Dendritic, backpropagating action potentials (bAPs) facilitate the induction of Hebbian long-term potentiation (LTP).

The functional connectivity of the cerebral cortex is shaped by experience during development, especially during a critical period early in life. In the prenatal and neonatal cortex, transient neuronal circuits are formed by a population of subplate neurons (SPNs). However, SPNs are absent in the adult cortex. While SPNs are crucial for normal development of the cerebral cortex and of thalamocortical synapses, little is known about how they are integrated in the developing thalamocortical circuit. We therefore investigated SPNs in vitro in thalamocortical slices of A1 and medial geniculate nucleus (MGN) in mouse from postnatal day 1 (P1) to P13. We found that SPNs can fire action potentials at P1 and that their intrinsic membrane properties are mature after P5. We find that SPNs receive functional excitatory inputs from the MGN as early as P2. The MGN projections to SPNs strengthen between P2 and P13 and are capable of inducing action potentials in SPNs. Selective activation of SPNs by photostimulation produced EPSCs in layer 4 neurons, demonstrating a functional excitatory connection. Thus SPNs are tightly integrated into the developing thalamocortical circuit and would be a reliable relay of early spontaneous and sound evoked activity. The role of SPNs in development likely results from their strong excitatory projection to layer 4 which might function to regulate activity dependent processes that enable mechanisms required for the functional maturation and plasticity of the developing cortex and thereby contribute to the development of normal cortical organization.

ABSTRACT:Active conductances located and operating on neuronal dendrites are expected to regulate synaptic integration and plasticity. We investigate how Kv4.2-mediated A-type K 1 channels and Ca 21 -activated K 1 channels are involved in the induction process of Hebbiantype plasticity that requires correlated pre-and postsynaptic activities. In CA1 pyramidal neurons, robust long-term potentiation (LTP) induced by a theta burst pairing protocol usually occurred within a narrow window during which incoming synaptic potentials coincided with postsynaptic depolarization. Elimination of dendritic A-type K 1 currents in Kv4.2 2/2 mice, however, resulted in an expanded time window, making the induction of synaptic potentiation less dependent on the temporal relation of pre-and postsynaptic activity. For the other type of synaptic plasticity, long-term depression, the threshold was significantly increased in Kv4.2 2/2 mice. This shift in depression threshold was restored to normal when the appropriate amount of internal free calcium was chelated during induction. In concert with A-type channels, Ca 21 -activated K 1 channels also exerted a sliding effect on synaptic plasticity. Blocking these channels in Kv4.2 2/2 mice resulted in an even larger potentiation while by contrast, the depression threshold was shifted further. In conclusion, dendritic A-type and Ca 21 -activated K 1 channels dually regulate the timing-dependence and thresholds of synaptic plasticity in an additive way. V V C 2010 Wiley-Liss, Inc.

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