Effects of α7 Nicotinic Receptor Activation on Cell Survival in Rat Organotypic Hippocampal Slice Cultures

Autor: R. Andrew Tasker, Denise F. Happ
Rok vydání: 2017
Předmět:
0301 basic medicine
Excitotoxicity
Receptors
Nicotinic
Hippocampal formation
Pharmacology
Toxicology
medicine.disease_cause
Hippocampus
Synaptic Transmission
Rats
Sprague-Dawley
Nicotinic receptor
chemistry.chemical_compound
0302 clinical medicine
NMDA RECEPTORS
Nicotinic Agonists
BRAIN
Receptor
IN-VIVO
OXYGEN-GLUCOSE DEPRIVATION
Chemistry
musculoskeletal
neural
and ocular physiology
General Neuroscience
POSITIVE ALLOSTERIC MODULATION
Temporal Lobe
Neurotoxicity Syndromes
Agonist
DOMOIC ACID
Propidium iodide
Cell Survival
medicine.drug_class
Aconitine
Receptors
N-Methyl-D-Aspartate
Neuroprotection
03 medical and health sciences
medicine
Animals
ACETYLCHOLINE-RECEPTORS
Methyllycaconitine
Dentate gyrus
NMDA receptor
Receptor interaction
NERVOUS-SYSTEM
CA1 INTERNEURONS
030104 developmental biology
nervous system
CHOLINE
Organotypic slice cultures
030217 neurology & neurosurgery
Zdroj: Happ, D F & Tasker, R A 2018, ' Effects of α7 Nicotinic Receptor Activation on Cell Survival in Rat Organotypic Hippocampal Slice Cultures ', Neurotoxicity Research, vol. 33, no. 4, pp. 887-895 . https://doi.org/10.1007/s12640-017-9854-2
ISSN: 1476-3524
1029-8428
Popis: Glutamatergic signaling via N-methyl-D-aspartate receptors (NMDARs) is important for physiological functioning, but can also induce cell death via excitotoxic mechanisms in many neuropathological diseases, such as stroke. Altering the cellular response to excitotoxic insults by modulating the downstream effects of NMDAR activation represents a promising therapeutic approach. For example, α7 nicotinic acetylcholine receptors (α7 nAChRs) signaling has been shown to be able to change NMDA-induced neurotoxicity in some models. However, both neuroprotective and neurotoxic effects have been reported. In this study, we examined the effect of co-activation of α7 nAChRs on NMDA-mediated cell death in rat organotypic hippocampal slice cultures (OHSCs). Our results show that α7 nAChR stimulation did not significantly influence NMDA-induced excitotoxic cell damage as measured by propidium iodide uptake. However, treatment of OHSCs with the α7 nAChR agonist choline alone induced an increase in the propidium iodide signal. Both the α7 nAChR antagonist methyllycaconitine (MLA) and the NMDAR antagonist (RS)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) were able to block this effect in the dentate gyrus and hippocampal subfield CA3.
Databáze: OpenAIRE
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