scholarly journals Cell type specific control of basolateral amygdala plasticity via feedforward inhibition

2018 ◽  
Author(s):  
E. Mae Guthman ◽  
Ming Ma ◽  
Philip Chu ◽  
Serapio M. Baca ◽  
Diego Restrepo ◽  
...  

AbstractThe basolateral amygdala (BLA) plays a vital role in associating specific sensory stimuli with salient valence information. Excitatory principal neurons (PNs) undergo plastic changes to encode this integrated sensory-valence information; however, local BLA inhibitory interneurons (INs) gate the plasticity of the PNs via feed forward inhibition (FFI). Despite extensive literature implicating parvalbumin expressing (PV+) INs in FFI in cortex and hippocampus, prior anatomical experiments in BLA implicate somatostatin expressing (Sst+) INs in BLA. In the present study, we combined patch clamp electrophysiology with chemogenetics, unsupervised cluster analysis, and predictive modeling and found that a previously unreported subpopulation of fast-spiking Sst+ INs mediate BLA FFI and gate plasticity.

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
E Mae Guthman ◽  
Joshua D Garcia ◽  
Ming Ma ◽  
Philip Chu ◽  
Serapio M Baca ◽  
...  

The basolateral amygdala (BLA) plays a vital role in associating sensory stimuli with salient valence information. Excitatory principal neurons (PNs) undergo plastic changes to encode this association; however, local BLA inhibitory interneurons (INs) gate PN plasticity via feedforward inhibition (FFI). Despite literature implicating parvalbumin expressing (PV+) INs in FFI in cortex and hippocampus, prior anatomical experiments in BLA implicate somatostatin expressing (Sst+) INs. The lateral entorhinal cortex (LEC) projects to BLA where it drives FFI. In the present study, we explored the role of interneurons in this circuit. Using mice, we combined patch clamp electrophysiology, chemogenetics, unsupervised cluster analysis, and predictive modeling and found that a previously unreported subpopulation of fast-spiking Sst+ INs mediate LEC→BLA FFI.


1990 ◽  
Vol 64 (4) ◽  
pp. 1657-1666 ◽  
Author(s):  
J R Erselius ◽  
B Jostes ◽  
A K Hatzopoulos ◽  
L Mosthaf ◽  
P Gruss

1997 ◽  
Vol 16 (4) ◽  
pp. 485-492 ◽  
Author(s):  
SEUNG-JAE LEE ◽  
YOUNG YIL BAHK ◽  
DOO HEE YUN ◽  
HE-JIN LEE ◽  
YOUNG HAN LEE ◽  
...  

2010 ◽  
Vol 30 (6) ◽  
pp. 2150-2159 ◽  
Author(s):  
S. Otte ◽  
A. Hasenstaub ◽  
E. M. Callaway

Cell ◽  
2016 ◽  
Vol 164 (3) ◽  
pp. 526-537 ◽  
Author(s):  
Thomas K. Roseberry ◽  
A. Moses Lee ◽  
Arnaud L. Lalive ◽  
Linda Wilbrecht ◽  
Antonello Bonci ◽  
...  

2011 ◽  
Vol 10 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Paola De Bartolo ◽  
Francesca Gelfo ◽  
Lorena Burello ◽  
Andrea De Giorgio ◽  
Laura Petrosini ◽  
...  

2019 ◽  
Author(s):  
Mark Aizenberg ◽  
Solymar Rolon Martinez ◽  
Tuan Pham ◽  
Winnie Rao ◽  
Julie Haas ◽  
...  

AbstractMany forms of behavior require selective amplification of neuronal representations of relevant environmental signals. Following emotional learning, sensory stimuli drive enhanced responses in the sensory cortex. However, the brain circuits that underlie emotionally driven control of the sensory representations remain poorly understood. Here we identify a novel pathway between the basolateral amygdala (BLA), an emotional learning center in the mouse brain, and the inhibitory nucleus of the thalamus (TRN). We demonstrate that activation of this pathway amplifies sound-evoked activity in the central auditory pathway. Optogenetic activation of BLA suppressed spontaneous, but not tone-evoked activity in the auditory cortex (AC), effectively amplifying tone-evoked responses in AC. Anterograde and retrograde viral tracing identified robust BLA projections terminating at TRN. Optogenetic activation of amygdala-TRN pathway mimicked the effect of direct BLA activation, amplifying tone-evoked responses in the auditory thalamus and cortex. The results are explained by a computational model of the thalamocortical circuitry. In our model, activation of TRN by BLA suppresses spontaneous activity in thalamocortical cells, and as a result, thalamocortical neurons are primed to relay relevant sensory input. These results demonstrate a novel circuit mechanism for shining a neural spotlight on behaviorally relevant signals and provide a potential target for treatment of neuropsychological disorders, in which emotional control of sensory processing is disrupted.


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