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Measuring Nonapoptotic Caspase Activity with a Transgenic Reporter in Mice

PJ. Nicholls, TF. Pack, NM. Urs, S. Kumar, Y. Zhou, G. Ichim, JD. Ginzel, G. Turu, E. Calabrese, WL. Roberts, P. Fan, VG. Ostapchenko, MS. Guzman Lenis, F. Beraldo, J. Hatina, VF. Prado, MAM. Prado, I. Spasojevic, JC. Snyder, K. Dzirasa, GA....

. 2022 ; 9 (5) : . [pub] 20221004

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, N.I.H., Extramural

Perzistentní odkaz   https://www.medvik.cz/link/bmc23004933

Grantová podpora
R21 NS081513 NINDS NIH HHS - United States
P41 EB015897 NIBIB NIH HHS - United States
R01 MH079201 NIMH NIH HHS - United States
R37 MH073853 NIMH NIH HHS - United States
MOP 93651 CIHR - Canada
12600 CIHR - Canada
89919 CIHR - Canada
HHSN271201300017C NIMH NIH HHS - United States

The protease caspase-3 is a key mediator of apoptotic programmed cell death. But weak or transient caspase activity can contribute to neuronal differentiation, axonal pathfinding, and synaptic long-term depression. Despite the importance of sublethal, or nonapoptotic, caspase activity in neurodevelopment and neural plasticity, there has been no simple method for mapping and quantifying nonapoptotic caspase activity (NACA) in rodent brains. We therefore generated a transgenic mouse expressing a highly sensitive and specific fluorescent reporter of caspase activity, with peak signal localized to the nucleus. As a proof of concept, we first obtained evidence that NACA influences neurophysiology in an amygdalar circuit. Then focusing on the amygdala, we were able to quantify a sex-specific persistent elevation in caspase activity in females after restraint stress. This simple in vivo caspase activity reporter will facilitate systems-level studies of apoptotic and nonapoptotic phenomena in behavioral and pathologic models.

Citace poskytuje Crossref.org

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$a The protease caspase-3 is a key mediator of apoptotic programmed cell death. But weak or transient caspase activity can contribute to neuronal differentiation, axonal pathfinding, and synaptic long-term depression. Despite the importance of sublethal, or nonapoptotic, caspase activity in neurodevelopment and neural plasticity, there has been no simple method for mapping and quantifying nonapoptotic caspase activity (NACA) in rodent brains. We therefore generated a transgenic mouse expressing a highly sensitive and specific fluorescent reporter of caspase activity, with peak signal localized to the nucleus. As a proof of concept, we first obtained evidence that NACA influences neurophysiology in an amygdalar circuit. Then focusing on the amygdala, we were able to quantify a sex-specific persistent elevation in caspase activity in females after restraint stress. This simple in vivo caspase activity reporter will facilitate systems-level studies of apoptotic and nonapoptotic phenomena in behavioral and pathologic models.
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