Welcome to the Felder Lab

The sympathetic nervous system is overactive in heart failure, and contributes to morbidity and mortality by promoting fluid accumulation, vasoconstriction, cardiac remodeling and serious ventricular arrhythmias. The Felder Laboratory studies the central nervous system mechanisms that activate the sympathetic nervous system in a rat model of heart failure that simulates human heart failure that develops after a myocardial infarction. We are particularly interested in the effects on the brain of humoral factors that increase in the circulation in heart failure as a result of activation of the immune system (i.e., pro-inflammatory cytokines) and of systems that attempt to compensate for the reduced pumping function of the failing heart (i.e., the renin-angiotensin-aldosterone system). Our molecular, immunohistochemical and electrophysiological and hemodynamic recording studies examine the effects of these humoral factors on the neurochemical milieu in central nervous system regions (in particular, the subfornical organ and the hypothalamic paraventricular nucleus) that regulate sympathetic nerve activity. The overall goal is to identify central nervous system mechanisms that might become the targets of therapeutic interventions to reduce sympathetic activity in this devastating disease.

Recent Publications

Yu, Y, Wei, SG, Weiss, RM, and Felder, RB: Silencing Epidermal Growth Factor Receptor in Hypothalamic Paraventricular Nucleus Reduces ERK1/2 Signaling and Sympathetic Excitation in Heart Failure Rats. Neuroscience, 463:227-237, 2021.

Wei, SG, Yu, Y, and Felder, RB: TNF-α-induced Sympathetic Excitation Requires EGFR and ERK1/2 Signaling in Cardiovascular Regulatory Regions of the Forebrain. Am J Physiol Heart Circ Physiol, 320:H772-H786, 2021.

Xue, B, Xue, J, Yu, Y, Wei, SG, Beltz, TG, Felder, RB, and Johnson, AK: Predator Scent-induced Sensitization of Hypertension and Anxiety-like Behaviors. Cell Mol Neurobiol, 2020 Nov 17. doi: 10.1007/s10571-020-01005-y. Epub ahead of print.

Naguib, YW, Yu, Y, Wei, SG, Morris, A, Givens, BE, Mekkawy, AI, Weiss, RM, Felder, RB, and Salem, AK: A Novel Injectable Microparticle Formulation Provides Long-Term Inhibition of Hypothalamic ERK1/2 Activity and Sympathetic Excitation in Rats with Heart Failure. Molecular Pharmaceutics, 17:3643-3648, 2020.

Naguib, YW, Givens, BE, Ho, G, Yu, Y, Wei, SG, Weiss, RM, Felder, RB, and Salem, AK: An Injectable Microparticle Formulation for the Sustained Release of the Specific MEK Inhibitor PD98059: In Vitro Evaluation and Pharmacokinetics. Drug Delivery and Translational Research, Epub Date: 05/07/2020, DOI: 10.1007/s13346-020-00758-9.

Xue, BJ, Yu, Y, Wei, SG, Beltz, TG, Guo, F, Felder, RB, and Johnson, AK: Stress-induced Sensitization of Angiotensin II Hypertension is Reversed by Blockade of Angiotensin-Converting Enzyme or Tumor Necrosis Factor-α. Am J Hypertens, 32:909-917, 2019.

Yu, Y, Cao, Y, Bell, B, Chen, X, Weiss, R, Felder, R, and Wei, SG: Brain TACE (Tumor Necrosis Factor-α-Converting Enzyme) Contributes to Sympathetic Excitation in Heart Failure Rats. Hypertension, 74:63-72, 2019.

Yu, Y, Wei, SG, Weiss, RM, and Felder, RB: Sex Differences in the Central and Peripheral Manifestations of Ischemia-induced Heart Failure in Rats. Am J Physiol Heart Circ Physiol, 316:H70-79, 2019.

All Publications

See Dr. Felder's complete list of publications on PubMed.

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ORCID

See Dr. Felder's ORCID profile.

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