sympathetic neurons
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2022 ◽  
Vol 15 ◽  
Author(s):  
Lukas Dehe ◽  
Shaaban A. Mousa ◽  
Noureddin Aboryag ◽  
Mohammed Shaqura ◽  
Antje Beyer ◽  
...  

Recent interest has focused on the mineralocorticoid receptor (MR) and its impact on the myocardium and the performance of the heart. However, there is a lack of evidence about MR expression and its endogenous ligand aldosterone synthesis with specific regard to the intrinsic cardiac nervous system. Therefore, we looked for evidence of MR and aldosterone in sympathetic and parasympathetic neurons of intracardiac ganglia. Tissue samples from rat heart atria were subjected to conventional reverse-transcriptase polymerase chain reaction (PCR), Western blot, and double immunofluorescence confocal analysis of MR, corticosterone-inactivating enzyme 11β-hydroxysteroid-dehydrogenase-2 (11β-HSD2), aldosterone, and its processing enzyme CYP11B2 together with the neuronal markers vesicular acetylcholine transporter (VAChT) and tyrosine hydroxylase (TH). Our results demonstrated MR, 11β-HSD2, and CYP11B2 specific mRNA and protein bands in rat heart atria. Double immunofluorescence labeling revealed coexpression of MR immunoreactivity with VAChT in large diameter parasympathetic principal neurons. In addition, MR immunoreactivity was identified in TH-immunoreactive small intensely fluorescent (SIF) cells and in nearby VAChT- and TH-immunoreactive nerve terminals. Interestingly, the aldosterone and its synthesizing enzyme CYP11B2 and 11β-HSD2 colocalized in MR– immunoreactive neurons of intracardiac ganglia. Overall, this study provides first evidence for the existence of not only local expression of MR, but also of 11β-HSD2 and aldosterone with its processing enzyme CYP11B2 in the neurons of the cardiac autonomic nervous system, suggesting a possible modulatory role of the mineralocorticoid system on the endogenous neuronal activity on heart performance.


2021 ◽  
Vol 2 (4) ◽  
pp. 101001
Author(s):  
Catia Andreassi ◽  
Antonella Riccio

2021 ◽  
Vol 22 (22) ◽  
pp. 12327
Author(s):  
Ekaterina K. Selivanova ◽  
Anastasia A. Shvetsova ◽  
Anna A. Borzykh ◽  
Dina K. Gaynullina ◽  
Oxana O. Kiryukhina ◽  
...  

Nitric oxide (NO) has been shown to stimulate differentiation and increase the survival of ganglionic sympathetic neurons. The proportion of neuronal NOS-immunoreactive sympathetic preganglionic neurons is particularly high in newborn rats and decreases with maturation. However, the role of NO in the development of vascular sympathetic innervation has never been studied before. We tested the hypothesis that intrauterine NO deficiency weakened the development of vascular sympathetic innervation and thereby changed the contractility of peripheral arteries and blood pressure level in two-week-old offspring. Pregnant rats consumed NOS inhibitor L-NAME (250 mg/L in drinking water) from gestational day 10 until delivery. Pups in the L-NAME group had a reduced body weight and blood level of NO metabolites at 1–2 postnatal days. Saphenous arteries from two-week-old L-NAME offspring demonstrated a lower density of sympathetic innervation, a smaller inner diameter, reduced maximal active force and decreased α-actin/β-actin mRNA expression ratio compared to the controls. Importantly, pups in the L-NAME group exhibited decreased blood pressure levels before, but not after, ganglionic blockade with chlorisondamine. In conclusion, intrauterine L-NAME exposure is followed by the impaired development of the sympathetic nervous system in early postnatal life, which is accompanied by the structural and functional remodeling of arterial blood vessels.


Author(s):  
Uwe Ernsberger ◽  
Thomas Deller ◽  
Hermann Rohrer

AbstractDuring the last 30 years, our understanding of the development and diversification of postganglionic sympathetic neurons has dramatically increased. In parallel, the list of target structures has been critically extended from the cardiovascular system and selected glandular structures to metabolically relevant tissues such as white and brown adipose tissue, lymphoid tissues, bone, and bone marrow. A critical question now emerges for the integration of the diverse sympathetic neuron classes into neural circuits specific for these different target tissues to achieve the homeostatic regulation of the physiological ends affected.


2021 ◽  
Author(s):  
Pedro Lourenco Katayama ◽  
Isabela de Paula Leirao ◽  
Alexandre Kanashiro ◽  
Joao Paulo Mesquita Luiz ◽  
Fernando Queiroz Cunha ◽  
...  

Recent evidence has suggested that the carotid bodies might act as immunological sensors, detecting pro-inflammatory mediators and signalling to the central nervous system, which, in turn, orchestrates autonomic responses. Here, we demonstrated that the TNF-α receptor type I is expressed in the carotid bodies of rats. The systemic administration of TNF-α increased carotid body afferent discharge and activated glutamatergic neurons in the nucleus tractus solitarius (NTS) that project to the rostral ventrolateral medulla (RVLM), where the majority of pre-sympathetic neurons reside. The activation of these neurons was accompanied by generalized activation of the sympathetic nervous system. Carotid body ablation blunted the TNF-α-induced activation of RVLM-projecting NTS neurons and the increase in splanchnic sympathetic nerve activity. Finally, plasma and spleen levels of cytokines after TNF-α administration were higher in rats subjected to either carotid body ablation or splanchnic sympathetic denervation. Collectively, our findings indicate that the carotid body detects circulating TNF-α to activate a counteracting sympathetic anti-inflammatory mechanism.


2021 ◽  
Author(s):  
Yuan Wang ◽  
Rong Huang ◽  
Zuying Chai ◽  
Changhe Wang ◽  
Xingyu Du ◽  
...  

A central principle of synaptic transmission is that action potential induced presynaptic neurotransmitter release occurs exclusively via Ca2+ dependent secretion (CDS). T he discovery and mechanistic investigations of Ca2+ independent but voltage dependent secretion (CiVDS) have demonstrated that the action potential per se is sufficient to trigger neurotransmission in the somata of primary sensory and sympathetic neurons in mammals. One key question remains, however, whether CiVDS contributes to central synaptic transmission. Here we report, in the central transmission from presynaptic (dorsal root ganglion) to postsynaptic (spinal dorsal horn) neurons, (1) excitatory postsynaptic currents (EPSCs) are mediated by glutamate transmission through both CiVDS up to 87%) and CDS; (2) CiVDS EPSC s are in dependent of extracellular and intracellular Ca2+; (3) CiVDS is >100 times faster than CDS in vesicle recycling with much less short term depression; 4) the fusion machinery of CiVDS includes Cav2.2 (voltage sensor) and SNARE (fusion pore). Together, an essential component of activity induced EPSCs is mediated by CiVDS in a central synapse.


2021 ◽  
Vol 11 (3) ◽  
pp. 257-262
Author(s):  
Roman V. Salyukov ◽  
Fedor A. Bushkov ◽  
Maria V. Frolova

Autonomic dysreflexia (AD) is a potentially life-threatening condition that develops in patients with spinal cord injury (SCI) at or above the T6 segment. First of all this condition is characterized by uncontrolled arterial hypertension, which can lead to catastrophic complications and even death. The trigger for the development of AD is often urological complications, as well as diagnostic and therapeutic manipulations on the lower urinary tract. It is important for urologists to be aware of the AD syndrome, clinical features of AD, acute and chronic management, as well as prevention episodes of AD in patients with neurogenic lower urinary dysfunction. AD is defined as an increase of systolic blood pressure of 20 mmHg from baseline in response to various afferent stimuli originating below the level of spinal cord injury. AD is based on exaltation of spinal reflex activity with irradiation of impulses in the spinal cord under conditions of dennervation preganglionic sympathetic neurons located above the T6 segment and hyperactivity of peripheral -adrenergic receptors. The main pathophysiological mechanism of AD is hypernoradrenalinemia, leading to vasoconstriction the vessels of the skin, abdominal cavity, muscles below the level of neurological injury.


2021 ◽  
Vol 27 (5) ◽  
pp. 499-508
Author(s):  
E. V. Shlyakhto ◽  
V. A. Tsyrlin ◽  
N. V. Kuzmenko ◽  
M. G. Pliss

This article is an analysis of modern data on the morphological, functional and neurochemical organization of the central mechanisms of blood circulation regulation, the violation of which can cause the development of essential hypertension. The data indicating the validity of the hypothesis of G.F. Lang that prolonged emotional stress leads to a violation of the neuronal activity of the hypothalamus structures are presented. The article describes the morphological connections of the hypothalamus with the neurons of the ventrolateral region of the medulla oblongata and the structures of the spinal cord that provide neurogenic vascular tone. The evidence of convergence of axons of neurons of the paraventricular nucleus of the hypothalamus on the preganglionic neurons of the spinal cord is presented. Neurochemical processes in the vasomotor center of the medulla oblongata are considered, morphological changes of preganglionic sympathetic neurons in experimental arterial hypertension are indicated.


2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jeanette M. Metzger ◽  
Helen N. Matsoff ◽  
Don Vu ◽  
Alexandra D. Zinnen ◽  
Kathryn M. Jones ◽  
...  

Minimal myelination is proposed to be a contributing factor to the preferential nigral neuronal loss in Parkinson’s disease (PD). Similar to nigral dopaminergic neurons, sympathetic neurons innervating the heart have long, thin axons which are unmyelinated or minimally myelinated. Interestingly, cardiac sympathetic loss in PD is heterogeneous across the heart, yet the spatial relationship between myelination and neurodegeneration is unknown. Here, we report the mapping of myelin basic protein (MBP) expression across the left ventricle of normal rhesus macaques (n = 5) and animals intoxicated with systemic 6-OHDA (50 mg/kg iv) to model parkinsonian cardiac neurodegeneration (n = 10). A subset of 6-OHDA-treated rhesus received daily dosing of pioglitazone (5 mg/kg po; n = 5), a PPARγ agonist with neuroprotective properties. In normal animals, MBP-immunoreactivity (-ir) was identified surrounding approximately 14% of axonal fibers within nerve bundles of the left ventricle, with more myelinated nerve fibers at the base level of the left ventricle than the apex p < 0.014 . Greater MBP-ir at the base was related to a greater number of nerve bundles at that level relative to the apex p < 0.05 , as the percent of myelinated nerve fibers in bundles was not significantly different between levels of the heart. Cardiac sympathetic loss following 6-OHDA was associated with decreased MBP-ir in cardiac nerve bundles, with the percent decrease of MBP-ir greater in the apex (84.5%) than the base (52.0%). Interestingly, cardiac regions and levels with more MBP-ir in normal animals showed attenuated sympathetic loss relative to areas with less MBP-ir in 6-OHDA + placebo (r = −0.7, p < 0.014 ), but not in 6-OHDA + pioglitazone (r = −0.1) subjects. Our results demonstrate that myelination is present around a minority of left ventricle nerve bundle fibers, is heterogeneously distributed in the heart of rhesus macaques, and has a complex relationship with cardiac sympathetic neurodegeneration and neuroprotection.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Di Bona ◽  
A Scalco ◽  
R Bariani ◽  
N Kuperwasser ◽  
P David ◽  
...  

Abstract Background Arrhythmogenic Cardiomyopathy (AC) is a genetic cardiac disorder, mainly caused by mutations in genes encoding desmosomal proteins, and accounts for most stress-related arrhythmic sudden cardiac deaths (SCD) in the young and athletes. The AC myocardium is hallmarked by cardiomyocyte (CM) death and fibro-fatty replacement, which generate a pro-arrhythmogenic substrate. Several pathogenetic factors in AC remain obscure and better understanding of the disease mechanisms is required to develop novel efficacious therapies to prevent SCD, which are sorely missing. The lexical analogy between desmosomes and desmosomal proteins has originally biased AC research towards CMs, the paradigmatic desmosome-bearing cells in heart. However, the myocardium is composed by different cell types, many of which express desmosomal proteins, albeit in the absence of desmosomes, including CMs, sympathetic neurons, vascular cells and fibroblasts. Notably, AC mutations are transmitted at germline, and thus may manifest in all cell types expressing desmosomal proteins. This might explain why the majority of preclinical AC models, using CM specific over-expression or deletion of the disease-causing mutation, failed to fully recapitulate the human disease phenotype. Hypothesis On these bases, we aimed to generate a knock-in (KI) AC mouse model for comprehensively studying AC pathogenesis. Methods As Desmoplakin (DSP) mutations occur in a large part of the Italian AC population, we used CRISP/Cas9 to generate a KI mouse strain harboring the Serine-to-Alanine substitution of S311, the murine homolog of human S299 [Bauce et al, 2005]. We successfully obtained DSPS311A/WT KI founders, which were viable and fertile and after backcrossing for &gt;10 generations, used to expand the new mouse strain. Mouse cardiac phenotype was characterized, at different stages (1,2,4,6,9 mo.) by functional (i.e. ECHO, telemetry-ECG, chronic exercise) and structural (i.e. EM, standard histology, confocal IF, TUNEL assay) analyses. Molecular/biochemical analyses probed the state of the main pathways involved in AC. Results Our analyses showed that, starting from 4 mo., DSP homozygous KI mice display contractile dysfunction, worsening during aging, and fibrotic myocardial remodelling with focal fatty lesions, accompanied by frequent arrhythmic beats, which become sustained ventricular arrhythmias upon Noradrenaline administration. Hearts showed desmosome alterations, particularly at advanced disease stages, and lateralization of cx43, which corresponded to the phenotype of human AC hearts. Heterozygous mice showed similar alterations, which only took longer to appear. Exercise accelerated disease progression and increased the incidence of SCD (DSPS311A: SCD=63%, n=11; ctrls: SCD=8%, n=12). Conclusion Our KI mice replicate the clinical and pathological phenotype of DSP-linked biventricular AC and are thus suited for the mechanistic study of the multicellular origin of the disease. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): PRIN Miur 2015


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