Phosphoproteomic of the acetylcholine pathway enables discovery of the PKC-β-PIX-Rac1-PAK cascade as a stimulatory signal for aversive learning.
Yukie YamahashiYou-Hsin LinAkihiro MouriSho IwanagaKazuhiro KawashimaYuya TokumotoYo WatanabeMd Omar FarukXinjian ZhangDaisuke TsuboiTakashi NakanoNaoaki SaitoTaku NagaiKiyofumi YamadaKozo KaibuchiPublished in: Molecular psychiatry (2022)
Acetylcholine is a neuromodulator critical for learning and memory. The cholinesterase inhibitor donepezil increases brain acetylcholine levels and improves Alzheimer's disease (AD)-associated learning disabilities. Acetylcholine activates striatal/nucleus accumbens dopamine receptor D2-expressing medium spiny neurons (D2R-MSNs), which regulate aversive learning through muscarinic receptor M1 (M1R). However, how acetylcholine stimulates learning beyond M1Rs remains unresolved. Here, we found that acetylcholine stimulated protein kinase C (PKC) in mouse striatal/nucleus accumbens. Our original kinase-oriented phosphoproteomic analysis revealed 116 PKC substrate candidates, including Rac1 activator β-PIX. Acetylcholine induced β-PIX phosphorylation and activation, thereby stimulating Rac1 effector p21-activated kinase (PAK). Aversive stimulus activated the M1R-PKC-PAK pathway in mouse D2R-MSNs. D2R-MSN-specific expression of PAK mutants by the Cre-Flex system regulated dendritic spine structural plasticity and aversive learning. Donepezil induced PAK activation in both accumbal D2R-MSNs and in the CA1 region of the hippocampus and enhanced D2R-MSN-mediated aversive learning. These findings demonstrate that acetylcholine stimulates M1R-PKC-β-PIX-Rac1-PAK signaling in D2R-MSNs for aversive learning and imply the cascade's therapeutic potential for AD as aversive learning is used to preliminarily screen AD drugs.
Keyphrases
- protein kinase
- diabetic rats
- oxidative stress
- functional connectivity
- high glucose
- multiple sclerosis
- metabolic syndrome
- white matter
- long non coding rna
- cell migration
- subarachnoid hemorrhage
- toll like receptor
- resting state
- drug induced
- uric acid
- inflammatory response
- dendritic cells
- binding protein
- endothelial cells
- regulatory t cells
- data analysis