Facial Nerve Axotomy Induces Changes on Hippocampal CA3-to-CA1 Long-term Synaptic Plasticity

[Display omitted] •Rats with facial axotomy-induced whisker palsy were followed up for 1–21 days.•Hippocampal CA3-to-CA1 synaptic transmission contralateral to axotomy was evaluated.•Facial axotomy induced transient release probability increase in CA3-to-CA1 synapse.•Facial axotomy persistently impaired CA3-to-CA1 LTP, mostly its presynaptic module. Peripheral facial axotomy induces functional and structural central nervous system changes beyond facial motoneurons, causing, among others, changes in sensorimotor cortex and impairment in hippocampal-dependent memory tasks. Here, we explored facial nerve axotomy effects on basal transmission and long-term plasticity of commissural CA3-to-CA1 synapses. Adult, male rats were submitted to unilateral axotomy of the buccal and mandibular branches of facial nerve and allowed 1, 3, 7, or 21 days of recovery before performing electrophysiological recordings of contralateral CA3 (cCA3) stimulation-evoked CA1 field postsynaptic potential in basal conditions and after high frequency stimulation (HFS) (six, one-second length, 100 Hz stimuli trains). Facial nerve axotomy induced transient release probability enhancement during the first week after surgery, without significant changes in basal synaptic strength. In addition, peripheral axotomy caused persistent long-term potentiation (LTP) induction impairment, affecting mainly its presynaptic component. Such synaptic changes may underlie previously reported impairments in hippocampal-dependent memory tasks and suggest a direct hippocampal implication in sensorimotor integration in whisking behavior.