Fig 6.

Direct calcineurin inhibition results in enhanced facial motor neuron survival following axotomy, but calcineurin A alpha (CNAα) 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 cypermethrintreated 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, axotomyinduced 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.