Antihypertensive and neuroprotective effects of catestatin in spontaneously hypertensive rats: Interaction with GABAergic transmission in amygdala and brainstem

Highlights • CST exerted antihypertensive and neuroprotective effects. • CST interacted with GABAergic systems and increased activities. • Akt and ERK signaling were involved in neuroprotective mechanisms. • CST + MUS may constitute new therapeutic agents for neurovascular disorders.

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Bibliographic Details
Published in:Neuroscience 2014-06, Vol.270, p.48-57
Main Authors: Avolio, E, Mahata, S.K, Mantuano, E, Mele, M, Alò, R, Facciolo, R.M, Talani, G, Canonaco, M
Format: Article
Language:English
Subjects:
Age Factors
Amygdala - drug effects
Amygdala - physiopathology
Animals
Antihypertensive Agents - pharmacology
Biological and medical sciences
Blood Pressure - drug effects
Blood Pressure - physiology
Brain Stem - drug effects
Brain Stem - physiopathology
catestatin
Chromogranin A - pharmacology
Fundamental and applied biological sciences. Psychology
GABA-A Receptor Agonists - pharmacology
GABAergic agonist
GABAergic Neurons - drug effects
GABAergic Neurons - physiology
hypertension
Hypertension - drug therapy
Hypertension - physiopathology
Inhibitory Postsynaptic Potentials - drug effects
Male
MAP Kinase Signaling System - drug effects
MAP Kinase Signaling System - physiology
Muscimol - pharmacology
Nerve Degeneration - drug therapy
Nerve Degeneration - physiopathology
neurodegeneration
Neurology
Neuroprotective Agents - pharmacology
Peptide Fragments - pharmacology
Proto-Oncogene Proteins c-akt - metabolism
Pyramidal Cells - drug effects
Pyramidal Cells - physiology
Rats, Inbred SHR
SHRs
Synaptic Transmission - drug effects
Synaptic Transmission - physiology
Vertebrates: nervous system and sense organs
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Description
Summary:Highlights • CST exerted antihypertensive and neuroprotective effects. • CST interacted with GABAergic systems and increased activities. • Akt and ERK signaling were involved in neuroprotective mechanisms. • CST + MUS may constitute new therapeutic agents for neurovascular disorders.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2014.04.001