Fig 8.

Direct calcineurin inhibition results in enhanced facial motor neuron survival following axotomy, but CNA-α plays a dispensable role in regulating neuronal survival. (A) Daily administration of cypermethrin (10 mg/kg) demonstrated enhanced facial motor neuron survival from 12 ± 1% in vehicle-treated animals to 32 ± 3% in cypermethrin-treated mice, thus suggesting a prominent role for calcineurin inhibition in promoting neuronal survival (** indicates statistical significance between cypermethrin treatment and controls at P < 0.01). (B) shows an increased number of motor neurons in whole facial nuclei of cypermethrin-treated animals compared to controls. To further examine the role of calcineurin inhibition in enhancing neuronal survival following injury, axotomy-induced injury was performed in Ppp3ca null mice and heterozygous controls. (C) Histogram of facial motor neuron survival in Ppp3ca null mice. Mice homozygous for a targeted deletion of the dominant isoform of CNA in the CNS did not exhibit enhanced motor neuron survival compared to heterozygous littermates (19 ± 1% versus 21 ± 3%, respectively). (D) A typical injured facial nucleus from Ppp3ca null animals following axotomy, with no observable enhancement in motor neuron survival compared to heterozygous controls.