Neuronal coexistence of trkB and glutamic acid decarboxylase67 mRNAs in rat hippocampus.
We have in earlier studies shown that brain derived neurotrophic factor (BDNF) mRNA expression is increased in the hippocampus following stimulation of excitatory cortical afferents and spatial learning. Furthermore, we have observed that excitatory influence in the hippocampus seems to increase in vivo release of gamma-aminobutyric acid (GABA), indicated by microdialysis perfusion of the CA1 region. In this study we have investigated whether the receptor for BDNF, TrkB, may be expressed in GABA containing neurons in the CA1, thereby suggesting a possible role for BDNF in the trophic regulation of these neurons. We provide evidence of a neuronal coexistence of the mRNA encoding TrkB and glutamic acid decarboxylase, the key enzyme in the synthesis of GABA. This finding indicates that TrkB can be synthesized in GABA producing neurons in the hippocampus.
Zachrisson
O
O
Department of Clinical Neuroscience, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden.
Falkenberg
T
T
Lindefors
N
N
D000818:Animals; D005968:Glutamate Decarboxylase / Q000235:genetics*; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000235:genetics*; D009474:Neurons / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020801:Receptor, Ciliary Neurotrophic Factor; D017475:Receptors, Nerve Growth Factor / Q000235:genetics*
D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D020801:Receptor, Ciliary Neurotrophic Factor; D017475:Receptors, Nerve Growth Factor; D005968:Glutamate Decarboxylase