PMID- 19144857 OWN - NLM STAT- MEDLINE DCOM- 20090408 LR - 20220310 IS - 1529-2401 (Electronic) IS - 0270-6474 (Print) IS - 0270-6474 (Linking) VI - 29 IP - 2 DP - 2009 Jan 14 TI - Complementary actions of BDNF and neurotrophin-3 on the firing patterns and synaptic composition of motoneurons. PG - 575-87 LID - 10.1523/JNEUROSCI.5312-08.2009 [doi] AB - Neurotrophins, as target-derived factors, are essential for neuronal survival during development, but during adulthood, their scope of actions widens to become also mediators of synaptic and morphological plasticity. Target disconnection by axotomy produces an initial synaptic stripping ensued by synaptic rearrangement upon target reinnervation. Using abducens motoneurons of the oculomotor system as a model for axotomy, we report that trophic support by brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) or a mixture of both, delivered to the stump of severed axons, results in either the prevention of synaptic stripping when administered immediately after lesion or in a promotion of reinnervation of afferents to abducens motoneurons once synaptic stripping had occurred, in concert with the recovery of synaptic potentials evoked from the vestibular nerve. Synaptotrophic effects, however, were larger when both neurotrophins were applied together. The axotomy-induced reduction in firing sensitivities related to eye movements were also restored to normal values when BDNF and NT-3 were administered, but discharge characteristics recovered in a complementary manner when only one neurotrophin was used. This is the first report to show selective retrograde trophic dependence of circuit-driven firing properties in vivo indicating that NT-3 restored the phasic firing, whereas BDNF supported the tonic firing of motoneurons during eye movement performance. Therefore, our data report a link between the synaptotrophic actions of neurotrophins, retrogradely delivered, and the alterations of neuronal firing patterns during motor behaviors. These trophic actions could be responsible, in part, for synaptic rearrangements that alter circuit stability and synaptic balance during plastic events of the brain. FAU - Davis-Lopez de Carrizosa, Maria A AU - Davis-Lopez de Carrizosa MA AD - Departamento de Fisiologia y Zoologia, Facultad de Biologia, Universidad de Sevilla, Sevilla, Spain. FAU - Morado-Diaz, Camilo J AU - Morado-Diaz CJ FAU - Tena, Juan J AU - Tena JJ FAU - Benitez-Temino, Beatriz AU - Benitez-Temino B FAU - Pecero, Maria L AU - Pecero ML FAU - Morcuende, Sara R AU - Morcuende SR FAU - de la Cruz, Rosa R AU - de la Cruz RR FAU - Pastor, Angel M AU - Pastor AM LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Carbazoles) RN - 0 (Enzyme Inhibitors) RN - 0 (Glial Fibrillary Acidic Protein) RN - 0 (Indole Alkaloids) RN - 0 (Neurotrophin 3) RN - 0 (Synaptophysin) RN - 0 (Vesicular Glutamate Transport Proteins) RN - 97161-97-2 (staurosporine aglycone) RN - EC 2.3.1.6 (Choline O-Acetyltransferase) SB - IM MH - Action Potentials/*drug effects MH - Analysis of Variance MH - Animals MH - Axotomy/methods MH - Brain-Derived Neurotrophic Factor/*pharmacology MH - Carbazoles/pharmacology MH - Cats MH - Choline O-Acetyltransferase/metabolism MH - Drug Interactions MH - Electric Stimulation/methods MH - Enzyme Inhibitors/pharmacology MH - Eye Movements/drug effects MH - Glial Fibrillary Acidic Protein/metabolism MH - Indole Alkaloids/pharmacology MH - Motor Neurons/*drug effects/metabolism MH - Nerve Regeneration/drug effects MH - Neurotrophin 3/*pharmacology MH - Pons/cytology MH - Synaptic Potentials/drug effects MH - Synaptic Transmission/*drug effects MH - Synaptophysin/metabolism MH - Time Factors MH - Vesicular Glutamate Transport Proteins/metabolism PMC - PMC6664940 EDAT- 2009/01/16 09:00 MHDA- 2009/04/09 09:00 PMCR- 2009/07/14 CRDT- 2009/01/16 09:00 PHST- 2009/01/16 09:00 [entrez] PHST- 2009/01/16 09:00 [pubmed] PHST- 2009/04/09 09:00 [medline] PHST- 2009/07/14 00:00 [pmc-release] AID - 29/2/575 [pii] AID - 3444240 [pii] AID - 10.1523/JNEUROSCI.5312-08.2009 [doi] PST - ppublish SO - J Neurosci. 2009 Jan 14;29(2):575-87. doi: 10.1523/JNEUROSCI.5312-08.2009.