Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala
Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at i...
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doaj-b5b86047f64641f7a527640b88458c4f2020-11-25T01:46:07ZengMDPI AGInternational Journal of Molecular Sciences1422-00672019-09-012017431010.3390/ijms20174310ijms20174310Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral AmygdalaSusanne Meis0Thomas Endres1Thomas Munsch2Volkmar Lessmann3Institut für Physiologie, Otto-von-Guericke-Universität, D-39120 Magdeburg, GermanyInstitut für Physiologie, Otto-von-Guericke-Universität, D-39120 Magdeburg, GermanyInstitut für Physiologie, Otto-von-Guericke-Universität, D-39120 Magdeburg, GermanyInstitut für Physiologie, Otto-von-Guericke-Universität, D-39120 Magdeburg, GermanyBrain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABA<sub>A</sub>-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF<sup>+/−</sup>). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF<sup>+/−</sup> mice compared to wild-type littermates. In addition, long-term potentiation (LTP) of IPSCs was similar in both genotypes. In contrast, facilitation of spontaneous IPSCs (sIPSCs) by norepinephrine (NE) was significantly reduced in BDNF<sup>+/−</sup> mice. These results argue against a generally impaired efficacy and plasticity at GABAergic synapses due to a chronic BDNF deficit. Importantly, the increase in GABAergic tone mediated by NE is reduced in BDNF<sup>+/−</sup> mice. As release of NE is elevated during aversive behavioral states in the amygdala, effects of a chronic BDNF deficit on GABAergic inhibition may become evident in response to states of high arousal, leading to amygdala hyper-excitability and impaired amygdala function.https://www.mdpi.com/1422-0067/20/17/4310amygdalaGABABDNFheterozygous BDNF knockout miceLTP |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Susanne Meis Thomas Endres Thomas Munsch Volkmar Lessmann |
spellingShingle |
Susanne Meis Thomas Endres Thomas Munsch Volkmar Lessmann Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala International Journal of Molecular Sciences amygdala GABA BDNF heterozygous BDNF knockout mice LTP |
author_facet |
Susanne Meis Thomas Endres Thomas Munsch Volkmar Lessmann |
author_sort |
Susanne Meis |
title |
Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala |
title_short |
Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala |
title_full |
Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala |
title_fullStr |
Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala |
title_full_unstemmed |
Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala |
title_sort |
impact of chronic bdnf depletion on gabaergic synaptic transmission in the lateral amygdala |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1422-0067 |
publishDate |
2019-09-01 |
description |
Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABA<sub>A</sub>-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF<sup>+/−</sup>). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF<sup>+/−</sup> mice compared to wild-type littermates. In addition, long-term potentiation (LTP) of IPSCs was similar in both genotypes. In contrast, facilitation of spontaneous IPSCs (sIPSCs) by norepinephrine (NE) was significantly reduced in BDNF<sup>+/−</sup> mice. These results argue against a generally impaired efficacy and plasticity at GABAergic synapses due to a chronic BDNF deficit. Importantly, the increase in GABAergic tone mediated by NE is reduced in BDNF<sup>+/−</sup> mice. As release of NE is elevated during aversive behavioral states in the amygdala, effects of a chronic BDNF deficit on GABAergic inhibition may become evident in response to states of high arousal, leading to amygdala hyper-excitability and impaired amygdala function. |
topic |
amygdala GABA BDNF heterozygous BDNF knockout mice LTP |
url |
https://www.mdpi.com/1422-0067/20/17/4310 |
work_keys_str_mv |
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