Abstract
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.
Highlights
Development of the somatosensory cortical body maps is an activity-dependent process controlled by serotonin
The maximal local field potential (LFP) signals, current sinks, oscillation power, and multiple unit activity (MUA) during the sensory-evoked responses were located in cortical layer 4 (L4) (Fig. 1a) that is in keeping with the results of previous studies [4, 5]
In order to quantify the effects of fluoxetine, we analyzed the following parameters: sensory-evoked potential (SEP) amplitude and onset latency, MUA during SEP and MUA during 500 ms time window after SEP, and spontaneous MUA that was calculated within 8 s long time window before the stimulus
Summary
Development of the somatosensory cortical body maps is an activity-dependent process controlled by serotonin. Elevation of extracellular serotonin levels through the inhibition of serotonin uptake with the selective serotonin uptake inhibitors (SSRIs) and genetic blockade of serotonin transporters or serotonin degrading enzyme monoamine oxidase A disturbs the formation of the cortical maps during the neonatal period in rodents (for review, see [1]). Studies using thalamocortical slices revealed that exogenously applied serotonin strongly inhibits the thalamocortical transmission in neonatal rodents [2, 3]. Along with these findings, a highly selective and potent SSRI citalopram has been shown to inhibit spontaneous and sensory-evoked responses, to prolong the delays of the sensory-evoked potentials (SEPs) and to reduce the frequency and power of the early gamma oscillations in the neonatal rat barrel cortex [4]. Laboratory of Neurobiology, Kazan Federal University, 18 Kremlevskaya st, Kazan 420008, Russia
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