The brain initiates activation of the gonadotropin-releasing hormone (GnRH) system at puberty onset. Since GnRH neurons are suggested to show a plasticity during postnatal development, remodeling of GnRH neurons may be involved in the onset of puberty. The present study was done by attempting to block plasticity in the GnRH neuronal network, by interfering with the synaptic delivery of GluR1 whose trafficking is critical in synaptic plasticity and thus necessary for memory. To this end, GluR1-C-tail, a dominant negative mutant of GluR1, was expressed in the POA of female rats at day 21 using lentivirus. GluR1-C-tail has been shown to act by competing with GluR1 for synaptic delivery during synaptic plasticity. As the result, the onset of puberty, by checking viginal opening, was significantly delayed. After that, the estrous cyclicity was checked by viginal smear and found that the rat injected with GluR1-C-tail exhibited a regular estrous cycle. However, the surge of luteinizing hormone (LH) secretion in the rat injected with GluR1-C-tail was significantly attenuated, compared to the control rat. Injection with GluR1-C-tail in mature rats had no effect on the surge of LH secretion. The present study suggests that GluR1-mediated plasticity occurs at the time of puberty and is important to maintain surge of LH secretion in adults. <b>[J Physiol Sci. 2008;58 Suppl:S140]</b>