Facial nerve axotomy is a good model for studying neuronal plasticity and regeneration in the peripheral nervous system. In the present study, we investigated the effect of axotomy on the different subunits of GABA(A) and GABA(B) receptors of facial motoneurons. The facial nerve trunk was unilaterally sectioned and operated rats were sacrificed at 1, 3, 8, 30, and 60 days later. mRNAs coding for alpha1, beta2, and gamma2 of GABA(A) receptors and for GABA(1B) and GABA(B2) receptors were down-regulated by axotomy. This decrease began as soon as 1 or 3 days after axotomy, and the minimum was 8 days post-lesion; the mRNA levels remained lower than normal at day post-lesion 60. The abundance of mRNAs coding for the three other alpha2, beta1, and beta3 facial subunits of GABA(A) receptors and for the pre-synaptic GABA(B1A) subunit remained unchanged during the period 1-8 days post-lesion. Immunohistochemistry using specific antibodies against alpha1, gamma2 subunits of GABA(A) and against GABA(B2) subunits confirmed this down-regulation. Colchicine treatment and blockade of action potential by tetrodotoxin significantly decreased GABA(A)alpha1 immunoreactivity in the axotomized facial nucleus after 7 days. Finally, muscle destruction by cardiotoxin or facial palsy induced by botulinum toxin failed to change GABA(A)alpha1 subunit expression. Our data demonstrate that axotomy strongly reduced the amounts of alpha1, beta2, and gamma2 subunits of GABA(A) receptors and B(1B) and B(2) subunits of GABA(B) receptors in the axotomized facial motoneurons. The loss of GABA(A)alpha1 subunit was most probably induced by both the loss of trophic factors transported from the periphery and a positive injury signal. It also seems to be dependent on activity disruption.