Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

We have recently shown that aged mice with haploinsufficiencies for the neurotrophin receptors trkB, trkC or both, trkB and trkC, display reduced cell numbers in the substantia nigra and in the dentate gyrus, but not in the amygdala. Moreover, both hippocampus and amygdala contain increased numbers of degenerated axonal fragments. Consistent with this observation and the expression of trkB and trkC by midbrain dopaminergic neurons, we show now that heterozygous deletion of the trkB or/and trkC receptor genes significantly reduces catecholaminergic, tyrosine hydroxylase (TH-) positive fiber densities in the hippocampus and amygdala mainly in aged (21-23 month old) mice. In the amygdala the phenotype was restricted to the lateral and basolateral nucleus of the amygdala. In adult (6 month old) mice, reductions in catecholaminergic fiber densities were only found in the hippocampal area CA3 and the dentate gyrus of heterozygous trkB and trkB/C mice. Our observations suggest that signaling through trkB and trkC neurotrophin receptors is important for the maintenance of the catecholaminergic innervation of two limbic key regions, the hippocampus and amygdala.

Original publication

DOI

10.1007/s00702-006-0498-2

Type

Journal article

Journal

J Neural Transm (Vienna)

Publication Date

12/2006

Volume

113

Pages

1829 - 1836

Keywords

Amygdala, Animals, Catecholamines, Dentate Gyrus, Heterozygote, Hippocampus, Immunohistochemistry, Mice, Nerve Fibers, Parasympathetic Nervous System, Phenotype, Receptors, Nerve Growth Factor, Terminology as Topic, Tyrosine 3-Monooxygenase