TY - JOUR
T1 - Cerebellar Learning Properties Are Modulated by the CRF Receptor
AU - Ezra-Nevo, Gili
AU - Prestori, Francesca
AU - Locatelli, Francesca
AU - Soda, Teresa
AU - ten Brinke, Michiel M.
AU - Engel, Mareen
AU - Boele, Henk-Jan
AU - Botta, Laura
AU - Leshkowitz, Dena
AU - Ramot, Assaf
AU - Tsoory, Michael
AU - Biton, Inbal E.
AU - Deussing, Jan
AU - D'Angelo, Egidio
AU - De Zeeuw, Chris I.
AU - Chen, Alon
N1 - Publisher Copyright: © 2018 the authors.
PY - 2018/7/25
Y1 - 2018/7/25
N2 - Corticotropin-releasing factor (CRF) and its type 1 receptor (CRFR1) play an important role in the responses to stressful challenges. Despite the well established expression of CRFR1 in granular cells (GrCs), its role in procedural motor performance and memory formation remains elusive. To investigate the role of CRFR1 expression in cerebellar GrCs, we used a mouse model depleted of CRFR1 in these cells. We detected changes in the cellular learning mechanisms in GrCs depleted of CRFR1 in that they showed changes in intrinsic excitability and long-term synaptic plasticity. Analysis of cerebella transcriptome obtained from KO and control mice detected prominent alterations in the expression of calcium signaling pathways components. Moreover, male mice depleted of CRFR1 specifically in GrCs showed accelerated Pavlovian associative eye-blink conditioning, but no differences in baseline motor performance, locomotion, or fear and anxiety-related behaviors. Our findings shed light on the interplay between stress-related central mechanisms and cerebellar motor conditioning, highlighting the role of the CRF system in regulating particular forms of cerebellar learning.
AB - Corticotropin-releasing factor (CRF) and its type 1 receptor (CRFR1) play an important role in the responses to stressful challenges. Despite the well established expression of CRFR1 in granular cells (GrCs), its role in procedural motor performance and memory formation remains elusive. To investigate the role of CRFR1 expression in cerebellar GrCs, we used a mouse model depleted of CRFR1 in these cells. We detected changes in the cellular learning mechanisms in GrCs depleted of CRFR1 in that they showed changes in intrinsic excitability and long-term synaptic plasticity. Analysis of cerebella transcriptome obtained from KO and control mice detected prominent alterations in the expression of calcium signaling pathways components. Moreover, male mice depleted of CRFR1 specifically in GrCs showed accelerated Pavlovian associative eye-blink conditioning, but no differences in baseline motor performance, locomotion, or fear and anxiety-related behaviors. Our findings shed light on the interplay between stress-related central mechanisms and cerebellar motor conditioning, highlighting the role of the CRF system in regulating particular forms of cerebellar learning.
UR - http://www.scopus.com/inward/record.url?scp=85051101120&partnerID=8YFLogxK
U2 - https://doi.org/10.1523/JNEUROSCI.3106-15.2018
DO - https://doi.org/10.1523/JNEUROSCI.3106-15.2018
M3 - مقالة
SN - 0270-6474
VL - 38
SP - 6751
EP - 6765
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 30
ER -