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The retinocollicular pathway undergoes activity-dependent refinement during postnatal development, which results in the precise retinotopic order seen in adults. This process is NMDA- and nitric oxide-dependent. Recent studies have shown that L-type Ca2+ channels may also play a role in synaptic plasticity, but such channel activity has not previously been reported in the developing superior colliculus (SC). Here we report the presence of a postsynaptic plateau potential mediated by L-type Ca2+ channels using whole-cell current clamp of the SC in an isolated brainstem preparation of rats. Seventy percent of SC neurons showed these potentials as early as postnatal day 0 (P0)-P2. The potential was blocked by nitrendipine and/or APV and facilitated by bicuculline, showing that the channel is activated by NMDA receptor-mediated EPSPs and deactivated by GABAA receptor-mediated IPSPs. Blockade of L-type Ca2+ channels also diminished long-term depression, which we could induce in the retinocollicular pathway in neonatal animals. The incidence of plateau potentials decreased to 39% of neurons by P10-P14, suggesting that L-type calcium channels may contribute to retinocollicular pathway refinement in the developing SC.

the journal of neuroscience/the journal of neuroscience

Synaptic Regulation of L-Type Ca<sup>2+</sup>Channel Activity and Long-Term Depression during Refinement of the Retinocollicular Pathway in Developing Rodent Superior Colliculus

Synaptic Regulation of L-Type Ca2+Channel Activity and Long-Term Depression during Refinement of the Retinocollicular Pathway in Developing Rodent Superior Colliculus

Synaptic Regulation of L-Type Ca²⁺Channel Activity and Long-Term Depression during Refinement of the Retinocollicular Pathway in Developing Rodent Superior Colliculus