TY  - JOUR
A1  - Reuter, Isabel
A1  - Jäckels, Jana
A1  - Kneitz, Susanne
A1  - Kuper, Jochen
A1  - Lesch, Klaus-Peter
A1  - Lillesaar, Christina
T1  - Fgf3 is crucial for the generation of monoaminergic cerebrospinal fluid contacting cells in zebrafish
JF  - Biology Open
N2  - In most vertebrates, including zebrafish, the hypothalamic serotonergic cerebrospinal fluid-contacting (CSF-c) cells constitute a prominent population. In contrast to the hindbrain serotonergic neurons, little is known about the development and function of these cells. Here, we identify fibroblast growth factor (Fgf)3 as the main Fgf ligand controlling the ontogeny of serotonergic CSF-c cells. We show that fgf3 positively regulates the number of serotonergic CSF-c cells, as well as a subset of dopaminergic and neuroendocrine cells in the posterior hypothalamus via control of proliferation and cell survival. Further, expression of the ETS-domain transcription factor etv5b is downregulated after fgf3 impairment. Previous findings identified etv5b as critical for the proliferation of serotonergic progenitors in the hypothalamus, and therefore we now suggest that Fgf3 acts via etv5b during early development to ultimately control the number of mature serotonergic CSF-c cells. Moreover, our analysis of the developing hypothalamic transcriptome shows that the expression of fgf3 is upregulated upon fgf3 loss-of-function, suggesting activation of a self-compensatory mechanism. Together, these results highlight Fgf3 in a novel context as part of a signalling pathway of critical importance for hypothalamic development.
KW  - Fgf-signalling
KW  - Serotonin
KW  - Dopamine
KW  - Hypothalamus
KW  - Central nervous system
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-200749
VL  - 8
ER  - 
TY  - JOUR
A1  - Kästner, Niklas
A1  - Richter, S. Helene
A1  - Urbanik, Sarah
A1  - Kunert, Joachim
A1  - Waider, Jonas
A1  - Lesch, Klaus-Peter
A1  - Kaiser, Sylvia
A1  - Sachser, Norbert
T1  - Brain serotonin deficiency affects female aggression
JF  - Scientific Reports
N2  - The neurotransmitter serotonin plays a key role in the control of aggressive behaviour. While so far most studies have investigated variation in serotonin levels, a recently created tryptophan hydroxylase 2 (Tph2) knockout mouse model allows studying effects of complete brain serotonin deficiency. First studies revealed increased aggressiveness in homozygous Tph2 knockout mice in the context of a resident-intruder paradigm. Focussing on females, this study aimed to elucidate effects of serotonin deficiency on aggressive and non-aggressive social behaviours not in a test situation but a natural setting. For this purpose, female Tph2 wildtype (n = 40) and homozygous knockout mice (n = 40) were housed with a same-sex conspecific of either the same or the other genotype in large terraria. The main findings were: knockout females displayed untypically high levels of aggressive behaviour even after several days of co-housing. Notably, in response to aggressive knockout partners, they showed increased levels of defensive behaviours. While most studies on aggression in rodents have focussed on males, this study suggests a significant involvement of serotonin also in the control of female aggression. Future research will show, whether the observed behavioural effects are directly caused by the lack of serotonin or by potential compensatory mechanisms.
KW  - animal behaviour
KW  - genetics of the nervous system
KW  - social behaviour
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-325386
VL  - 9
ER  -