered in a use-dependent manner came from targeted recordings in acute brain slices (Ouardouz and Lacaille, 1995; McMahon and Kauer, 1997; Cowan et al., 1998; Mahanty and Sah, 1998; Alle et al., 2001). Restricting attention to subsets of interneurons, consistent patterns of plasticity are beginning to emerge. Thus, LTP can be elicited in a subset of interneurons in stratum oriens (Ouardouz and Lacaille, 1995; Perez et al., 2001; Lamsa et al., 2007b; Jia et al., selleck inhibitor 2010), which can be recruited by axon collaterals of local pyramidal neurons and contribute

to feedback inhibition. They include bistratified, basket, and axo-axonic cells, as well as oriens-lacunosum/moleculare (O-LM) cells. Although LTP in many of these cells can be induced by pairing presynaptic theta-burst stimulation with postsynaptic depolarization (Perez et al., 2001; Lapointe

et al., 2004), it can also be triggered when the postsynaptic neuron is kept at resting membrane potential or even hyperpolarized (Lamsa et al., 2007b; Oren et al., 2009). Both induction Mannose-binding protein-associated serine protease protocols probably converge on a common cascade that depends on postsynaptic Ca2+ signaling and mGluR1 receptors but not NMDA receptors. Roles have also been proposed for TRP channels, Src/ERK, and intracellular Ca2+ release (Topolnik et al., 2006). LTP can also be induced by applying a group I mGluR agonist paired with hyperpolarization (Le Duigou and Kullmann, 2011). The preferential induction at relatively negative potentials is consistent with a role for inward rectifying, Ca2+-permeable AMPA receptors (Oren et al., 2009). In keeping with an induction role for such receptors, excitatory postsynaptic currents recorded in cells exhibiting this form of plasticity show strong inward rectification and express low levels of GluA2 (Lamsa et al., 2007b; Szabo et al., 2012). Because a requirement for postsynaptic hyperpolarization is diametrically opposite to the conventional view of NMDA receptor-dependent LTP as a substrate for Hebb’s postulate (Brown et al.