NDLI: Neuronal NT-3 is not required for synaptic transmission or long-term potentiation in area CA1 of the adult rat hippocampus.

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Neuronal NT-3 is not required for synaptic transmission or long-term potentiation in area CA1 of the adult rat hippocampus.

Content Provider	Semantic Scholar
Author	Ma, Long Reis, Giuliano Schuman, Erin M.
Copyright Year	1999
Abstract	Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field potential recordings at the Schaffer collateral-CA1 synapse in hippocampal slices from homozygous knockout and wild-type mice. We examined the following indices of synaptic transmission: (1) input-output relationship; (2) paired-pulse facilitation; (3) post-tetanic potentiation; and (4) long-term potentiation: induced by two different protocols: (a) two trains of 100-Hz stimulation and (b) theta burst stimulation. We found no difference between the knockout and wild-type mice in any of the above measurements. These results suggest that neuronal NT-3 does not play an essential role in normal synaptic transmission and some forms of plasticity in the mouse hippocampus.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://learnmem.cshlp.org/content/6/3/267.full.pdf
PubMed reference number	10492008v1
Volume Number	6
Issue Number	3
Journal	Learning & memory
Language	English
Access Restriction	Open
Subject Keyword	Brain-Derived Neurotrophic Factor CA1 field Deletion (action) Homozygote Long-Term Potentiation Neuronal Ceroid-Lipofuscinoses Protocols documentation Synapsins chemosensitization/potentiation facilitation modulation of synaptic transmission recombinase
Content Type	Text
Resource Type	Article

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