Neural mechanisms underlying the deficit of learning and memory by exposure to Di(2-ethylhexyl) phthalate in rats.

Di(2-ethylhexyl) phthalate (DEHP), as one of the most broadly representative phthalic acid esters, is used as a plasticizer in Polyvinyl chloride production. The exact neurotoxicologically effects of DEHP to human have not been adequately researched. In order to investigate the effects and mechanisms of DEHP exposure on neural circuit, the spatial learning and memory of Sprague Dawley (SD) rats was measured, and the cellular mechanisms underlying synaptic plasticity, cellular excitability and ion channels were detected. Our data showed that the spatial learning and memory was changed by DEHP (100 and 300 mg) treatment. Meanwhile, the frequency of mini Excitatory Postsynaptic Current (mEPSC) from CA3 pyramidal cells were significantly decreased by DEHP exposure (0.1 and 0.3 M); the firing threshold, membrane potential threshold, number, amplitude and latency of Action Potentials (Aps) of CA1 pyramidal cells were altered with the application of DEHP (0.1 and 0.3 M); furthermore, DEHP, both in 0.1 and 0.3 M could inhibit the voltage-gated potassium channel of CA1 pyramidal cells. Our results indicated that DEHP could impair the spatial learning and memory, and this impairment might due to the DEHP-induced suppression of the neuronal excitability and synaptic plasticity by inhibiting the voltage-gated potassium channel, supporting the hypothesis that DEHP could cause the disruption of neural function.