PMID- 10322075
OWN - NLM
STAT- MEDLINE
DCOM- 19990614
LR  - 20171213
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 81
IP  - 5
DP  - 1999 May
TI  - Effects of BDNF and NT-3 on development of Ia/motoneuron functional connectivity 
      in neonatal rats.
PG  - 2398-405
AB  - Effects of BDNF and NT-3 on development of Ia/motoneuron functional connectivity 
      in neonatal rats. The effects of neurotrophin administration and neurotrophin 
      removal via administration of tyrosine kinase (trk) immunoadhesins (trk receptor 
      extracellular domains fused with IgG heavy chain) on the development of segmental 
      reflexes were studied in neonatal rats. Brain derived neurotrophic factor (BDNF), 
      neurotrophin-3 (NT-3), trkB-IgG, and trkC-IgG were delivered via subcutaneous 
      injection on days 0, 2, 4, and 6 of postnatal life. Electrophysiological analysis 
      of EPSPs recorded intracellularly in L5 motoneurons in response to stimulation of 
      dorsal root L5 was carried out on postnatal day 8 in the in vitro hemisected 
      spinal cord. Treatment with BDNF resulted in smaller monosynaptic EPSPs with 
      longer latency than those in controls. EPSP amplitude became significantly larger 
      when BDNF was sequestered with trkB-IgG, suggesting that BDNF has a tonic action 
      on the development of this synapse in neonates. Treatment with NT-3 resulted in 
      larger EPSPs, but the decrease noted after administration of trkC-IgG was not 
      significant. Neurotrophins had little effect on the response to high-frequency 
      dorsal root stimulation or on motoneuron properties. Polysynaptic components were 
      exaggerated in BDNF-treated rats and reduced after NT-3 compared with controls. 
      As in control neonates the largest monosynaptic EPSPs in NT-3 and 
      trkB-IgG-treated preparations were observed in motoneurons with relatively large 
      values of rheobase, probably those that are growing the most rapidly. We conclude 
      that supplementary NT-3 and BDNF administered to neonates can influence 
      developing Ia/motoneuron synapses in the spinal cord but with opposite net 
      effects.
FAU - Seebach, B S
AU  - Seebach BS
AD  - Department of Neurobiology and Behaviour, State University of New York at Stony 
      Brook, Stony Brook, New York 11794-5230, USA.
FAU - Arvanov, V
AU  - Arvanov V
FAU - Mendell, L M
AU  - Mendell LM
LA  - eng
GR  - P01 NS-14899/NS/NINDS NIH HHS/United States
GR  - R01 NS-16996/NS/NINDS NIH HHS/United States
GR  - R01 NS-32264/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neurotrophin 3)
SB  - IM
MH  - Animals
MH  - Animals, Newborn/*physiology
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Electric Stimulation
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Motor Neurons/*drug effects/*physiology
MH  - Nerve Growth Factors/*pharmacology
MH  - Neural Pathways/drug effects/physiology
MH  - Neurotrophin 3
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reaction Time/drug effects
MH  - Synapses/drug effects/physiology
MH  - Synaptic Transmission/drug effects
EDAT- 1999/05/13 00:00
MHDA- 1999/05/13 00:01
CRDT- 1999/05/13 00:00
PHST- 1999/05/13 00:00 [pubmed]
PHST- 1999/05/13 00:01 [medline]
PHST- 1999/05/13 00:00 [entrez]
AID - 10.1152/jn.1999.81.5.2398 [doi]
PST - ppublish
SO  - J Neurophysiol. 1999 May;81(5):2398-405. doi: 10.1152/jn.1999.81.5.2398.