Chemical Stimulation of Rodent and Human Cortical Synaptosomes: Implications in Neurodegeneration.

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI

Stimulation, Chemical*; Alzheimer Disease/*metabolism ; Long-Term Potentiation/*physiology ; Neuronal Plasticity/*physiology ; Synapses/*metabolism ; Synaptosomes/*metabolism; Actins/metabolism ; Aged ; Animals ; Brain/physiology ; Colforsin/administration & dosage ; Female ; Frontal Lobe/pathology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate/metabolism ; Rolipram/administration & dosage

Synaptic plasticity events, including long-term potentiation (LTP), are often regarded as correlates of brain functions of memory and cognition. One of the central players in these plasticity-related phenomena is the α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor (AMPAR). Increased levels of AMPARs on postsynaptic membranes thus constitute a biochemical measure of LTP. Isolated synaptic terminals (synaptosomes) are an excellent ex vivo tool to monitor synaptic physiology in healthy and diseased brains, particularly in human research. We herein describe three protocols for chemically-induced LTP (cLTP) in synaptosomes from both rodent and human brain tissues. Two of these chemical stimulation protocols are described for the first time in synaptosomes. A pharmacological block of synaptosomal actin dynamics confirmed the efficiency of the cLTP protocols. Furthermore, the study prototypically evaluated the deficiency of cLTP in cortical synaptosomes obtained from human cases of early-onset Alzheimer's disease (EOAD) and frontotemporal lobar degeneration (FLTD), as well as an animal model that mimics FLTD.

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1835-PG Neurological Foundation of New Zealand; 16-597 Health Research Council of New Zealand; NA Department of Anatomy, University of Otago, New Zealand

Keywords: KCl; NMDAR; PS19 mice; depolarization; forskolin; glycine; latrunculin A; radio-labelled; rolipram; tetraethyl ammonium

0 (Actins)
0 (Receptors, Glutamate)
0 (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptor, human)
1F7A44V6OU (Colforsin)
K676NL63N7 (Rolipram)

Date Created: 20210602 Date Completed: 20211025 Latest Revision: 20211025

20240829

PMC8151714

10.3390/cells10051174

34065927