miRNA-132/212 Gene-Deletion Aggravates the Effect of Oxygen-Glucose Deprivation on Synaptic Functions in the Female Mouse Hippocampus.

Tytuł:: miRNA-132/212 Gene-Deletion Aggravates the Effect of Oxygen-Glucose Deprivation on Synaptic Functions in the Female Mouse Hippocampus.
Autorzy:: Bormann D; Center for Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria.; Laboratory for Cardiac and Thoracic Diagnosis, Department of Surgery, Regeneration and Applied Immunology, Medical University of Vienna, Research Laboratories Vienna General Hospital, Waehringer Guertel 18-20, 1090 Vienna, Austria.; Division of Thoracic Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
Stojanovic T; Center for Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria.
Cicvaric A; Department of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, New York, NY 10461, USA.
Schuld GJ; Center for Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria.
Cabatic M; Center for Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria.
Ankersmit HJ; Laboratory for Cardiac and Thoracic Diagnosis, Department of Surgery, Regeneration and Applied Immunology, Medical University of Vienna, Research Laboratories Vienna General Hospital, Waehringer Guertel 18-20, 1090 Vienna, Austria.; Division of Thoracic Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.; Aposcience AG, Dresdner Straße 87/A 21, 1200 Vienna, Austria.
Monje FJ; Center for Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria.
Źródło:: Cells [Cells] 2021 Jul 06; Vol. 10 (7). Date of Electronic Publication: 2021 Jul 06.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: Basel, Switzerland : MDPI
MeSH Terms:: Base Sequence*
Sequence Deletion*
Brain Ischemia/*genetics
Dentate Gyrus/*metabolism
MicroRNAs/*genetics
Acetylcholine/metabolism ; Acetylcholinesterase/genetics ; Acetylcholinesterase/metabolism ; Animals ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Cholinergic Neurons/drug effects ; Cholinergic Neurons/metabolism ; Cholinergic Neurons/pathology ; Dentate Gyrus/pathology ; Excitatory Postsynaptic Potentials/physiology ; Female ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Gene Expression Regulation ; Glucose/deficiency ; Glucose/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; MicroRNAs/metabolism ; Microtomy ; Oxygen/pharmacology ; Patch-Clamp Techniques ; Receptor, Muscarinic M1/genetics ; Receptor, Muscarinic M1/metabolism ; Synaptic Transmission ; Tissue Culture Techniques
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Grant Information:: P 31004 Austria FWF_ Austrian Science Fund FWF
Contributed Indexing:: Keywords: acetylcholine; dentate gyrus; field excitatory postsynaptic potentials (fEPSP); hippocampus; hypoxia; ischemia; miRNA 132/212; oxygen-glucose deprivation (OGD)
Substance Nomenclature:: 0 (GPI-Linked Proteins)
0 (MIRN132 microRNA, mouse)
0 (MIRN212 microRNA, mouse)
0 (MicroRNAs)
0 (Receptor, Muscarinic M1)
EC 3.1.1.7 (Acetylcholinesterase)
EC 3.1.1.7 (Ache protein, mouse)
IY9XDZ35W2 (Glucose)
N9YNS0M02X (Acetylcholine)
S88TT14065 (Oxygen)
Entry Date(s):: Date Created: 20210807 Date Completed: 20211028 Latest Revision: 20231206
Update Code:: 20240105
PubMed Central ID:: PMC8306255
DOI:: 10.3390/cells10071709
PMID:: 34359879
: Czasopismo naukowe

Pełny tekst

Cerebral ischemia and its sequelae, which include memory impairment, constitute a leading cause of disability worldwide. Micro-RNAs (miRNA) are evolutionarily conserved short-length/noncoding RNA molecules recently implicated in adaptive/maladaptive neuronal responses to ischemia. Previous research independently implicated the miRNA-132/212 cluster in cholinergic signaling and synaptic transmission, and in adaptive/protective mechanisms of neuronal responses to hypoxia. However, the putative role of miRNA-132/212 in the response of synaptic transmission to ischemia remained unexplored. Using hippocampal slices from female miRNA-132/212 double-knockout mice in an established electrophysiological model of ischemia, we here describe that miRNA-132/212 gene-deletion aggravated the deleterious effect of repeated oxygen-glucose deprivation insults on synaptic transmission in the dentate gyrus, a brain region crucial for learning and memory functions. We also examined the effect of miRNA-132/212 gene-deletion on the expression of key mediators in cholinergic signaling that are implicated in both adaptive responses to ischemia and hippocampal neural signaling. miRNA-132/212 gene-deletion significantly altered hippocampal AChE and mAChR-M1, but not α7-nAChR or MeCP2 expression. The effects of miRNA-132/212 gene-deletion on hippocampal synaptic transmission and levels of cholinergic-signaling elements suggest the existence of a miRNA-132/212-dependent adaptive mechanism safeguarding the functional integrity of synaptic functions in the acute phase of cerebral ischemia.

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