GABAB receptor‐mediated feed‐forward circuit dysfunction in the mouse model of fragile X syndrome

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp6819-list-0001">Cortico‐hippocampal feed‐forward circuits formed by the temporoammonic (TA) pathway exhibit a marked increase in excitation/inhibition ratio and abnormal spike modulation functions in Fmr1 knock‐out (KO) mice.Inhibitory, but not excitatory, synapse dysfunction underlies cortico‐hippocampal feed‐forward circuit abnormalities in Fmr1 KO mice.GABA release is reduced in TA‐associated inhibitory synapses of Fmr1 KO mice in a GABAB receptor‐dependent manner.Inhibitory synapse and feed‐forward circuit defects are mediated predominately by presynaptic GABAB receptor signalling in the TA pathway of Fmr1 KO mice.GABAB receptor‐mediated inhibitory synapse defects are circuit‐specific and are not observed in the Schaffer collateral pathway‐associated inhibitory synapses in stratum radiatum.