Topic: spike timing-dependent long-term depression

During development, critical periods of synaptic plasticity facilitate the reordering and refinement of neural connections, allowing the definitive synaptic circuits responsible for correct adult physiology to be established. The L4-L2/3 synapses in the somatosensory cortex (S1) exhibit a presynaptic form of spike timing-dependent long-term depression (t-LTD) that probably fulfills a role in synaptic refinement. This t-LTD persists until the 4rd postnatal week in mice, disappearing thereafter. When we investigated the mechanisms underlying this maturation-related loss of t-LTD in mouse slices,

The entorhinal cortex (EC) connects to the hippocampus sending different information from cortical areas that is first processed at the dentate gyrus (DG) including spatial, limbic, and sensory and information. Excitatory afferents from lateral (LPP) and medial (MPP) perforant pathways of the EC connecting to granule cells (GC) of the DG play a role in memory encoding and information processing. LPP- and MPP-GC synapses have distinct electrophysiological properties, and these differences potentially affecting the functional processing of information. However, the plasticity of these synapses i

N-methyl-D-aspartate receptors (NMDAR) are heteromeric, cation-selective, ligand- and voltage-gated ion channels with critical roles in both excitatory synaptic transmission and in the induction of many forms of synaptic plasticity, the process by which synaptic weight is dynamically modified in an activity-dependent manner. The principal aim of this project is to resolve the long-standing debate surrounding NMDAR expression and function in the presynaptic axonal compartment, specifically in the induction of spike timing-dependent long-term depression (tLTD) at the layer 4 to layer 2/3 synapse