Vinicia C. Biancardi

ORCID: 0000-0001-7301-1702
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About
Contact & Profiles
Research Areas
  • Neuroscience of respiration and sleep
  • Neuroendocrine regulation and behavior
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Renin-Angiotensin System Studies
  • Neuroscience and Neuropharmacology Research
  • Circadian rhythm and melatonin
  • Nitric Oxide and Endothelin Effects
  • Neuropeptides and Animal Physiology
  • Heme Oxygenase-1 and Carbon Monoxide
  • Photoreceptor and optogenetics research
  • Protein Hydrolysis and Bioactive Peptides
  • Neonatal and fetal brain pathology
  • Eicosanoids and Hypertension Pharmacology
  • Sleep and Wakefulness Research
  • Heart Rate Variability and Autonomic Control
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Ion channel regulation and function
  • Biochemical effects in animals
  • Receptor Mechanisms and Signaling
  • Birth, Development, and Health
  • Apelin-related biomedical research
  • Regulation of Appetite and Obesity
  • Diet and metabolism studies
  • Sodium Intake and Health
  • Sexual function and dysfunction studies

Auburn University
2017-2025

Center for Neurosciences
2019-2023

Augusta University
2008-2019

Georgia Regents Medical Center
2013-2016

University of Nebraska Medical Center
2011-2016

Universidade Estadual Paulista (Unesp)
2015

University of Alberta
2015

Augusta University Health
2011-2013

Wright State University
2011

University of Cincinnati
2007-2008

Angiotensin II–mediated vascular brain inflammation emerged as a novel pathophysiological mechanism in neurogenic hypertension. However, the precise underlying mechanisms and functional consequences relation to blood–brain barrier (BBB) integrity central angiotensin II actions mediating neurohumoral activation hypertension are poorly understood. Here, we aimed determine whether BBB permeability within critical hypothalamic stem regions involved regulation was altered during Using digital...

10.1161/hypertensionaha.113.01743 article EN Hypertension 2013-12-17

ANG II is thought to increase sympathetic outflow by increasing oxidative stress and promoting local inflammation in the paraventricular nucleus (PVN) of hypothalamus. However, relative contributions drive remain poorly understood, underlying cellular molecular targets have yet be examined. has been shown enhance Toll-like receptor (TLR)4-mediated signaling on microglia. Thus, present study, we aimed determine whether II-mediated activation microglial TLR4 a key target initiating PVN. We...

10.1152/ajpheart.00247.2015 article EN AJP Heart and Circulatory Physiology 2015-12-05

Angiotensin II (AngII) is a key neuropeptide that acting within the brain hypothalamic paraventricular nucleus regulates neurohumoral outflow to circulation. Moreover, an exacerbated AngII action contributes activation in hypertension. Although effects involve changes neuronal activity, precise underlying mechanisms, cellular targets, and distribution of receptors remain largely unknown. Thus, whether direct actions on neurons, or it acts via intermediary cells, such as astrocytes, still...

10.1161/hypertensionaha.116.07747 article EN Hypertension 2016-10-04

Angiotensin II (AngII) is implicated in neuroinflammation, blood-brain barrier (BBB) disruption, and autonomic dysfunction hypertension. We have previously shown that exogenous AngII stimulates Toll-like receptor 4 (TLR4) via type 1 (AT1R), inducing activation of hypothalamic microglia ex vivo, AngII-AT1R signaling necessary for the loss BBB integrity spontaneously hypertensive rats (SHRs). Herein, we hypothesized microglial TLR4 AT1R interactions represent a crucial mechanistic link between...

10.1016/j.phrs.2021.105877 article EN cc-by-nc-nd Pharmacological Research 2021-10-04

A dynamic balance between the excitatory and inhibitory neurotransmitters glutamate GABA is critical for maintaining proper neuronal activity in brain. This partly achieved via presynaptic interactions glutamatergic ergic synapses converging into same targets. Here, we show that hypothalamic magnocellular neurosecretory neurons (MNCs), a direct crosstalk postsynaptic NMDA receptors (NMDARs) (GABA Rs) contributes to excitatory/inhibitory this system. We found activation of NMDARs by...

10.1523/jneurosci.3936-12.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-01-09

Heart failure (HF) is a debilitating disease affecting >64 million people worldwide. In addition to impaired cardiovascular performance and associated systemic complications, most patients with HF suffer from depression substantial cognitive decline. Although neuroinflammation brain hypoperfusion occur in humans rodents HF, the underlying neuronal substrates, mechanisms, their relative contribution deficits remains unknown.

10.1161/hypertensionaha.123.21070 article EN Hypertension 2023-04-10

Abstract An imbalance of excitatory and inhibitory functions has been shown to contribute numerous pathological disorders. Accumulating evidence supports the idea that a change in hypothalamic γ‐aminobutyric acid (GABA)‐ergic glutamatergic synaptic contributes exacerbated neurohumoral drive prevalent cardiovascular disorders, including hypertension. However, precise underlying mechanisms neuronal substrates are still not fully elucidated. In present study, we combined quantitative...

10.1002/cne.22256 article EN The Journal of Comparative Neurology 2009-11-20

We evaluated the hemodynamic pattern and contribution of sympathetic nervous system in conscious anesthetized (1.4 g/kg urethane, iv) Wistar rats with L-NAME-induced hypertension (20 mg/kg daily). The basal profile was similar for hypertensive animals, (N = 12) or treated L-NAME 2 7 days: increase total peripheral resistance associated a decrease cardiac output (CO) compared to normotensive 14) 14). Sympathetic blockade hexamethonium essentially caused animals (conscious, from (means +/-...

10.1590/s0100-879x2006005000077 article EN cc-by Brazilian Journal of Medical and Biological Research 2007-03-05

Neurohumoral activation, a hallmark in heart failure (HF), is linked to the progression and mortality of HF patients. Thus, elucidating its precise underlying mechanisms critical importance. Other than classic peripheral vasodilatory actions, gas NO pivotal neurotransmitter central nervous system control circulation. While accumulating evidence supports contribution blunted function neurohumoral activation HF, cellular sources, synthase (NOS) isoforms involved, remain unknown. Here, we used...

10.1161/hypertensionaha.111.175810 article EN Hypertension 2011-08-09

Neurohumoral activation, which includes augmented plasma levels of the neurohormone vasopressin (VP), is a common finding in heart failure (HF) that contributes to morbidity and mortality this disease. While an increased activation magnocellular neurosecretory cells (MNCs) enhanced glutamate function HF well documented, precise underlying mechanisms remain be elucidated. Here, we combined electrophysiology protein measurements determine whether altered glial transporter and/or expression...

10.1152/ajpregu.00056.2012 article EN AJP Regulatory Integrative and Comparative Physiology 2012-06-14

Despite the well-established contribution of neurohumoral activation to morbidity and mortality in heart failure (HF) patients, relatively little is known about underlying central nervous system mechanisms. In this study, we aimed determine whether changes GABAergic inhibitory glutamatergic excitatory synaptic function contribute altered hypothalamic magnocellular neurosecretory cell (MNC) activity HF rats. Patch-clamp recordings were obtained from MNCs brain slices sham Glutamate (EPSCs)...

10.1152/jn.00218.2011 article EN Journal of Neurophysiology 2011-06-23

Cardiovascular (CV) representation has been identified within the insular cortex (IC) and a lateralization of function previously suggested. In order to further understand role IC on cardiovascular control, present study compared CV responses evoked by stimulation N-metil-D-aspartate (NMDA) receptors in right left posterior at different rostrocaudal levels. Intracortical microinjections NMDA were performed into male Wistar rats anaesthetized with urethane (1.4 g/kg) prepared for blood...

10.1111/1440-1681.12542 article EN Clinical and Experimental Pharmacology and Physiology 2016-01-10

Neurovascular coupling (NVC), the process that links neuronal activity to cerebral blood flow changes, has been mainly studied in superficial brain areas, namely neocortex. Whether conventional, rapid, and spatially restricted NVC response can be generalized deeper functionally diverse regions remains unknown. Implementing an approach for vivo two-photon imaging from ventral surface of brain, we show a systemic homeostatic challenge, acute salt loading, progressively increases hypothalamic...

10.1016/j.celrep.2021.109925 article EN cc-by-nc-nd Cell Reports 2021-11-01

Abstract Cell migration through confining three dimensional (3D) topographies can lead to loss of nuclear envelope integrity, DNA damage, and genomic instability. Despite these detrimental phenomena, cells transiently exposed confinement do not usually die. Whether this is also true for subjected long‐term remains unclear at present. To investigate this, photopatterning microfluidics are employed fabricate a high‐throughput device that circumvents limitations previous cell models enables...

10.1002/advs.202302228 article EN cc-by Advanced Science 2023-06-02

The suprachiasmatic nucleus (SCN) sets the phase of oscillation throughout brain and body. Anatomical evidence reveals a portal system linking SCN organum vasculosum lamina terminalis (OVLT), begging question direction blood flow nature diffusible signals that in this specialized vasculature. Using combination anatomical vivo two-photon imaging approaches, we unequivocally show flows unidirectionally from to OVLT, rate displays daily oscillations with higher at night than day, circulating...

10.1126/sciadv.adn8350 article EN cc-by-nc Science Advances 2024-06-21
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