Muskelin regulates actin-dependent synaptic changes and intrinsic brain activity relevant to behavioral and cognitive processes
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Muskelin regulates actin-dependent synaptic changes and intrinsic brain activity relevant to behavioral and cognitive processes. / Muhia, Mary; YuanXiang, PingAn; Sedlacik, Jan; Schwarz, Jürgen R; Heisler, Frank F; Gromova, Kira V; Thies, Edda; Breiden, Petra; Pechmann, Yvonne; Kreutz, Michael R; Kneussel, Matthias.
in: COMMUN BIOL, Jahrgang 5, Nr. 1, 589, 15.06.2022.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Muskelin regulates actin-dependent synaptic changes and intrinsic brain activity relevant to behavioral and cognitive processes
AU - Muhia, Mary
AU - YuanXiang, PingAn
AU - Sedlacik, Jan
AU - Schwarz, Jürgen R
AU - Heisler, Frank F
AU - Gromova, Kira V
AU - Thies, Edda
AU - Breiden, Petra
AU - Pechmann, Yvonne
AU - Kreutz, Michael R
AU - Kneussel, Matthias
N1 - © 2022. The Author(s).
PY - 2022/6/15
Y1 - 2022/6/15
N2 - Muskelin (Mkln1) is implicated in neuronal function, regulating plasma membrane receptor trafficking. However, its influence on intrinsic brain activity and corresponding behavioral processes remains unclear. Here we show that murine Mkln1 knockout causes non-habituating locomotor activity, increased exploratory drive, and decreased locomotor response to amphetamine. Muskelin deficiency impairs social novelty detection while promoting the retention of spatial reference memory and fear extinction recall. This is strongly mirrored in either weaker or stronger resting-state functional connectivity between critical circuits mediating locomotor exploration and cognition. We show that Mkln1 deletion alters dendrite branching and spine structure, coinciding with enhanced AMPAR-mediated synaptic transmission but selective impairment in synaptic potentiation maintenance. We identify muskelin at excitatory synapses and highlight its role in regulating dendritic spine actin stability. Our findings point to aberrant spine actin modulation and changes in glutamatergic synaptic function as critical mechanisms that contribute to the neurobehavioral phenotype arising from Mkln1 ablation.
AB - Muskelin (Mkln1) is implicated in neuronal function, regulating plasma membrane receptor trafficking. However, its influence on intrinsic brain activity and corresponding behavioral processes remains unclear. Here we show that murine Mkln1 knockout causes non-habituating locomotor activity, increased exploratory drive, and decreased locomotor response to amphetamine. Muskelin deficiency impairs social novelty detection while promoting the retention of spatial reference memory and fear extinction recall. This is strongly mirrored in either weaker or stronger resting-state functional connectivity between critical circuits mediating locomotor exploration and cognition. We show that Mkln1 deletion alters dendrite branching and spine structure, coinciding with enhanced AMPAR-mediated synaptic transmission but selective impairment in synaptic potentiation maintenance. We identify muskelin at excitatory synapses and highlight its role in regulating dendritic spine actin stability. Our findings point to aberrant spine actin modulation and changes in glutamatergic synaptic function as critical mechanisms that contribute to the neurobehavioral phenotype arising from Mkln1 ablation.
KW - Actins/metabolism
KW - Animals
KW - Brain/metabolism
KW - Cognition
KW - Extinction, Psychological
KW - Fear
KW - Mice
U2 - 10.1038/s42003-022-03446-1
DO - 10.1038/s42003-022-03446-1
M3 - SCORING: Journal article
C2 - 35705737
VL - 5
JO - COMMUN BIOL
JF - COMMUN BIOL
SN - 2399-3642
IS - 1
M1 - 589
ER -
