Vascular Pharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 107458 - 107458
Published: Dec. 1, 2024
Language: Английский
Vascular Pharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 107458 - 107458
Published: Dec. 1, 2024
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(16), P. 9071 - 9071
Published: Aug. 21, 2024
Nitric oxide (NO) is a highly versatile gasotransmitter that has first been shown to regulate cardiovascular function and then exert tight control over much broader range of processes, including neurotransmitter release, neuronal excitability, synaptic plasticity. Endothelial NO synthase (eNOS) usually far from the mind neurophysiologists, who have focused most their attention on (nNOS) as primary source at neurovascular unit (NVU). Nevertheless, available evidence suggests eNOS could also contribute generating burst that, serving volume intercellular messenger, produced in response activity brain parenchyma. Herein, we review role both regulation cerebral blood flow plasticity discuss mechanisms by which cerebrovascular endothelial cells may transduce inputs into signal. We further suggest play critical vascular-to-neuronal communication integrating signals converging onto streaming active neurons.
Language: Английский
Citations
4Biomedicines, Journal Year: 2024, Volume and Issue: 12(10), P. 2387 - 2387
Published: Oct. 18, 2024
Within the central nervous system, synaptic plasticity, fundamental to processes like learning and memory, is largely driven by activity-dependent changes in strength. This plasticity often manifests as long-term potentiation (LTP) depression (LTD), which are bidirectional modulations of efficacy. Strong epidemiological experimental evidence show that heart-brain axis could be severely compromised both neurological cardiovascular disorders. Particularly, disorders, such heart failure, hypertension, obesity, diabetes insulin resistance, arrhythmias, may lead cognitive impairment, a condition known cardiogenic dementia. Herein, we review available knowledge on molecular mechanisms dementia arise describe how LTP and/or LTD induction maintenance CA1 region hippocampus metabolic syndrome, arrhythmias. We also discuss emerging endothelial dysfunction contribute directly altering hippocampal impairing synaptically induced activation nitric oxide synthase. A better understanding CV disorders impact proper function synapses will shed novel light underpinnings dementia, thereby providing new perspective for more specific pharmacological treatments.
Language: Английский
Citations
3Journal of Neuroscience Methods, Journal Year: 2024, Volume and Issue: 410, P. 110248 - 110248
Published: Aug. 6, 2024
Language: Английский
Citations
1Vascular Pharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 107458 - 107458
Published: Dec. 1, 2024
Language: Английский
Citations
0