| First Author | Kratovac S | Year | 2013 |
| Journal | Brain Res | Volume | 1537 |
| Pages | 69-78 | PubMed ID | 24008143 |
| Mgi Jnum | J:315923 | Mgi Id | MGI:6829158 |
| Doi | 10.1016/j.brainres.2013.08.052 | Citation | Kratovac S, et al. (2013) Developmental changes in expression of inhibitory neuronal proteins in the Fragile X Syndrome mouse basolateral amygdala. Brain Res 1537:69-78 |
| abstractText | In humans, Fragile X Syndrome (FXS) is characterized by enhanced fear, hyperactivity, social anxiety, and, in a subset of individuals, autism. Many of the emotional and social deficits point to defects in the amygdala. We have previously shown defects in inhibitory neuron drive onto excitatory projection neurons in the basolateral amygdala (BLA) of juvenile Fmr1(-/y) knockout (KO) mice. Using pharmacological approaches, we have also previously revealed dynamic functional deficits in alpha1, alpha2, and alpha3 subunit-containing GABAA receptors (GABAARs alpha1, alpha2, and alpha3) during early postnatal development. In this study, we sought to determine whether these defects in GABAAR function are accompanied by changes in protein expression of GABAARs alpha1, alpha2, and alpha3 and the post-synaptic GABAAR-clustering protein gephyrin. Interestingly, we found that while the expression of these proteins did not significantly differ between wildtype (WT) and KO mice at each time point, the timing of developmental expression of GABAAR alpha1, alpha2, and gephyrin was altered. Collectively, these data reveal novel defects in inhibitory synapse protein expression during critical periods of early postnatal development that could contribute to observed inhibitory neurotransmission deficits in the KO mouse BLA. |
