Sensory input plays critical roles in the development of the somatosensory cortex during the neonatal period. This early sensory input may involve: (1) stimulation arising from passive interactions with the mother and littermates and (2) sensory feedback arising from spontaneous infant movements. The relative contributions of these mechanisms under natural conditions remain largely unknown, however. Here, we show that, in the whisker-related barrel cortex of neonatal rats, spontaneous whisker movements and passive stimulation by the littermates cooperate, with comparable efficiency, in driving cortical activity. Both tactile signals arising from the littermate's movements under conditions simulating the littermates' position in the litter, and spontaneous whisker movements efficiently triggered bursts of activity in barrel cortex. Yet, whisker movements with touch were more efficient than free movements. Comparison of the various experimental conditions mimicking the natural environment showed that tactile signals arising from the whisker movements with touch and stimulation by the littermates, support: (1) a twofold higher level of cortical activity than in the isolated animal, and (2) a threefold higher level of activity than in the deafferented animal after the infraorbital nerve cut. Together, these results indicate that endogenous (self-generated movements) and exogenous (stimulation by the littermates) mechanisms cooperate in driving cortical activity in newborn rats and point to the importance of the environment in shaping cortical activity during the neonatal period.

During development, sensory systems switch from an immature to an adult mode of function along with the emergence of the active cortical states. Here, we used patch-clamp recordings from neocortical slices in vitro to characterize the developmental changes in the basic electrophysiological properties of excitatory L4 neurons and their connectivity before and after the developmental switch, which occurs in the rat barrel cortex in vivo at postnatal day P8. Prior to the switch, L4 neurons had higher resting membrane potentials, higher input resistance, lower membrane capacity, as well as action potentials (APs) with smaller amplitudes, longer durations and higher AP thresholds compared to the neurons after the switch. A sustained firing pattern also emerged around the switch. Dual patch-clamp recordings from L4 neurons revealed that recurrent connections between L4 excitatory cells do not exist before and develop rapidly across the switch. In contrast, electrical coupling between these neurons waned around the switch. We suggest that maturation of electrophysiological features, particularly acquisition of a sustained firing pattern, and a transition from the immature electrical to mature chemical synaptic coupling between excitatory L4 neurons, contributes to the developmental switch in the cortical mode of function.

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Inhibition of serotonin uptake disrupts the development of thalamocortical barrel maps in neonatal rodents. Previous studies, using the selective serotonin reuptake inhibitor citalopram, have suggested that this may involve a suppression of the early activity in the developing cortex. Here, we addressed the acute effects of another frequently used serotonin uptake inhibitor, fluoxetine (10-120 mg/kg, intraperitoneally), on the sensory-evoked electrical responses in the neonatal (postnatal days P2-6) rat barrel cortex. We found that the administration of fluoxetine minimally affected the sensory-evoked responses in the rat pups. Two hours after the fluoxetine administration, there was a slight increase in the sensory-evoked potential (SEP) onset latency. There also was a tendency of SEP's amplitude to decrease, but this was not significant. Fluoxetine also had no significant effect on the multiple unit activity during the SEP and sensory-evoked bursts and neither did it affect the spontaneous multiple unit activity. We suggest that the inhibitory effects of fluoxetine on the activity in the neonatal rat barrel cortex are much weaker, or that they develop over a slower time scale, than those evoked by citalopram, probably reflecting a lower potency of fluoxetine to inhibit the serotonin uptake.