Furthermore, in the fragile X syndrome loss of FMRP protein lead to decrease in current BK channel, slowing in repolarization and expanding the action potential and ultimately increase influx calcium and enhance neurotransmission(Deng et all 2013). Another potassium channel, H channels plays an important role in controlling neuronal excitability (Robinson RB1, Siegelbaum SA. In 2003). Consistent with the hypothesis, the depolarizing sag voltage was disappeared in neurons from treated VPA rats. The Electrophysiology results showed that VPA treatment induced membrane depolarization which was related to increases in the input resistance. These might be as a result of a decrease in the Ih current as demonstrated by voltage-clamp recording.