Proteomics

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Inhibitory and Excitatory Synaptic Neuroadaptations in the diazepam tolerant brain

ABSTRACT: Benzodiazepine (BZ) drugs treat seizures, anxiety, insomnia, and alcohol withdrawal by potentiating γ2 subunit containing GABA type A receptors (GABAARs). BZ clinical use is hampered by tolerance and withdrawal symptoms, which include heightened seizure susceptibility, panic, and sleep disturbances. Here, we undergo a comprehensive investigation of inhibitory GABAergic and excitatory glutamatergic plasticity in mice tolerant to benzodiazepine sedation. Using quantitative proteomics approaches, we reveal cortex neuroadaptations of key pro-excitatory mediators and synaptic plasticity pathways, highlighted by Ca2+/calmodulin-dependent protein kinase II (CAMKII), MAPK, and PKC signaling.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Tija Jacob  

LAB HEAD: Tija Jacob

PROVIDER: PXD041332 | Pride | 2023-10-24

REPOSITORIES: pride

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Dataset's files

Source:
Action DRS
Old_Hom_MzIdent.mzid.gz Mzid
Old_Hom_Protein_For_Merge.mzML Mzml
Old_Hom_TMT.msf Msf
P127595.raw Raw
P127596.raw Raw
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Publications

Benzodiazepine (BZ) drugs treat seizures, anxiety, insomnia, and alcohol withdrawal by potentiating γ2 subunit containing GABA type A receptors (GABA<sub>A</sub>Rs). BZ clinical use is hampered by tolerance and withdrawal symptoms including heightened seizure susceptibility, panic, and sleep disturbances. Here, we investigated inhibitory GABAergic and excitatory glutamatergic plasticity in mice tolerant to benzodiazepine sedation. Repeated diazepam (DZP) treatment diminished sedative effects and  ...[more]

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