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In vivo MEMRI Reveals Decreased Activation of the Hippocampal and Amygdaloid Regions in a Rodent Model of RAS‐Dependent Hypertension
Author(s) -
Zubcevic Jasenka,
Perez Pablo,
Ahmari Niousha,
Marulanda Carvajal Jessica,
Raizada Mohan,
Febo Marcelo
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.983.8
Subject(s) - hippocampal formation , neuroinflammation , neuroscience , amygdala , hippocampus , premovement neuronal activity , medicine , psychology , endocrinology , disease
Brain RAS affects pathogenesis of neuronal disease by contributing to neuroinflammation in animal models including hypertension. Thus, we hypothesized that the overactive brain RAS will directly contribute to decreased neuronal activity in cognitive brain areas. METHODS: Manganese‐enhanced magnetic resonance imaging (MEMRI) yielded in vivo mapping of spontaneous neuronal activity in the amygdala and hippocampus in a rodent model of overactive brain RAS and neuroinflammation, the spontaneously hypertensive rat (SHR) compared to the Wistar Kyoto (WKY). Rats were treated with manganese chloride (MnCl 2 30 mM, i.p.; 16‐20 hrs) and T 1 ‐weighted images were obtained (4.7T). Coronal slice scans were automatically segmented (FMRIB FSL and Ekam Solutions) and analyzed for differences in normalized signal intensity. RESULTS: We observed lower signal intensity in basal/central amygdala (53%), lateral (73%) and medial amygdala (50%), CA2 (46%) and CA3 hippocampal nuclei (30%), central gray (49%), and habenula (15%), in the SHR vs WKY rats. CONCLUSION To our knowledge, this is the first MEMRI assessment of neuronal activity suggesting abnormal hippocampal and amygdaloid neurocognitive functioning in the SHR. This supports the role of hypertension in cognitive decline and advocates for a therapeutic approach for neuronal disease by regulating the brain RAS. NIH HL33610.