Binocular input coincidence mediates critical period plasticity in the mouse primary visual cortex.

Classical studies on the development of ocular dominance (OD) organization in primary visual cortex (V1) have revealed a postnatal critical period (CP), during which visual inputs between the two eyes are most effective in shaping cortical circuits through synaptic competition. A brief closure of one eye during CP caused a pronounced shift of response preference of V1 neurons toward the open eye, a form of CP plasticity in the developing V1. However, it remains unclear what particular property of binocular inputs during CP is responsible for mediating this experience-dependent OD plasticity.

Synaptic mechanisms of direction selectivity in primary auditory cortex.

Frequency modulation (FM) is a prominent feature in animal vocalization and human speech. Although many neurons in the auditory cortex are known to be selective for FM direction, the synaptic mechanisms underlying this selectivity are not well understood. Previous studies of both visual and auditory neurons have suggested two general mechanisms for direction selectivity: (1) differential delays of excitatory inputs across the spatial/spectral receptive field and (2) spatial/spectral offset between excitatory and inhibitory inputs.

Coincidence detection of synaptic inputs is facilitated at the distal dendrites after long-term potentiation induction.

Two major aspects of dendritic integration, coincidence detection and temporal integration, depend critically on the spatial and temporal properties of the dendritic summation of synaptic inputs. Neuronal activity capable of inducing synaptic long-term potentiation (LTP) leads to increased linearity of the spatial summation of synchronous EPSPs. Whether such activity can also modulate the temporal summation of EPSPs is unknown.

ATP released by astrocytes mediates glutamatergic activity-dependent heterosynaptic suppression.

Extracellular ATP released from axons is known to assist activity-dependent signaling between neurons and Schwann cells in the peripheral nervous system. Here we report that ATP released from astrocytes as a result of neuronal activity can also modulate central synaptic transmission. In cultures of hippocampal neurons, endogenously released ATP tonically suppresses glutamatergic synapses via presynaptic P2Y receptors, an effect that depends on the presence of cocultured astrocytes.