Structural and functional consequences in the amygdala of leptin-deficient mice
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SHORT COMMUNICATION
Structural and functional consequences in the amygdala of leptin-deficient mice Jens Schepers 1 & Christine Gebhardt 2 & Alexander Bracke 1 & Ina Eiffler 1 & Oliver von Bohlen und Halbach 1 Received: 18 May 2020 / Accepted: 22 July 2020 # The Author(s) 2020
Abstract On the one hand, the emotional state can influence food intake and on the other hand, hunger can have an impact on the emotional state. Leptin, which is encoded by the ob gene, is involved in the energy homeostasis and plays a role in development of obesity. Mice deficient for leptin (ob/ob) are obese and display several behavioral alterations. It has been shown that ob/ob mice display striking changes in neuronal plasticity within the limbic system, e.g., hippocampal formation. We focus on alterations in ob/ob mice that can be related to alter processing in another part of the limbic system, the amygdala. ob/ob mice have a higher food consumption than age-matched controls, which might have an impact on the emotional state of these mice. Since the amygdala is involved in emotional processing, we analyze whether ob/ob mice display alterations in plasticity at the electrophysiological and structural level. No changes were seen in dendritic spine densities in the basolateral and lateral (LA) nucleus of the amygdala. Interestingly and in contrast to the hippocampus (Porter et al. 2013), long-term potentiation in the LA was increased in ob/ob mice. Our results indicate that amygdalar and hippocampal synaptic plasticity are regulated in different ways by leptin deficiency in accordance with the different functions of these limbic structures in stress and anxiety. Keywords Amygdala . Dendritic spines . Leptin . LTP . Obesity
Introduction Obesity is associated with increased morbidity and mortality having a dramatic effect on individual and public health. Previous cross-sectional studies on body-weightrelated alterations in brain structures revealed profound changes in white and gray matter resembling findings obtained from aged individuals (Mueller et al. 2015). Leptin is involved in the development of obesity and leptin deficiency (due to mutations in the ob gene) can be causal for obesity (Finger et al. 2010). Ob/ob mice, which were discovered in the 1950s (Ingalls et al. 1950), represent an animal model of obesity. At birth, ob/ob mice have nearly
* Oliver von Bohlen und Halbach [email protected] 1
Institut für Anatomie und Zellbiologie, Universitätsmedizin Greifswald, Friedrich Loeffler Str. 23c, 17487 Greifswald, Germany
2
Institut für Neurophysiologie, Charité—Universitätsmedizin Berlin, Virchowweg 6, 10117 Berlin, Germany
the same body weight as their controls but within 2 weeks postnatally, they become heavier. In contrast to diabetic leptin receptor (db/db)-deficient mice, blood glucose concentration is unaltered in ob/ob mice (Giesbertz et al. 2015). During the first 120 postnatal days, weight nearly doubles in ob/ob mice (Bracke et al. 2019). Moreover, they display deficits in hippocampal synaptic plastic
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