title: Effects of p75NTR deficiency on cholinergic innervation of the amygdala and anxiety-like behavior.
abstract: The p75 neurotrophin receptor (p75NTR) is a low-affinity receptor that is capable of binding neurotrophins. Two different p75NTR knockout mouse lines are available either with a deletion in Exon III (p75NTRExIII-/-) or in Exon IV (p75NTRExIV-/-). In p75NTRExIIIknockout mice, only the full-length p75NTR is deleted, whereas in p75NTRExIVknockout mice, the full-length as well as the truncated isoform of the receptor is deleted. Deletion of p75NTR has been shown to affect, among others, the septohippocampal cholinergic innervation pattern and neuronal plasticity within the hippocampus. We hypothesize that deletion of p75NTR also alters the morphology and physiology of a further key structure of the limbic system, the amygdala. Our results indicate that deletion of p75NTR also increases cholinergic innervation in the basolateral amygdala in adult as well as aged p75NTRExIII-/-and p75NTRExIV-/-mice. The p75NTRExIV-/-mice did not display altered long-term potentiation (LTP) in the basolateral amygdala as compared to age-matched control littermates. However, p75NTRExIII-/-mice display stronger LTP in the basolateral amygdala compared to age-matched controls. Bath-application of K252a (a trk antagonist) did not inhibit the induction of LTP in the basolateral amygdala, but reduced the level of LTP in p75NTRExIII-/-mice to levels seen in respective controls. Moreover, p75NTRExIII-/-mice display altered behavior in the dark/light box. Thus, deletion of p75NTR in mice leads to physiological and morphological changes in the amygdala and altered behavior that is linked to the limbic system.
authors.affiliation: Institute of Anatomy and Cell Biology, University Medicine Greifswald, Friedrich-Löffler Straße-23c, Greifswald, Germany.
authors.forename: Ruben
authors.initials: R
authors.lastname: Busch
authors.affiliation: Institute of Anatomy and Cell Biology, University Medicine Greifswald, Friedrich-Löffler Straße-23c, Greifswald, Germany.
authors.forename: Marian
authors.initials: M
authors.lastname: Baldus
authors.affiliation: Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
authors.forename: Miriam A
authors.initials: MA
authors.lastname: Vogt
authors.affiliation: Department of Molecular Biology, Central Institute of Mental Health and Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
authors.forename: Stefan M
authors.initials: SM
authors.lastname: Berger
authors.affiliation: Department of Molecular Biology, Central Institute of Mental Health and Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
authors.forename: Dusan
authors.initials: D
authors.lastname: Bartsch
authors.affiliation: Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
authors.forename: Peter
authors.initials: P
authors.lastname: Gass
authors.affiliation: Institute of Anatomy and Cell Biology, University Medicine Greifswald, Friedrich-Löffler Straße-23c, Greifswald, Germany.
authors.forename: Oliver
authors.identifier: 0000-0002-2613-2517
authors.initials: O
authors.lastname: von Bohlen Und Halbach
mesh_terms: D000679:Amygdala / Q000737:chemistry; D000818:Animals; D001007:Anxiety / Q000523:psychology*; D001522:Behavior, Animal; D001923:Brain Chemistry / Q000235:genetics; D002799:Cholinergic Fibers; D003213:Conditioning, Psychological; D055724:Electrophysiological Phenomena; D005091:Exons; D005239:Fear; D007150:Immunohistochemistry; D017774:Long-Term Potentiation; D051379:Mice; D018345:Mice, Knockout; D010275:Parasympathetic Nervous System / Q000737:chemistry; D017475:Receptors, Nerve Growth Factor / Q000172:deficiency* / Q000235:genetics
chemical_list: D017475:Receptors, Nerve Growth Factor; C517634:Ngfr protein, mouse
keywords: 
  HPLC
  ; acetylcholine; amygdala; long-term potentiation; mice; p75NTR