Table 1.

Postnatal Treatment with Ketanserin Prevents Specific Transcriptional Changes Induced by Maternal Separation in the Adult Prefrontal Cortex

Gene	Ctl	MS	Ket	MS + Ket
Prkcb1	1.00 ± .02	1.22 ± .04a	1.04 ± .10	1.01 ± .13b
Plek	1.00 ± .07	1.25 ± .03a	1.12 ± .08	1.03 ± .13b
Ppp3ca	1.00 ± .04	1.17 ± .03a	1.06 ± .02	.99 ± .04b
Plcd4	1.00 ± .03	1.24 ± .05a	.99 ± .13	1.07 ± .19
Nlgn1	1.00 ± .09	1.30 ± .05a	1.20 ± .09	1.22 ± .16
Grin2d	1.00 ± .05	1.28 ± .03a	1.15 ± .15	1.29 ± .18a

Animals from the control (Ctl) and maternal separation (MS) groups received treatment from postnatal days 2 to 14 with either the serotonin type 2 receptor antagonist ketanserin (Ket) or vehicle, and gene expression was examined at postnatal day 90. We examined the expression of genes of specific interest implicated in G-protein signaling and known to contribute to serotonin type 2 receptor-mediated signal transduction, cellular excitability, and neuronal plasticity. Quantitative polymerase chain reaction analysis for the following genes, protein kinase C (Prkcb1), pleckstrin (Plek), calcineurin (Ppp3ca), phospholipase C (Plcd4), neuroligin 1(Nlgn1), and N-methyl-D aspartate-receptor subunit 2D (Grin2d) was performed from the prefrontal cortex as described in Methods and Materials. The expression of these transcripts was significantly induced in the prefrontal cortex of MS animals in adulthood. Postnatal Ket treatment blocked the messenger RNA induction of Prkcb1, Ppp3ca, and Plek but not of Plcd4, Nlgn1, and Grin2d in the prefrontal cortex. Data are expressed as fold change and are the mean ± SEM (n = 5–10 per group). (Analysis of variance and Bonferroni post hoc test).

^ap < .05 compared with Ctl.

^bp < .01 significantly different from MS.