Eye opening and PSD95 are required for long-term potentiation in developing superior colliculus

Area of Science:

• Neuroscience
• Synaptic Plasticity
• Developmental Neuroscience

Background:

• The young superficial superior colliculus (SC) expresses synapse-associated protein 102 (SAP102) and postsynaptic density protein 95 (PSD95) as major glutamate receptor scaffolds.
• Synaptic PSD95 levels increase rapidly after eyelid opening (EO) in visual brain regions.

Purpose of the Study:

• To investigate the roles of EO and PSD95 in SC NMDA receptor (NMDAR)-dependent long-term potentiation (LTP).
• To understand how PSD95 influences synaptic function and maturation in the developing SC.

Main Methods:

• In vivo PSD95 knockdown (KD) in the SC.
• Electrophysiological recordings of miniature AMPA receptor and NMDAR currents.
• Manipulation of EO to assess its effect on LTP and synaptic currents.

Main Results:

• EO and PSD95 are essential for SC NMDAR-dependent LTP; manipulating EO alters LTP.
• PSD95 KD blocks LTP but not long-term depression, reducing miniature NMDAR and AMPA receptor current frequencies without affecting presynaptic release.
• PSD95 KD reveals activity-triggered calcineurin sensitivity in NMDAR currents, characteristic of the pre-EO period.

Conclusions:

• Young SC LTP results from PSD95-mediated unsilencing of silent synapses.
• Synaptic potentiation is labile in the young brain.
• PSD95, not SAP102, facilitates synaptic maturation in the SC, despite both binding to NMDARs.