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Mechanisms underlying induction of LTP-associated changes in short-term dynamics of transmission at immature synapses

Natalia V Luchkina1, Marko Sallert, Vernon R J Clarke

  • 1Neuroscience Center and Department of Biosciences, University of Helsinki, Finland.

Neuropharmacology
|December 19, 2012
PubMed

Insights

During early development, postsynaptic activity can alter presynaptic function at CA3-CA1 synapses. This study reveals a critical period for activity-dependent presynaptic regulation via NMDA-receptor and PKC signaling.

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Developmental Neurobiology

Background:

  • Postsynaptic mechanisms of synaptic transmission maturation are well understood.
  • Presynaptic mechanisms governing functional maturation remain less characterized.
  • Understanding presynaptic plasticity is crucial for comprehending neural circuit development.

Purpose of the Study:

  • To investigate activity-dependent presynaptic mechanisms during early synaptic maturation.
  • To elucidate the role of NMDA-receptors and protein kinase C (PKC) in neonatal synaptic plasticity.
  • To differentiate presynaptic and postsynaptic contributions to long-term potentiation (LTP) at immature synapses.

Main Methods:

  • Electrophysiological recordings from CA3-CA1 synapses in the hippocampus during the first postnatal week.
  • Induction of postsynaptically expressed LTP using physiologically relevant pairing protocols.
  • Pharmacological manipulation to assess the roles of NMDA-receptors, L-type calcium channels, and PKC.

Main Results:

  • Postsynaptically induced LTP at immature CA3-CA1 synapses is associated with decreased synaptic facilitation, indicating increased release probability (P(r)).
  • This loss of facilitation is NMDA-receptor dependent but independent of L-type calcium channels.
  • Protein kinase C (PKC) activity is specifically required for the decrease in facilitation (presynaptic component) but not for the potentiation itself (postsynaptic component).

Conclusions:

  • Synaptic maturation involves a critical developmental window where presynaptic function is highly sensitive to activity-dependent regulation.
  • NMDA-receptor activation and subsequent PKC signaling are key mediators of presynaptic plasticity at immature glutamatergic synapses.
  • These findings highlight a novel mechanism for activity-dependent presynaptic refinement during early brain development.

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