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[P3–045]: BENEFICIAL EFFECTS OF ANGIOTENSIN CONVERTING ENZYME INHIBITOR CAPTOPRIL ON SLEEP DEPRIVATION‐INDUCED COGNITIVE IMPAIRMENT
Author(s) -
Parameswari R.P.,
Girish R.,
Babu C. Saravana,
Thyagarajan S.P.,
Dwarakanath B.S.
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.06.1858
Subject(s) - captopril , neun , hippocampus , synapsin i , synaptic plasticity , sleep deprivation , neuroprotection , medicine , endocrinology , hippocampal formation , neuroplasticity , neuroscience , psychology , cognition , chemistry , blood pressure , synaptic vesicle , immunohistochemistry , biochemistry , vesicle , receptor , membrane
Background: In early stages of Alzheimer’s disease (AD) neuronal hyperexcitability contributes to network dysfunction observed in regions such as hippocampus. Inhibitory neurotransmission impairments underly this excitability increase. G-protein gated potassium (GirK) channels induce the neurons to hyperpolarize, compensating the excitatory excess between neurotransmission systems. Previously, we have shown Methods:We have studied the relationship between GirK channel and the effects of acute intracerebroventricular injections of Ab1-42 in behaving mice 1) at the synaptic level, by using I/O and PPF protocols in CA3-CA1 synapse, 2) at the circuit and network levels, by studying LTP in CA3-CA1 synapse and oscillatory properties of CA1 region and 3) at the behavioral level, on learning and memory capabilities CA3-CA1 synapse-dependent. Results: Our data suggest that GirK channels are necessary for normal hippocampal activity at synaptic, neural network and behavioral levels. Interestingly, we found that increasing GirK activity re-establishes hippocampal synaptic plasticity, network activity, and memory deficits induced by Ab. Conclusions:Taken together, our results support the contention that manipulations focused on the prevention of network hyperexcitability would provide new therapeutic approaches in the pathogenesis of AD.