scholarly journals Fear learning triggers structural changes at GABAergic synapses in the basal amygdala

2010 ◽  
Vol 10 (S1) ◽  
Author(s):  
Yu Kasugai ◽  
Markus Hauschild ◽  
Werner Sieghart ◽  
Ryuichi Shigemoto ◽  
Nicolas Singewald ◽  
...  
Neuron ◽  
2019 ◽  
Vol 104 (4) ◽  
pp. 781-794.e4 ◽  
Author(s):  
Yu Kasugai ◽  
Elisabeth Vogel ◽  
Heide Hörtnagl ◽  
Sabine Schönherr ◽  
Enrica Paradiso ◽  
...  

2011 ◽  
Vol 11 (Suppl 2) ◽  
pp. A42
Author(s):  
Yu Kasugai ◽  
Elisabeth Vogel ◽  
Markus Hauschild ◽  
Ramon O Tasan ◽  
Yvan Peterschmitt ◽  
...  

2019 ◽  
Author(s):  
Wei Tang ◽  
Olexiy Kochubey ◽  
Michael Kintscher ◽  
Ralf Schneggenburger

SummaryThe amygdala is a brain area critical for the formation of threat memories. However, the nature of the teaching signal(s) that drive plasticity in the amygdala are still under debate. Here, we use optogenetic methods to investigate whether dopamine release in the amygdala contributes to fear learning. Antero- and retrograde labeling showed that a sparse, and relatively evenly distributed population of ventral tegmental area (VTA) neurons projects to the basal amygdala (BA). In-vivo optrode recordings in behaving mice showed that many VTA neurons, amongst them putative dopamine neurons, are excited by footshocks. Correspondingly, in-vivo fiber photometry of dopamine in the BA revealed robust dopamine concentration transients upon footshock presentation. Finally, silencing VTA dopamine neurons, or their axon terminals in the BA during the footshock, reduced the extent of threat memory retrieval one day later. Thus, VTA dopamine neurons projecting to the BA code for the saliency of the footshock event, and the resulting dopamine release in the BA facilitates threat memory formation.


eNeuro ◽  
2018 ◽  
Vol 5 (5) ◽  
pp. ENEURO.0272-18.2018 ◽  
Author(s):  
Megan Tipps ◽  
Ezequiel Marron Fernandez de Velasco ◽  
Allee Schaeffer ◽  
Kevin Wickman

2019 ◽  
Vol 20 (17) ◽  
pp. 4310 ◽  
Author(s):  
Susanne Meis ◽  
Thomas Endres ◽  
Thomas Munsch ◽  
Volkmar Lessmann

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 GABAA-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF+/−). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF+/− 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+/− 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+/− 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.


2020 ◽  
Vol 40 (20) ◽  
pp. 3969-3980 ◽  
Author(s):  
Wei Tang ◽  
Olexiy Kochubey ◽  
Michael Kintscher ◽  
Ralf Schneggenburger
Keyword(s):  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Junghwa Lee ◽  
Bobae An ◽  
Sukwoo Choi

AbstractThe balance between activities of fear neurons and extinction neurons in the basolateral nucleus of the basal amygdala (BAL) has been hypothesized to encode fear states after extinction. However, it remains unclear whether these neurons are solely responsible for encoding fear states. In this study, we stably recorded single-unit activities in the BAL during fear conditioning and extinction for 3 days, providing a comprehensive view on how different BAL neurons respond during fear learning. We found BAL neurons that showed excitatory responses to the conditioned stimulus (CS) after fear conditioning (‘conditioning-potentiated neurons’) and another population that showed excitatory responses to the CS after extinction (‘extinction-potentiated neurons’). Interestingly, we also found BAL neurons that developed inhibitory responses to the CS after fear conditioning (‘conditioning-inhibited neurons’) or after extinction (‘extinction-inhibited neurons’). BAL neurons that showed excitatory responses to the CS displayed various functional connectivity with each other, whereas less connectivity was observed among neurons with inhibitory responses to the CS. Intriguingly, we found correlative neuronal activities between conditioning-potentiated neurons and neurons with inhibitory responses to the CS. Our findings suggest that distinct BAL neurons, which are responsive to the CS with excitation or inhibition, encode various facets of fear conditioning and extinction.


Author(s):  
S. Phyllis Steamer ◽  
Rosemarie L. Devine

The importance of radiation damage to the skin and its vasculature was recognized by the early radiologists. In more recent studies, vascular effects were shown to involve the endothelium as well as the surrounding connective tissue. Microvascular changes in the mouse pinna were studied in vivo and recorded photographically over a period of 12-18 months. Radiation treatment at 110 days of age was total body exposure to either 240 rad fission neutrons or 855 rad 60Co gamma rays. After in vivo observations in control and irradiated mice, animals were sacrificed for examination of changes in vascular fine structure. Vessels were selected from regions of specific interest that had been identified on photomicrographs. Prominent ultrastructural changes can be attributed to aging as well as to radiation treatment. Of principal concern were determinations of ultrastructural changes associated with venous dilatations, segmental arterial stenosis and tortuosities of both veins and arteries, effects that had been identified on the basis of light microscopic observations. Tortuosities and irregularly dilated vein segments were related to both aging and radiation changes but arterial stenosis was observed only in irradiated animals.


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