Cardiac sympathetic nerve transdifferentiation reduces action potential heterogeneity after myocardial infarction.

Cardiac sympathetic nerves undergo cholinergic transdifferentiation following reperfused myocardial infarction (MI), whereby the sympathetic nerves release both norepinephrine (NE) and acetylcholine (ACh). The functional electrophysiological consequences of post-MI transdifferentiation have never been explored. We performed MI or sham surgery in wild-type (WT) mice and mice in which choline acetyltransferase was deleted from adult noradrenergic neurons [knockout (KO)].

Sex differences in sympathetic gene expression and cardiac neurochemistry in Wistar Kyoto rats.

The stellate ganglia are the predominant source of sympathetic innervation to the heart. Remodeling of sympathetic nerves projecting to the heart has been observed in several cardiovascular diseases, and sympathetic dysfunction contributes to cardiac pathology. Wistar Kyoto rats are a common model for the study of cardiovascular diseases, but we lack a profile of the baseline transcriptomic and neurochemical characteristics of their cardiac sympathetic neurons.

Transient denervation of viable myocardium after myocardial infarction does not alter arrhythmia susceptibility.

Cardiac sympathetic nerves stimulate heart rate and force of contraction. Myocardial infarction (MI) leads to the loss of sympathetic nerves within the heart, and clinical studies have indicated that sympathetic denervation is a risk factor for arrhythmias and cardiac arrest. Two distinct types of denervation have been identified in the mouse heart after MI caused by ischemia-reperfusion: transient denervation of peri-infarct myocardium and sustained denervation of the infarct.

Molecular Signals Involved in Human B Cell Migration into the Retina: In Vitro Investigation of ICAM-1, VCAM-1, and CXCL13.

Purpose: B cells participate in diverse retinal immunopathologies. Endothelial adhesion molecules and chemokines direct leukocyte trafficking. We examined the involvement of three molecular signals in retinal transendothelial migration of human B cells: ICAM-1, VCAM-1, and CXCL13.

Myocardial Infarction Causes Transient Cholinergic Transdifferentiation of Cardiac Sympathetic Nerves via gp130.

Unlabelled: Sympathetic and parasympathetic control of the heart is a classic example of norepinephrine (NE) and acetylcholine (ACh) triggering opposing actions. Sympathetic NE increases heart rate and contractility through activation of β receptors, whereas parasympathetic ACh slows the heart through muscarinic receptors. Sympathetic neurons can undergo a developmental transition from production of NE to ACh and we provide evidence that mouse cardiac sympathetic nerves transiently produce ACh after myocardial infarction (MI).

Disrupting protein tyrosine phosphatase σ does not prevent sympathetic axonal dieback following myocardial infarction.

The neuronal receptor protein tyrosine phosphatase receptor σ (PTPσ) inhibits axonal extension upon binding to chondroitin sulfate proteoglycans (CSPGs) in scar tissue. We recently demonstrated that modulating or deleting PTPσ promoted re-innervation of the CSPG-containing cardiac scar after ischemia-reperfusion (I-R). However, it remains unknown if the lack of PTPσ or early treatment with the PTPσ modulator, intracellular sigma peptide (ISP), prevents the initial injury-induced axonal dieback.

Migration of toxoplasma gondii-infected dendritic cells across human retinal vascular endothelium.

Purpose: Toxoplasma gondii, the parasite responsible for ocular toxoplasmosis, accesses the retina from the bloodstream. We investigated the dendritic cell as a potential taxi for T. gondii tachyzoites moving across the human retinal endothelium, and examined the participation of adhesion molecules and chemokines in this process.

Effect of caloric restriction on base-excision repair (BER) in the aging rat brain.

Apyrimidinic/apurinic endonuclease (APE) is a key protein involved in the base-excision DNA repair (BER) pathway of oxidative DNA lesions. Using a novel oligonucleotide substrate, we demonstrate that APE activity in the frontal/parietal cortex (F/PCTX), cerebellum, brainstem, midbrain and hypothalamus declined with age in rats on an ad libitum (AL) diet. In contrast, APE activity for these brain regions was approximately 1.

Genotoxicants target distinct molecular networks in neonatal neurons.

Background: Exposure of the brain to environmental agents during critical periods of neuronal development is considered a key factor underlying many neurologic disorders.

Objectives: In this study we examined the influence of genotoxicants on cerebellar function during early development by measuring global gene expression changes.

Methods: We measured global gene expression in immature cerebellar neurons (i.