Adrenal medullary chromaffin cell culture systems are extremely useful for the study of excitation-secretion coupling in an in vitro...
Since the work of Katz, Douglas, and their collaborators almost half a century ago (Katz, 1969), a central concept in the physiology of neurosecretion is that a rise in cytosolic [Ca2+], resulting from Ca2+ influx, triggers exocytosis. More recently it has become clear that the rise in [Ca2+] occurs in a microdomain within the vicinity (i.e., at a distance of 200-300 nm in chromaffin cells) of plasmalemmal Ca2+ channels (García et al., 2006; Neher and Sakaba, 2008). This finding raises the possibility of other microdomains where a rise in focal [Ca2+] might mediate other processes, allowing Ca2+ to subserve several functions without cross talk. This possibility receives further support from the study of Ca2+ sparks in smooth muscle cells. Ca2+ sparks are focal Ca2+ transients found in striated and smooth muscle and mediated by RYRs (Cheng and Lederer, 2008). In striated muscle, they are the quanta or building blocks that make up a global increase in [Ca2+] to trigger contraction (Csernoch, ...
Synaptotagmin-1, the canonical isoform of the synaptotagmin family, is a Ca(2+) sensor for fast synchronous neurotransmitter release in forebrain neurons and chromaffin cells. Even though deletion of synaptotagmin-1 abolishes fast exocytosis in chromaffin cells, it reduces overall secretion by only 20% because of the persistence of slow exocytosis. Therefore, another Ca(2+) sensor dominates release in these cells. Synaptotagmin-7 has a higher Ca(2+) affinity and slower binding kinetics than synaptotagmin-1, matching the proposed properties for the second, slower Ca(2+) sensor. Here, we examined Ca(2+)-triggered exocytosis in chromaffin cells from KO mice lacking synaptotagmin-7, and from knockin mice containing normal levels of a mutant synaptotagmin-7 whose C(2)B domain does not bind Ca(2+). In both types of mutant chromaffin cells, Ca(2+)-triggered exocytosis was decreased dramatically. Moreover, in chromaffin cells lacking both synaptotagmin-1 and -7, only a very slow release component, ...
In a previous report, we described the ability of two secretogogues, histamine and nicotine, to stimulate additive effects on catecholamine (CA) release and synapsin II phosphorylation in bovine adrenal chromaffin cells (BACC) [Firestone and Browning (1992), J. Neurochem., 58:441-447]. We hypothesized that these results were due to the combined effects on cytosolic Ca++ of the two distinct signalling pathways. We therefore examined the intracellular Ca++ signals stimulated by histamine and nicotine, alone and together. In Ca(++)-deficient medium, nicotine-stimulated signals were abolished, whereas histamine-stimulated signals were maintained, demonstrating that nicotine depended entirely on Ca++ influx for its effects. Indeed, the nicotine-stimulated signal could also be prevented using a Ca++ channel blocker, nicardipine. Further, the observation that exposure of BACC to thapsigargin reduced histamine-stimulated Ca++ signals verified that histamine mobilizes Ca++ from intracellular stores. Thus, the
Investigations into the effects of culturing bovine adrenal chromaffin cells in the presence (72 h) of dibutyryl cyclic AMP, forskolin, and reserpine on the level and release of [Met]enkephalyl-Arg6-Phe7 immunoreactivity, noradrenaline, and adrenaline are reported. The assay for [Met]enkephalyl-Arg6-Phe7 immunoreactivity recognises both peptide B, the 31-amino acid carboxy-terminal segment of proenkephalin, and its heptapeptide fragment, [Met]enkephalyl-Arg6-Phe7. Treatments that elevate cyclic AMP increase the amount of peptide immunoreactivity in these cells; this is predominantly peptide B-like immunoreactivity in both control cells and cyclic AMP-elevated cells. Treatment with reserpine gives no change in total immunoreactivity levels, but does not result in increased accumulation of the heptapeptide [Met]enkephalyl-Arg6-Phe7 at the expense of immunoreactivity that elutes with its immediate precursor, peptide B. Cyclic AMP treatment causes either no change or a decrease in levels of accumulated
In bovine adrenal chromaffin cells, prostaglandin E2 (PGE2) stimulates the formation of inositol phosphates and Ca2+ mobilization through its specific receptor [Yokohama, Tanaka, Ito, Negishi, Hayashi & Hayaishi (1988) J. Biol. Chem. 263, 1119-1122]. Here we show that PGE2-induced phosphoinositide metabolism was blocked by pretreatment with 12-O-tetradecanoylphorbol 13-acetate (TPA). Using intact cells, we also examined the inhibitory effect of TPA on the individual steps of the activation process of phosphoinositide metabolism. The inhibition was observed within 1 min and complete by 10 min after addition of 1 microM-TPA, and half-maximal inhibition by TPA occurred at 20 nM. TPA prevented Ca2+ mobilization induced by PGE2, but not by the Ca2+ ionophore ionomycin. The inactive phorbol ester 4 alpha-phorbol 12,13-didecanoate did not inhibit the formation of inositol phosphates and Ca2+ mobilization by PGE2. TPA treatment affected neither the high-affinity binding of [3H]PGE2 to intact cells and ...
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TY - JOUR. T1 - Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells. AU - Török, Tamás L.. AU - Pauló, Tünde. AU - Tóth, Péter T.. AU - Azzidani, Awad M.. AU - Powis, David A.. AU - Magyar, K.. PY - 1989. Y1 - 1989. N2 - 1. 1. The spontaneous release of [3H]noradrenaline ([3H]NA) has been measured from rabbit pulmonary arteries and bovine chromaffin cells in the presence of neuronal uptake blocker cocaine (3 × 10-5 M). 2. 2. The Na+-pump inhibitor sodium-azide (NaN3, 2 mM) produced a moderate increase of [3H]NA release from both preparations and relaxed the arteries. The [3H]releasing action of NaN3 was accompanied by a 30% inhibition of 86Rb-uptake into chromaffin cells. 3. 3. In both preparations, ouabain (10-4 M) markedly increased the release of [3H], contracted the arteries and inhibited the 86Rb-uptake of chromaffin cells by about 75%. A combined application of NaN3 and ouabain produced a similar inhibition of ...
Synaptotagmin-1 and -7 constitute the main calcium sensors mediating SNARE-dependent exocytosis in mouse chromaffin cells, but the role of a closely related calcium-binding protein, Doc2b, remains enigmatic. We investigated its role in chromaffin cells using Doc2b knock-out mice and high temporal resolution measurements of exocytosis. We found that the calcium dependence of vesicle priming and release triggering remained unchanged, ruling out an obligatory role for Doc2b in those processes. However, in the absence of Doc2b, release was shifted from the readily releasable pool to the subsequent sustained component. Conversely, upon overexpression of Doc2b, the sustained component was largely inhibited whereas the readily releasable pool was augmented. Electron microscopy revealed an increase in the total number of vesicles upon Doc2b overexpression, ruling out vesicle depletion as the cause for the reduced sustained component. Further experiments showed that, in the absence of Doc2b, the ...
Synaptophysin (syp) is a major integral membrane protein of secretory vesicles. Previous work has demonstrated functions for syp in synaptic vesicle cycling, endocytosis, and synaptic plasticity, but the role of syp in the process of membrane fusion during Ca2+-triggered exocytosis remains poorly understood. Furthermore, although syp resides on both large dense-core and small synaptic vesicles, its role in dense-core vesicle function has received less attention compared with synaptic vesicle function. To explore the role of syp in membrane fusion and dense-core vesicle function, we used amperometry to measure catecholamine release from single vesicles in male and female mouse chromaffin cells with altered levels of syp and the related tetraspanner protein synaptogyrin (syg). Knocking out syp slightly reduced the frequency of vesicle fusion events below wild-type (WT) levels, but knocking out both syp and syg reduced the frequency 2-fold. Knocking out both proteins stabilized initial fusion ...
Adrenal chromaffin cells (ACCs) secrete several neuroactive substances that are effective in influencing pain sensitivity in the central nervous system as well as enhancing the recovery of the intrinsic nigrostriatal dopaminergic system in patients w
TY - JOUR. T1 - Neuropeptide Y inhibition of nicotinic receptor-mediated chromaffin cell secretion. AU - Hexum, T. D.. AU - Zheng, Jialin C. AU - Zhu, J.. PY - 1994/1/1. Y1 - 1994/1/1. N2 - Neuropeptide Y (NPY), a widely distributed peptide with varied activities, inhibits nicotinic receptor-induced [3H]norepinephrine ([3H]NE) secretion from bovine chromaffin cells. The secretion produced by membrane depolarization with high KCl concentrations or veratridine is not inhibited. Fragments of NPY, such as NPY18-36, are potent inhibitors of [3H]NE secretion, whereas [Leu31,Pro34]-NPY and peptide YY have no effect. The response to NPY18-36 is not sensitive to pertussis toxin pretreatment of chromaffin cells. NPY fragments also inhibit nicotinic receptor-induced 45Ca++ influx but not that induced by KCl or veratridine. The rank orders of potency for inhibition of [3H]NE secretion and 45Ca++ influx are the same: NPY18-36 ≥ NPY26-36 , NPY13-36. NPY and NPY(free acid) are weak inhibitors of secretion ...
TY - JOUR. T1 - Recapture after exocytosis causes differential retention of protein in granules of bovine chromaffin cells. AU - Perrais, David. AU - Kleppe, Ingo C.. AU - Taraska, Justin W.. AU - Almers, Wolfhard. PY - 2004/10/15. Y1 - 2004/10/15. N2 - After exocytosis, chromaffin granules release essentially all their catecholamines in small fractions of a second, but it is unknown how fast they release stored peptides and proteins. Here we compare the exocytic release of fluorescently labelled neuropeptide Y (NPY) and tissue plasminogen activator from single granules. Exocytosis was tracked by measuring the membrane capacitance, and single granules in live cells were imaged by evanescent field microscopy. Neuropeptide Y left most granules in small fractions of a second, while tissue plasminogen activator remained in open granules for minutes. Taking advantage of the dependence on pH of the fluorescence of green fluorescent protein, we used rhythmic external acidification to determine whether ...
Other articles where Chromaffin cell is discussed: human nervous system: The endocrine system: Within the adrenal medulla are chromaffin cells, which are homologous to sympathetic neurons and, like sympathetic neurons, are developed from embryonic neural crest cells. Chromaffin cells produce epinephrine (adrenaline) and, to a much lesser extent, norepinephrine as well as other chemicals such as chromogranins, enkephalins, and neuropeptide Y-all of which…
Author: Nili, U. et al.; Genre: Journal Article; Published in Print: 2006-12-01; Title: Munc18-1 phosphorylation by protein kinase C potentiates vesicle pool replenishment in bovine chromaffin cells
The previous sections describe the different exocytotic responses obtained when the amount of Ca2+ entry is altered at a constant interpulse interval (200 msec). To examine whether the exocytotic response of a cell is also influenced by the time span between bouts of Ca2+ entry, we tested various interpulse intervals.. Trains of 40 msec pulses at 200 msec intervals evoked depressed responses in most cells (Figs. 3C, 4). Prolonging the interpulse interval increased the Ca2+ efficacy without significant changes to total Ca2+ entry (Fig. 8). Three examples comparing a 200 and a 1000 msec interval stimulus train within individual cells are shown in Figure 8A. Cells with strong depression during the 200 msec train showed a partial relief of depression at 1000 msec intervals (Fig. 8A,i) or followed the standard curve (Fig. 8A,ii), whereas cells with less depression often gave large responses with enhanced Ca2+ efficacy (Fig. 8A,iii). A summary of 17 experiments is presented in Figure 8B, in which the ...
The properties of Ca(2+)- and voltage-dependent K+ currents and their role in defining membrane potential were studied in cultured rat chromaffin cells. Two variants of large-conductance, Ca2+ and voltage-dependent BK channels, one noninactivating and one inactivating, were largely segregated among patches. Whole-cell noninactivating and inactivating currents resulting from each of these channels were segregated among different chromaffin cells. Cell-to-cell variation in the rate and extent of whole-cell current decay was not explained by differences in cytosolic [Ca2+] regulation among cells; rather, variation was due to differences in the intrinsic properties of the underlying BK channels. About 75% of rat chromaffin cells and patches express inactivating BK current (termed BKi) while the remainder express noninactivating BK current (termed BKs). The activation time course of both currents is similar, as is the dependence of activation on [Ca2+] and membrane potential. However, deactivation of ...
Adrenal chromaffin cells are excitable neuroendocrine cells that have been widely used as a simple model of neurosecretion. In vivo, acetylcholine released from preganglionic neurons binds to nicotinic receptors, which are Na+ ionophores, causing Na+ influx that depolarizes the plasma membrane. Depolarization in turn causes voltage-gated calcium channels (VGCCs) to open, leading to an influx of Ca2+ that activates the fusion of secretory granules with the plasma membrane, resulting in catecholamine release that occurs within milliseconds. This Ca2+-dependent secretory process is referred to as exocytosis. Previous investigations exploring the potential for nanosecond electric pulses (NEPs) to serve as a novel bioelectric stimulus of neurosecretion in chromaffin cells have shown that in chromaffin cells exposed to 5 ns, 5 MV/m electric pulses, catecholamine release is stimulated in a manner that relies on Ca2+ influx via VGCCs. The goal of the present study was to further understand this novel ...
Chromaffin cells are neuroendocrine cells found predominantly in the medulla of the adrenal gland. They are also found in other ganglia of the sympathetic nervous system and are derived from the embryonic neural crest. Embryology They arise in ...
TY - JOUR. T1 - The effect of ACTH, renin, angiotensin II, and various precursors on biosynthesis of aldosterone by adrenal slices.. AU - Kaplan, Norman M. AU - BARTER, F. C.. PY - 1962/4. Y1 - 1962/4. UR - http://www.scopus.com/inward/record.url?scp=0001053852&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0001053852&partnerID=8YFLogxK. U2 - 10.1172/JCI104530. DO - 10.1172/JCI104530. M3 - Article. C2 - 14453776. AN - SCOPUS:0001053852. VL - 41. SP - 715. EP - 724. JO - Journal of Clinical Investigation. JF - Journal of Clinical Investigation. SN - 0021-9738. ER - ...
Adrenomedullary chromaffin cells have been used as an excellent experimental model to study the exocytosis and therefore the molecular mechanisms of neurotransmission. It is now clear that the proteins involved in the processes of vesicle docking, membrane fusion and neurotransmitter release are common to many cellular systems (SNARE hypothesis). Our research interest is focused in two different aspects of the molecular mechanisms of neurotransmission: Implication of molecular motors such myosin-actin in vesicle transport during neurosecretion and the determination of essential aminoacids of synaptobrevin or SNAP-25 implicated in the process of membrane fusion. Experimental approaches involve strategies using antibodies, sequence peptide design and protein overexpression that demonstrate the participation of specific protein domains in exocytosis. In addition, the role of these proteins on the secretory stages have been studied using amperometry, technique that resolves single fusion events ...
Adrenomedullary chromaffin cells have been used as an excellent experimental model to study the exocytosis and therefore the molecular mechanisms of neurotransmission. It is now clear that the proteins involved in the processes of vesicle docking, membrane fusion and neurotransmitter release are common to many cellular systems (SNARE hypothesis). Our research interest is focused in two different aspects of the molecular mechanisms of neurotransmission: Implication of molecular motors such myosin-actin in vesicle transport during neurosecretion and the determination of essential aminoacids of synaptobrevin or SNAP-25 implicated in the process of membrane fusion. We coined the term Molecular cytoarchitecture of exocytosis to define the interaction between SNARE proteins, calcium channel and lately nicotinic receptors (integrating Dr. Criado main line) and the cohesive F-actin cortical network in order to improve secretory efficiency ...
RT-PCR and Western blotting techniques established the expression of APC protein both in bovine adrenal chromaffin cells, which express native alpha 3 beta 4* nAChRs, and in a HEK293 cell line expressing recombinant bovine adrenal alpha 3 beta 4 nAChRs (BM alpha 3 beta 4 cells). Transfection of BM alpha 3 beta 4 cells with siRNA to APC, reduced APC protein. levels to 52.4% and 61.9% of control values at 24 and 48 h after transfection. To investigate the effects of APC on the cellular distribution of alpha 3 beta 4 nAChRs, [(3)H]epibatidine binding approaches, coupled with APC siRNA treatment, were used. Twenty-four and 48 h after APC siRNA transfection, intracellular nAChRs were significantly reduced to 71% and 68% of control, respectively, while the total population of nAChRs were. not significantly changed. Given that total cellular nAChRs represent IKK inhibitor the sum of surface and intracellular nAChRs, these studies support a re-distribution of nAChRs to the plasma membrane with APC siRNA ...
Video articles in JoVE about adrenal glands include A Novel Method: Super-selective Adrenal Venous Sampling, Monitoring the Effect of Osmotic Stress on Secretory Vesicles and Exocytosis, Methods for Cell-attached Capacitance Measurements in Mouse Adrenal Chromaffin Cell, Mouse Adipose Tissue Collection and Processing for RNA Analysis, Imaging Plasma Membrane Deformations With pTIRFM, An Alternant Method to the Traditional NASA Hindlimb Unloading Model in Mice, Pre-Conditioning the Airways of Mice with Bleomycin Increases the Efficiency of Orthotopic Lung Cancer Cell Engraftment, 5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat, Isolation and Transplantation of Different Aged Murine Thymic Grafts., In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis, Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors, Murine Prostate Micro-dissection
The differentiation of neuronal cell progenitors depends on complex interactions between intrinsic cellular programs and environmental cues. Such interactions have recently been explored using an immortalized sympathoadrenal progenitor cell line, MAH. These studies have revealed that depolarizing conditions, in combination with exposure to FGF, can induce responsiveness to NGF. Here we report that CNTF, which utilizes an intracellular signaling pathway distinct from that of both FGF and NGF, can collaborate with FGF to promote efficiently the differentiation of MAH progenitor cells to a stage remarkably reminiscent of NGF-dependent, postmitotic sympathetic neurons. We also find that similar collaborative interactions can occur during transdifferentiation of normal cultured chromaffin cells into sympathetic neurons ...
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Nili, U.; de Wit, H.; Gulyas-Kovacs, A.; Toonen, R. F.; Soerensen, J. B.; Verhage, M.; Ashery, U.: Munc18-1 phosphorylation by protein kinase C potentiates vesicle pool replenishment in bovine chromaffin cells. Neuroscience 143 (2), pp. 487 - 500 (2006 ...
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Fingerprint Dive into the research topics of The actions of propofol on inhibitory amino acid receptors of bovine adrenomedullary chromaffin cells and rodent central neurones. Together they form a unique fingerprint. ...
During exocytosis, the fusion pore expands to allow release of neurotransmitters and hormones to the extracellular space. To understand the process of synaptic transmission, it is of outstanding importance to know the properties of the fusion pore and how these properties affect the release process. Many proteins have been implicated in vesicle fusion; however, there is little evidence for proteins involved in fusion pore expansion. Myosin II has been shown to participate in the transport of vesicles and, surprisingly, in the final phases of exocytosis, affecting the kinetics of catecholamine release in adrenal chromaffin cells as measured by amperometry. Here, we have studied single vesicle exocytosis in chromaffin cells overexpressing an unphosphorylatable form (T18AS19A RLC-GFP) of myosin II that produces an inactive protein by patch amperometry. This method allows direct determination of fusion pore expansion by measuring its conductance, whereas the release of catecholamines is recorded ...
Cleavage of the disulfide bond linking the heavy and the light chains of tetanus toxin is necessary for its inhibitory action on exocytotic release ofcatecholamines from permeabi1ized chromaffin cells [(1989) FEBS Lett. 242, 245-248; (1989) J. Neurochern., in press]. The related botulinum A toxin also consists of a heavy and a light chain linked by a disulfide bond. The actions ofboth neurotoxins on exocytosis were presently compared using streptolysin O-permeabilized bovine adrenal chromaffin cells. Botulinum A toxin inhibited Ca2 +-stimulated catecholamine release from these cells. Addition of dithiothreitollowered the effective doses to values below 5 nM. Under the same conditions, the effective doses of tetanus toxin were decreased by a factor of five. This indicates that the interchain S-S bond of botulinum A toxin must also be split before the neurotoxin can exert its effect on exocytosis. ...
Start Over You searched for: Authors International Symposium on Chromaffin Cell Biology 1986 : Coolfont, W. Va.) ✖Remove constraint Authors: International Symposium on Chromaffin Cell Biology 1986 : Coolfont, W. Va.) Languages English ✖Remove constraint Languages: English Subjects Cellular Structures ✖Remove constraint Subjects: Cellular Structures ...
TY - JOUR. T1 - Neurosecretory cell-based biosensor. T2 - Monitoring secretion of adrenal chromaffin cells by local extracellular acidification using light-addressable potentiometric sensor. AU - Liu, Qingjun. AU - Hu, Ning. AU - Zhang, Fenni. AU - Wang, Hua. AU - Ye, Weiwei. AU - Wang, Ping. N1 - Funding Information: This work was supported by the National Natural Science Foundation of China (Grant no. 81071226 , 60725102 ), the Research on Public Welfare Technology Application Projects of Zhejiang Province, China (no. 2011C23096 ), the Zhejiang Provincial Natural Science Foundation of China (no. Y2100684 ), and the Fundamental Research Funds for the Central Universities .. PY - 2012/5/15. Y1 - 2012/5/15. N2 - Vesicular exocytosis plays an important role in many physiological processes. The dense-core vesicles release of chromaffi{ligature}n cells is a suitable model for the presynaptic process in neurosecretory cells. In this study, light-addressable potentiometric sensor (LAPS) was introduced ...
S. Karanth, W. H. Yu, A. Walczewska, C. Mastronardi, S. M. McCann, Ascorbic acid acts as an inhibitory transmitter in the hypothalamus to inhibit stimulated luteinizing hormone-releasing hormone release by scavenging nitric oxide, Proceedings of the National Academy of Sciences, 2000, 97, 4, ...
xml version=1.0 encoding=UTF-8?, ,Pathway xmlns=http://genmapp.org/GPML/2010a Name=Nicotine in Chromaffin Cells Version=20100831 Organism=Homo sapiens, ,Comment Source=WikiPathways-description,Nicotine is an alkaloid found in tobacco plants. It is a substance that acts as a stimulant in humans and is one of the main factors responsible for tobacco dependence. When nicotine enters the body, it is distributed quickly through the bloodstream, and it can cross the blood-brain barrier to enter the central nervous system (CNS). It binds to two main types of nicotinic acetylcholine receptors: the ganglion type and the CNS type. In chromaffin cells in the adrenal medulla, nicotine binds to the ganglion-type nicotinic acetylcholine receptor, which is composed of alpha 3 (CHRNA3) and beta 4 (CHRNB4) subunits. By binding to the receptors, nicotine causes cell depolarization and an influx of calcium through voltage dependent calcium channels. Calcium triggers the release of epinephrine from ...
MUNC18-1 (also known as STXBP1) is an essential protein for docking and fusion of secretory vesicles. Mouse chromaffin cells (MCCs) lacking MUNC18-1 show impaired secretory vesicle docking, but also mistargeting of SNARE protein syntaxin1 and an abnormally dense submembrane F-actin network. Here, we tested the contribution of both these phenomena to docking and secretion defects in MUNC18-1-deficient MCCs. We show that an abnormal F-actin network and syntaxin1 targeting defects are not observed in Snap25- or Syt1-knockout (KO) MCCs, which are also secretion deficient. We identified a MUNC18-1 mutant (V263T in β-sheet 10) that fully restores syntaxin1 targeting but not F-actin abnormalities in Munc18-1-KO cells. MUNC18-2 and -3 (also known as STXBP2 and STXBP3, respectively), which lack the hydrophobic residue at position 263, also did not restore a normal F-actin network in Munc18-1-KO cells. However, these proteins did restore the normal F-actin network when a hydrophobic residue was ...
Hypoglycemia activates the counterregulatory response (CRR), a neural-endocrine reflex that restores euglycemia. Although effective if occasionally activated, repeated induction of the CRR leads to a decline in responsiveness and prolonged exposure to hypoglycemia. The mechanism underlying this impairment is not known. We found that the reduction in epinephrine release that characterizes a suppressed CRR involves a long-lasting form of sympatho-adrenal synaptic plasticity. Using optogenetically evoked catecholamine release, we show that recurrent hypoglycemia reduced the secretory capacity of mouse adrenal chromaffin cells. Single activation of the CRR increased the adrenal levels of tyrosine hydroxylase (TH), the rate-limiting enzyme for catecholamine synthesis, but this was prevented by repeated activation. In contrast, the level of neuropeptide Y (NPY), an adrenal cotransmitter, remained elevated after recurrent hypoglycemia. Inhibition of NPY or Y1 signaling, either transgenically or ...
Hypoglycemia activates the counterregulatory response (CRR), a neural-endocrine reflex that restores euglycemia. Although effective if occasionally activated, repeated induction of the CRR leads to a decline in responsiveness and prolonged exposure to hypoglycemia. The mechanism underlying this impairment is not known. We found that the reduction in epinephrine release that characterizes a suppressed CRR involves a long-lasting form of sympatho-adrenal synaptic plasticity. Using optogenetically evoked catecholamine release, we show that recurrent hypoglycemia reduced the secretory capacity of mouse adrenal chromaffin cells. Single activation of the CRR increased the adrenal levels of tyrosine hydroxylase (TH), the rate-limiting enzyme for catecholamine synthesis, but this was prevented by repeated activation. In contrast, the level of neuropeptide Y (NPY), an adrenal cotransmitter, remained elevated after recurrent hypoglycemia. Inhibition of NPY or Y1 signaling, either transgenically or ...
The sympathetic nervous system is activated by a variety of threats to organismal homeostasis. The adrenomedullary chromaffin cell is the core effector of sympathetic activity in the peripheral nervous system. By design, the chromaffin cell secretory response is mutable so that release can be rapidly tuned to drive context-dependent changes in physiological function. However, the mechanisms by which this tuning is achieved with such high temporal fidelity and context specificity remain unclear. This represents a major gap in our understanding of the sympatho-adrenal system since it is known to modify the function of nearly every organ system in the body. In chromaffin cells, the trigger for stimulus-evoked exocytosis is a rise in intracellular Ca2+. The level of intracellular Ca2+ accumulation varies with the stimulus intensity and secretagogue. Ca2+ regulates release by acting on the Ca2+-binding synaptotagmin (Syt) protein family, driving their penetration into membranes that harbor anionic lipids,
Area of interest: Mechanisms of stress transduction at the sympatho-adrenal synapse; optical studies of hormone trafficking and secretion in the adrenomedullary chromaffin cell.
TY - CHAP. T1 - Adrenomedullin. AU - Abel, Peter. AU - Rorabaugh, Boyd. PY - 2007/1/1. Y1 - 2007/1/1. N2 - Adrenomedullin is a member of the calcitonin family of peptides. It is produced by vascular smooth muscle cells, vascular endothelial cells, cardiomyocytes, adrenal chromaffin cells, macrophages, bronchial epithelium, and many other cell types. This peptide is a potent vasodilator in most vascular beds and has been implicated in the regulation of blood pressure, ..... AB - Adrenomedullin is a member of the calcitonin family of peptides. It is produced by vascular smooth muscle cells, vascular endothelial cells, cardiomyocytes, adrenal chromaffin cells, macrophages, bronchial epithelium, and many other cell types. This peptide is a potent vasodilator in most vascular beds and has been implicated in the regulation of blood pressure, ..... UR - http://www.scopus.com/inward/record.url?scp=84884021496&partnerID=8YFLogxK. UR - ...
Ahnert-Hilger, G.; Wegenhorst, U.; Stecher, B.; Spicher, K.; Rosenthal, W.; Gratzl, Manfred (1992): Exocytosis from permeabilized bovine adrenal chromaffin cells is differently modulated by guanosine 5-[gamma-thio]triphosphate and guanosine 5-[beta gamma-imido]triphosphate. Evidence for the involvement of various guanine nucleotide-binding proteins. In: Biochemical Journal, Vol. 284: pp. 321-326 [PDF, 3MB] ...
TY - CHAP. T1 - Carbon-Fiber Amperometry in the Study of Exocytosis. AU - Duffield, Michael. AU - Raghupathi, RaviNarayan. AU - Keating, Damien. PY - 2014. Y1 - 2014. N2 - Understanding how signaling molecules are released from cells is essential for furthering our knowledge of the basic biological mechanisms controlling many significant biological pathways. These molecules, including neurotransmitters, hormones, growth factors, and peptides, are released from cells via a process called exocytosis. Our laboratory has utilized a noninvasive method of measuring the release of oxidizable molecules from cells, known as carbon-fiber amperometry. In this chapter we will describe how we undertake such measurements, how the resulting data is analyzed, and what the outcomes mean in terms of physiology. We provide examples of our work measuring catecholamine release in single chromaffin cells as well as serotonin release from intact sections of colon.. AB - Understanding how signaling molecules are ...
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