ausblenden:
Schlagwörter:
3T3 Cells
Animals
Antibody Specificity
Binding, Competitive/immunology
Brain-Derived Neurotrophic Factor/*pharmacology
Electrophysiology
Gene Expression/physiology
Hippocampus/chemistry/drug effects/*physiology
Immunoglobulin G/pharmacology
Long-Term Potentiation/drug effects/*physiology
Male
Mice
Neuronal Plasticity/drug effects/physiology
Organ Culture Techniques
Rabbits
Rats
Rats, Sprague-Dawley
Receptor Protein-Tyrosine Kinases/genetics/immunology/*metabolism
Receptor, Ciliary Neurotrophic Factor
Receptors, Nerve Growth Factor/genetics/immunology/*metabolism
Signal Transduction/*drug effects/physiology
Synaptic Transmission/drug effects/immunology
Time Factors
Zusammenfassung:
We examined the role of TrkB ligands in hippocampal long-term potentiation (LTP) using function-blocking TrkB antiserum (Ab) and Trk-IgG fusion proteins. Incubation of hippocampal slices with TrkB Ab had no effect on basal synaptic transmission, short-term plasticity, or LTP induced by several trains of tetanic stimulation. The TrkB Ab-treated slices, however, showed significant deficits in LTP induced by either theta-burst stimulation (TBS) or "pairing." Slices exposed to the same number of inducing stimuli, delivered either as TBS or as a single 100 Hz epoch, only exhibited TrkB-sensitive LTP when TBS was used, indicating that the temporal pattern of stimulation determines the neurotrophin dependence. The late phase of LTP (2-3 hr) was also significantly impaired in slices pretreated with TrkB Ab or a TrkB-IgG. The application of a TrkB-IgG 30 min after LTP induction caused previously potentiated synaptic transmission to return to baseline levels, indicating that TrkB ligands are required to maintain LTP for up to 1 hr after induction. Taken together, these results indicate that both the temporal patterns of synaptic activity and the different temporal phases of synaptic enhancement are important in determining the neurotrophin dependence of plasticity in the hippocampus.
