PMID- 35538828
OWN - NLM
STAT- MEDLINE
DCOM- 20230315
LR  - 20230321
IS  - 1996-3181 (Electronic)
IS  - 1871-5273 (Linking)
VI  - 22
IP  - 5
DP  - 2023
TI  - The Role of Ca(2+) Permeable AMPA Receptors in Neurodegeneration, Neurotoxicity, 
      and Neuroinflammation.
PG  - 624-633
LID - 10.2174/1871527321666220510141735 [doi]
AB  - It is believed that degenerative conditions that give rise to neurological 
      diseases may share an abnormal influx of Ca(2+), mainly through glutamate 
      receptors. Current research on the glutamatergic system indicates that the 
      N-methyl-D-aspartate receptor (NMDAR) is not the only receptor permeable to 
      Ca(2+). Under certain conditions, alpha 
      -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) are able 
      to rapidly and potently mediate a neurotoxic Ca(2+) influx. AMPARs are encoded by 
      four genes designated GluR 1-4. The presence of the edited GluA2 subunit makes 
      the heteromeric AMPAR impermeable to Ca(2+) (CI-AMPAR's). On the other hand, the 
      lack of GluA2 or disruptions in its post-translational editing result in 
      Ca(2+)-permeable AMPA receptors (CP-AMPARs). In addition to triggering behavioral 
      changes, the increase in CP-AMPARs is documented in several neurodegenerative, 
      neuroinflammatory and neurotoxic conditions, demonstrating that AMPAR changes may 
      play a role in the emergence and evolution of pathological conditions of the 
      central nervous system (CNS). Seeking to better understand how CP-AMPARs 
      influence CNS neuropathology, and how it may serve as a pharmacological target 
      for future molecules, in this article, we summarize and discuss studies 
      investigating changes in the composition of AMPARs and their cellular and 
      molecular effects, to improve the understanding of the therapeutic potential of 
      the CP-AMPAR in neurodegenerative, neurotoxic and neuroinflammatory diseases.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - da Silva, Jose Afonso Correa
AU  - da Silva JAC
AD  - Department of Physiology, Institute for Basic Health Sciences, Federal University 
      of Rio Grande do Sul, Porto Alegre, Brazil.
FAU - Schroder, Nadja
AU  - Schroder N
AD  - Department of Physiology, Institute for Basic Health Sciences, Federal University 
      of Rio Grande do Sul, Porto Alegre, Brazil.
AD  - National Institute of Science and Technology for Translational Medicine 
      (INCT-TM), Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), 
      Brasilia, Brazil.
LA  - eng
PT  - Journal Article
PL  - United Arab Emirates
TA  - CNS Neurol Disord Drug Targets
JT  - CNS & neurological disorders drug targets
JID - 101269155
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Humans
MH  - *Receptors, AMPA
MH  - *Neuroinflammatory Diseases
MH  - Receptors, N-Methyl-D-Aspartate
MH  - Calcium/metabolism
OTO - NOTNLM
OT  - AMPA receptors
OT  - calcium
OT  - calcium-permeable AMPA receptors (CP-AMPAR)
OT  - neurodegenerative diseases
OT  - neurotoxicity
OT  - pharmacological target
EDAT- 2022/05/12 06:00
MHDA- 2023/03/16 06:00
CRDT- 2022/05/11 03:14
PHST- 2021/11/12 00:00 [received]
PHST- 2022/02/25 00:00 [revised]
PHST- 2022/03/03 00:00 [accepted]
PHST- 2022/05/12 06:00 [pubmed]
PHST- 2023/03/16 06:00 [medline]
PHST- 2022/05/11 03:14 [entrez]
AID - CNSNDDT-EPUB-123332 [pii]
AID - 10.2174/1871527321666220510141735 [doi]
PST - ppublish
SO  - CNS Neurol Disord Drug Targets. 2023;22(5):624-633. doi: 
      10.2174/1871527321666220510141735.