Zeitschriftenartikel: „Chromaffin cells“

1

Coupland, R. E. "MAST CELLS AND CHROMAFFIN CELLS." Annals of the New York Academy of Sciences 103, no. 1 (December 15, 2006): 139–50. http://dx.doi.org/10.1111/j.1749-6632.1963.tb53694.x.

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Shepherd, S. P., and M. A. Holzwarth. "Chromaffin-adrenocortical cell interactions: effects of chromaffin cell activation in adrenal cell cocultures." American Journal of Physiology-Cell Physiology 280, no. 1 (January 1, 2001): C61—C71. http://dx.doi.org/10.1152/ajpcell.2001.280.1.c61.

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Although the adrenal cortex and medulla are both involved in the maintenance of homeostasis and stress response, the functional importance of intra-adrenal interactions remains unclear. When primary cocultures of frog ( Rana pipiens) adrenocortical and chromaffin cells were used, selective chromaffin cell activation dramatically affected both chromaffin and adrenocortical cells. Depolarization with 50 μm veratridine enhanced chromaffin cell neuronal phenotype, contacts with adrenocortical cells, and secretion of norepinephrine, epinephrine, and serotonin. Time-lapse video microscopy recorded the rapid establishment of growth cones on the activated chromaffin cell neurites, neurite branching, and outgrowth toward adrenocortical cells. Simultaneously, adrenocortical cells migrated toward chromaffin cells. Following chromaffin cell activation, adrenocortical cell Fos protein expression and corticosteroid secretion were increased, indicating that chromaffin cell modulation of adrenocortical cells is at the transcriptional level. These results provide evidence that intra-adrenal interactions affect cellular differentiation and modulate steroidogenesis. Furthermore, this suggests that the activity-related plasticity of chromaffin and adrenocortical cells is developmentally and physiologically important.

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Furlan, Alessandro, Vyacheslav Dyachuk, Maria Eleni Kastriti, Laura Calvo-Enrique, Hind Abdo, Saida Hadjab, Tatiana Chontorotzea, et al. "Multipotent peripheral glial cells generate neuroendocrine cells of the adrenal medulla." Science 357, no. 6346 (July 6, 2017): eaal3753. http://dx.doi.org/10.1126/science.aal3753.

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Adrenaline is a fundamental circulating hormone for bodily responses to internal and external stressors. Chromaffin cells of the adrenal medulla (AM) represent the main neuroendocrine adrenergic component and are believed to differentiate from neural crest cells. We demonstrate that large numbers of chromaffin cells arise from peripheral glial stem cells, termed Schwann cell precursors (SCPs). SCPs migrate along the visceral motor nerve to the vicinity of the forming adrenal gland, where they detach from the nerve and form postsynaptic neuroendocrine chromaffin cells. An intricate molecular logic drives two sequential phases of gene expression, one unique for a distinct transient cellular state and another for cell type specification. Subsequently, these programs down-regulate SCP-gene and up-regulate chromaffin cell–gene networks. The AM forms through limited cell expansion and requires the recruitment of numerous SCPs. Thus, peripheral nerves serve as a stem cell niche for neuroendocrine system development.

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Kim, Yu Mi, Young Hoon Jeon, Gwang Chun Jin, Jeong Ok Lim, and Woon Yi Baek. "In Vivo Biocompatibility of Alginate-PLL Microcapsules with Chromaffin Cells for the Alleviation of Chronic Pain." Key Engineering Materials 277-279 (January 2005): 62–66. http://dx.doi.org/10.4028/www.scientific.net/kem.277-279.62.

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Intrathecal implants of adrenal medullary chromaffin cells relieve chronic pain by secreting catecholamines, opioids and other neuroactive substances. Recently, macrocapsules with hollow fibers were employed to isolate immunologically xenogeneic chromaffin cells, but the poor viability in vivo of the encapsulated chromaffin cells limited the usefulness of this method. In this study, we used microencapsulation technology to increase the viability of chromaffin cells. Bovine adrenal chromaffin cells were microencapsulated with alginate and poly-L-lysine and implanted intrathecally in a rat using the neuropathic pain model. Intrathecal implants of microencapsulated cells relieved cold allodynia, which is the most prominent symptom of the neuropathic pain model in a rat. Furthermore, the microencapsulated chromaffin cells were morphologically normal and retained their functionality. These findings suggest that the intrathecal implant of microencapsulated chromaffin cells might be a useful method for treating chronic pain.

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Finotto, S., K. Krieglstein, A. Schober, F. Deimling, K. Lindner, B. Bruhl, K. Beier, et al. "Analysis of mice carrying targeted mutations of the glucocorticoid receptor gene argues against an essential role of glucocorticoid signalling for generating adrenal chromaffin cells." Development 126, no. 13 (July 1, 1999): 2935–44. http://dx.doi.org/10.1242/dev.126.13.2935.

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Molecular mechanisms underlying the generation of distinct cell phenotypes is a key issue in developmental biology. A major paradigm of determination of neural cell fate concerns the development of sympathetic neurones and neuroendocrine chromaffin cells from a common sympathoadrenal (SA) progenitor cell. Two decades of in vitro experiments have suggested an essential role of glucocorticoid receptor (GR)-mediated signalling in generating chromaffin cells. Targeted mutation of the GR should consequently abolish chromaffin cells. The present analysis of mice lacking GR gene product demonstrates that animals have normal numbers of adrenal chromaffin cells. Moreover, there are no differences in terms of apoptosis and proliferation or in expression of several markers (e.g. GAP43, acetylcholinesterase, adhesion molecule L1) of chromaffin cells in GR-deficient and wild-type mice. However, GR mutant mice lack the adrenaline-synthesizing enzyme PNMT and secretogranin II. Chromaffin cells of GR-deficient mice exhibit the typical ultrastructural features of this cell phenotype, including the large chromaffin granules that distinguish them from sympathetic neurones. Peripherin, an intermediate filament of sympathetic neurones, is undetectable in chromaffin cells of GR mutants. Finally, when stimulated with nerve growth factor in vitro, identical proportions of chromaffin cells from GR-deficient and wild-type mice extend neuritic processes. We conclude that important phenotypic features of chromaffin cells that distinguish them from sympathetic neurones develop normally in the absence of GR-mediated signalling. Most importantly, chromaffin cells in GR-deficient mice do not convert to a neuronal phenotype. These data strongly suggest that the dogma of an essential role of glucocorticoid signalling for the development of chromaffin cells must be abandoned.

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Hong, Hai Yan, Jeong Ok Lim, and Woon Yi Baek. "Effect of Morphine and Bupivacaine on Nicotine-Induced Catecholamine Secretion from Encapsulated Chromaffin Cells." Key Engineering Materials 277-279 (January 2005): 56–61. http://dx.doi.org/10.4028/www.scientific.net/kem.277-279.56.

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The control of intractable pain through transplanted of chromaffin cells has been recently reported where the analgesic effects are principally due to the production of opioid peptides and catecholamines (CAs) by the chromaffin cells. Currently many cancer patients receive general opioids or local anesthetics, such as bupivacaine. Therefore, the present study investigated the effect of morphine or bupivacaine on the secretion of nicotine-induced CAs from encapsulated chromaffin cells over a period of 180 min. As such, bovine chromaffin cells were isolated and encapsulated with alginate–poly–L–lysine–alginate (APA) biomaterials to prevent immunorejection. The capsules were then pre-incubated with nicotine for 5 min prior to morphine or bupivacaine stimulation, and the quantity of CAs analyzed using a high performance liquid chromatography (HPLC) analysis system. The resulting data showed that the encapsulated chromaffin cells retained the ability of their parent chromaffin cells when responding to opioids by suppressing the release of CAs. In contrast, bupivacaine did not have any statistically significant affect on the basal and nicotine-induced CA release from the encapsulated chromaffin cells.

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Sol, J. C., R. Y. Li, B. Sallerin, S. Jozan, H. Zhou, V. Lauwers-Cances, F. Tortosa, et al. "Intrathecal Grafting of Porcine Chromaffin Cells Reduces Formalin-Evoked c-Fos Expression in the Rat Spinal Cord." Cell Transplantation 14, no. 6 (July 2005): 353–65. http://dx.doi.org/10.3727/000000005783982963.

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Chromaffin cells from the adrenal gland secrete a combination of neuroactive compounds including catecholamines, opioid peptides, and growth factors that have strong analgesic effects, especially when administered intrathecally. Preclinical studies of intrathecal implantation with xenogeneic bovine chromaffin cells in rats have provided conflicting data with regard to analgesic effects, and recent concern over risk of prion transmission has precluded their use in human clinical trials. We previously developed a new, safer source of adult adrenal chromaffin cells of porcine origin and demonstrated an in vivo antinociceptive effect in the formalin test, a rodent model of tonic pain. The goal of the present study was to confirm porcine chromaffin cell analgesic effects at the molecular level by evaluating neural activity as reflected by spinal cord c-Fos protein expression. To this end, the expression of c-Fos in response to intraplantar formalin injection was evaluated in animals following intrathecal grafting of 106 porcine or bovine chromaffin cells. For the two species, adrenal chromaffin cells significantly reduced the tonic phases of the formalin response. Similarly, c-Fos-like immunoreactive neurons were markedly reduced in the dorsal horns of animals that had received injections of xenogeneic chromaffin cells. This reduction was observed in both the superficial (I—II) and deep (V—VI) lamina of the dorsal horn. The present study demonstrates that both xenogeneic porcine and bovine chromaffin cells transplanted into the spinal subarachnoid space of the rat can suppress formalin-evoked c-Fos expression equally, in parallel with suppression of nociceptive behaviors in the tonic phase of the test. These findings confirm previous reports that adrenal chromaffin cells may produce antinociception by inhibiting activation of nociceptive neurons in the spinal dorsal horn. Taken together these results support the concept that porcine chromaffin cells may offer an alternative xenogeneic cell source for transplants delivering pain-reducing neuroactive substances.

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Eaton, M. J., M. Martinez, S. Karmally, T. Lopez, and J. Sagen. "Initial Characterization of the Transplant of Immortalized Chromaffin Cells for the Attenuation of Chronic Neuropathic Pain." Cell Transplantation 9, no. 5 (September 2000): 637–56. http://dx.doi.org/10.1177/096368970000900509.

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Cultures of embryonic day 17 (E17) rat adrenal and neonatal bovine adrenal cells were conditionally immortalized with the temperature-sensitive allele of SV40 large T antigen (tsTag) and chromaffin cell lines established. Indicative of the adrenal chromaffin phenotype, these cells expressed immunoreactivity (ir) for tyrosine hydroxylase (TH), the first enzyme in the synthetic pathway for catecholamines. At permissive temperature in vitro (33°C), these chromaffin cells are proliferative, have a typical rounded chromaffin-like morphology, and contain detectable TH-ir. At nonpermissive temperature in vitro (39°C), these cells stop proliferating and express increased TH-ir. When these immortalized chromaffin cells were transplanted in the lumbar subarachnoid space of the spinal cord 1 week after a unilateral chronic constriction injury (CCI) of the rat sciatic nerve, they survived longer than 7 weeks on the pia mater around the spinal cord and continued to express TH-ir. Conversely, grafted chromaffin cells lost Tag-ir after transplant and Tag-ir was undetectible in the grafts after 7 weeks in the subarachnoid space. At no time did the grafts form tumors after transplant into the host animals. These grafted chromaffin cells also expressed immunoreactivities for the other catecholamine-synthesizing enzymes 7 weeks after grafting, including: dopamine-β-hydroxylase (DβH) and phenylethanolamine-N-methyltransferase (PNMT). The grafted cells also expressed detectable immunoreactivities for the opioid met-enkephalin (ENK), the peptide galanin (GAL), and the neurotransmitters γ-aminobutyric acid (GABA) and serotonin (5-HT). Furthermore, after transplantation, tactile and cold allodynia and tactile and thermal hyperalgesia induced by CCI were significantly reduced during a 2–8-week period, related to the chromaffin cell transplants. The maximal antinociceptive effect occurred 1–3 weeks after grafting. Control adrenal fibroblasts, similarly immortalized and similarly transplanted after CCI, did not express any of the chromaffin antigenic markers, and fibroblast grafts had no effect on the allodynia and hyperalgesia induced by CCI. These data suggest that embryonic and neonatal chromaffin cells can be conditionally immortalized and will continue to express the phenotype of primary chromaffin cells in vitro and in vivo; grafted cells will ameliorate neuropathic pain after nerve injury and can be used as a homogeneous source to examine the mechanisms by which chromaffin transplants reverse chronic pain. The use of such chromaffin cell lines that are able to deliver antinociceptive molecules in models of chronic pain after nerve and spinal cord injury (SCI) offers a novel approach to pain management.

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DUNCAN, Rory R., Andrew C. DON-WAUCHOPE, Sompol TAPECHUM, Michael J. SHIPSTON, Robert H. CHOW, and Peter ESTIBEIRO. "High-efficiency Semliki Forest virus-mediated transduction in bovine adrenal chromaffin cells." Biochemical Journal 342, no. 3 (September 5, 1999): 497–501. http://dx.doi.org/10.1042/bj3420497.

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Adrenal chromaffin cells are commonly used in studies of exocytosis. Progress in characterizing the molecular mechanisms has been slow, because no simple, high-efficiency technique is available for introducing and expressing heterologous cDNA in chromaffin cells. Here we demonstrate that Semliki Forest virus (SFV) vectors allow high-efficiency expression of heterologous protein in chromaffin cells.

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Vukicevic, Vladimir, Janine Schmid, Andreas Hermann, Sven Lange, Nan Qin, Linda Gebauer, Kuei-Fang Chung, et al. "Differentiation of Chromaffin Progenitor Cells to Dopaminergic Neurons." Cell Transplantation 21, no. 11 (November 2012): 2471–86. http://dx.doi.org/10.3727/096368912x638874.

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The differentiation of dopamine-producing neurons from chromaffin progenitors might represent a new valuable source for replacement therapies in Parkinson's disease. However, characterization of their differentiation potential is an important prerequisite for efficient engraftment. Based on our previous studies on isolation and characterization of chromaffin progenitors from adult adrenals, this study investigates their potential to produce dopaminergic neurons and means to enhance their dopaminergic differentiation. Chromaffin progenitors grown in sphere culture showed an increased expression of nestin and Mash1, indicating an increase of the progenitor subset. Proneurogenic culture conditions induced the differentiation into neurons positive for neural markers β-III-tubulin, MAP2, and TH accompanied by a decrease of Mash1 and nestin. Furthermore, Notch2 expression decreased concomitantly with a downregulation of downstream effectors Hes1 and Hes5 responsible for self-renewal and proliferation maintenance of progenitor cells. Chromaffin progenitor-derived neurons secreted dopamine upon stimulation by potassium. Strikingly, treatment of differentiating cells with retinoic and ascorbic acid resulted in a twofold increase of dopamine secretion while norepinephrine and epinephrine were decreased. Initiation of dopamine synthesis and neural maturation is controlled by Pitx3 and Nurr1. Both Pitx3 and Nurr1 were identified in differentiating chromaffin progenitors. Along with the gained dopaminergic function, electrophysiology revealed features of mature neurons, such as sodium channels and the capability to fire multiple action potentials. In summary, this study elucidates the capacity of chromaffin progenitor cells to generate functional dopaminergic neurons, indicating their potential use in cell replacement therapies.

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BROOKS, J., and M. BROOKS. "Thiophosphorylated proteins in chromaffin cells are chromaffin vesicle matrix proteins." Neurochemistry International 20, no. 4 (June 1992): 501–9. http://dx.doi.org/10.1016/0197-0186(92)90029-q.

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12

Cheek, T. R., T. R. Jackson, A. J. O'Sullivan, R. B. Moreton, M. J. Berridge, and R. D. Burgoyne. "Simultaneous measurements of cytosolic calcium and secretion in single bovine adrenal chromaffin cells by fluorescent imaging of fura-2 in cocultured cells." Journal of Cell Biology 109, no. 3 (September 1, 1989): 1219–27. http://dx.doi.org/10.1083/jcb.109.3.1219.

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The cytosolic free calcium concentration ([Ca2+]i) and exocytosis of chromaffin granules were measured simultaneously from single, intact bovine adrenal chromaffin cells using a novel technique involving fluorescent imaging of cocultured cells. Chromaffin cell [Ca2+]i was monitored with fura-2. To simultaneously follow catecholamine secretion, the cells were cocultured with fura-2-loaded NIH-3T3t cells, a cell line chosen because of their irresponsiveness to chromaffin cell secretagogues but their large Ca2+ response to ATP, which is coreleased with catecholamine from the chromaffin cells. In response to the depolarizing stimulus nicotine (a potent secretagogue), chromaffin cell [Ca2+]i increased rapidly. At the peak of the response, [Ca2+]i was evenly distributed throughout the cell. This elevation in [Ca2+]i was followed by a secretory response which originated from the entire surface of the cell. In response to the inositol 1,4,5-trisphosphate (InsP3)-mobilizing agonist angiotensin II (a weak secretagogue), three different responses were observed. Approximately 30% of chromaffin cells showed no rise in [Ca2+]i and did not secrete. About 45% of the cells responded with a large (greater than 200 nM), transient elevation in [Ca2+]i and no detectable secretory response. The rise in [Ca2+]i was nonuniform, such that peak [Ca2+]i was often recorded only in one pole of the cell. And finally, approximately 25% of cells responded with a similar Ca2+-transient to that described above, but also gave a secretory response. In these cases secretion was polarized, being confined to the pole of the cell in which the rise in [Ca2+]i was greatest.(ABSTRACT TRUNCATED AT 250 WORDS)

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Kordower, Jeffrey H., Massimo S. Fiandaca, Mary F. D. Notter, John T. Hansen, and Don M. Gash. "NGF-like trophic support from peripheral nerve for grafted rhesus adrenal chromaffin cells." Journal of Neurosurgery 73, no. 3 (September 1990): 418–28. http://dx.doi.org/10.3171/jns.1990.73.3.0418.

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✓ Autopsy results on patients and corresponding studies in nonhuman primates have revealed that autografts of adrenal medulla into the striatum, used as a treatment for Parkinson's disease, do not survive well. Because adrenal chromaffin cell viability may be limited by the low levels of available nerve growth factor (NGF) in the striatum, the present study was conducted to determine if transected peripheral nerve segments could provide sufficient levels of NGF to enhance chromaffin cell survival in vitro and in vivo. Aged female rhesus monkeys, rendered hemiparkinsonian by the drug MPTP (n-methyl-4-phenyl-1,2,3,6 tetrahydropyridine), received autografts into the striatum using a stereotactic approach, of either sural nerve or adrenal medulla, or cografts of adrenal medulla and sural nerve (three animals in each group). Cell cultures were established from tissue not used in the grafts. Adrenal chromaffin cells either cocultured with sural nerve segments or exposed to exogenous NGF differentiated into a neuronal phenotype. Chromaffin cell survival, when cografted with sural nerve into the striatum, was enhanced four- to eightfold from between 8000 and 18,000 surviving cells in grafts of adrenal tissue only up to 67,000 surviving chromaffin cells in cografts. In grafts of adrenal tissue only, the implant site consisted of an inflammatory focus. Surviving chromaffin cells, which could be identified by both chromogranin A and tyrosine hydroxylase staining, retained their endocrine phenotype. Cografted chromaffin cells exhibited multipolar neuritic processes and numerous chromaffin granules, and were also immunoreactive for tyrosine hydroxylase and chromogranin A. Blood vessels within the graft were fenestrated, indicating that the blood-brain barrier was not intact. Additionally, cografted chromaffin cells were observed in a postsynaptic relationship with axon terminals from an undetermined but presumably a host origin.

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Parlato, Rosanna, Christiane Otto, Jan Tuckermann, Stefanie Stotz, Sylvia Kaden, Hermann-Josef Gröne, Klaus Unsicker та Günther Schütz. "Conditional Inactivation of Glucocorticoid Receptor Gene in Dopamine-β-Hydroxylase Cells Impairs Chromaffin Cell Survival". Endocrinology 150, № 4 (26 листопада 2008): 1775–81. http://dx.doi.org/10.1210/en.2008-1107.

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Glucocorticoid hormones (GCs) have been thought to determine the fate of chromaffin cells from sympathoadrenal progenitor cells. The analysis of mice carrying a germ line deletion of the glucocorticoid receptor (GR) gene has challenged these previous results because the embryonic development of adrenal chromaffin cells is largely unaltered. In the present study, we have analyzed the role of GC-dependent signaling in the postnatal development of adrenal chromaffin cells by conditional inactivation of the GR gene in cells expressing dopamine-β-hydroxylase, an enzyme required for the synthesis of noradrenaline and adrenaline. These mutant mice are viable, allowing to study whether in the absence of GC signaling further development of the adrenal medulla is affected. Our analysis shows that the loss of GR leads not only to the loss of phenylethanolamine-N-methyl-transferase expression and, therefore, to inhibition of adrenaline synthesis, but also to a dramatic reduction in the number of adrenal chromaffin cells. We provide evidence that increased apoptotic cell death is the main consequence of GR loss. These findings define the essential role of GCs for survival of chromaffin cells and underscore the specific requirement of GCs for adrenergic chromaffin cell differentiation and maintenance.

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Huber, Katrin, Barbara Brühl, François Guillemot, Eric N. Olson, Uwe Ernsberger, and Klaus Unsicker. "Development of chromaffin cells depends on MASH1 function." Development 129, no. 20 (October 15, 2002): 4729–38. http://dx.doi.org/10.1242/dev.129.20.4729.

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The sympathoadrenal (SA) cell lineage is a derivative of the neural crest (NC), which gives rise to sympathetic neurons and neuroendocrine chromaffin cells. Signals that are important for specification of these two types of cells are largely unknown. MASH1 plays an important role for neuronal as well as catecholaminergic differentiation. Mash1 knockout mice display severe deficits in sympathetic ganglia, yet their adrenal medulla has been reported to be largely normal suggesting that MASH1 is essential for neuronal but not for neuroendocrine differentiation. We show now that MASH1 function is necessary for the development of the vast majority of chromaffin cells. Most adrenal medullary cells in Mash1–/– mice identified by Phox2b immunoreactivity, lack the catecholaminergic marker tyrosine hydroxylase. Mash1 mutant and wild-type mice have almost identical numbers of Phox2b-positive cells in their adrenal glands at embryonic day (E) 13.5; however, only one-third of the Phox2b-positive adrenal cell population seen in Mash1+/+ mice is maintained in Mash1–/– mice at birth. Similar to Phox2b, cells expressing Phox2a and Hand2 (dHand) clearly outnumber TH-positive cells. Most cells in the adrenal medulla of Mash1–/– mice do not contain chromaffin granules, display a very immature, neuroblast-like phenotype, and, unlike wild-type adrenal chromaffin cells, show prolonged expression of neurofilament and Ret comparable with that observed in wild-type sympathetic ganglia. However, few chromaffin cells in Mash1–/– mice become PNMT positive and downregulate neurofilament and Ret expression. Together, these findings suggest that the development of chomaffin cells does depend on MASH1 function not only for catecholaminergic differentiation but also for general chromaffin cell differentiation.

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Czech, Kimberly A., Raymond Pollak, George D. Pappas, and Jacqueline Sagen. "Bovine Chromaffin Cells for CNS Transplantation do not Elicit Xenogeneic T Cell Proliferative Responses in Vitro." Cell Transplantation 5, no. 2 (March 1996): 257–67. http://dx.doi.org/10.1177/096368979600500214.

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Adrenal chromaffin cells have been utilized for several neural grafting applications, but limitations in allogeneic donor availability and dangers inherent in auto-grafting limit the widespread use of this approach clinically. While xenogeneic donors offer promise as a source for cell transplantation in the central nervous system (CNS), immunologic responses to cellular components of the adrenal medulla have not been well characterized. To further study the host T cell xenogeneic response to chromaffin and passenger cells of the adrenal medulla, an in vitro lymphocyte proliferation assay was used. Lymphocyte proliferation was determined by mixing rat lymphocytes with potential stimulator cell subpopulations of the bovine adrenal medulla: isolated chromaffin cells, isolated endothelial cells, or passenger nonchromaffin cells, which include a mixture of fibroblasts, smooth muscle cells, and endothelial cells. As a positive control, bovine aortic endothelial cells were also used. 3[H]-thymidine incorporation, corresponding to lymphocyte proliferation, was measured. Results indicated that isolated bovine chromaffin cells produce only a mild, statistically insignificant stimulation of rat lymphocytes. In contrast, there was a significant response to passenger nonchromaffin cells of the adrenal medulla, especially endothelial cells. The inclusion of low levels of cyclosporin A in the cultures completely eliminated the mild proliferative response to isolated bovine chromaffin cells, while near toxic levels were necessary to abrogate the response to endothelial cells. Immunocytochemical analysis revealed that routine chromaffin cell isolation procedures result in the inclusion of a small percentage of endothelial cells, which may be responsible for the slight lymphocyte stimulation. The results of this study indicate that isolated chromaffin cells possess low immunogenicity, and suggest that passenger cells in the adrenal medulla, particularly endothelial cells, may be primarily responsible for progressive rejection in CNS grafts. Thus, removal of passenger nonchromaffin cells from xenogeneic donor tissues prior to transplantation may produce a more tolerated graft in rodent models of neural transplantation.

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Bornstein, S. R., M. Ehrhart-Bornstein, A. Androutsellis-Theotokis, G. Eisenhofer, V. Vukicevic, J. Licinio, M. L. Wong, et al. "Chromaffin cells: the peripheral brain." Molecular Psychiatry 17, no. 4 (January 17, 2012): 354–58. http://dx.doi.org/10.1038/mp.2011.176.

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Barg, S., and J. D. Machado. "Compensatory endocytosis in chromaffin cells." Acta Physiologica 192, no. 2 (November 16, 2007): 195–201. http://dx.doi.org/10.1111/j.1748-1716.2007.01813.x.

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VITALE, NICOLAS, SYLVETTE CHASSEROT-GOLAZ, and MARIE-FRANCE BADER. "Regulated Secretion in Chromaffin Cells." Annals of the New York Academy of Sciences 971, no. 1 (October 2002): 193–200. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04463.x.

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Boarder, M. R. "Phospholipase D in Chromaffin Cells?" Journal of Neurochemistry 60, no. 5 (May 1993): 1978–79. http://dx.doi.org/10.1111/j.1471-4159.1993.tb13435.x.

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Caumont, Anne-Sophie, Marie-Christine Galas, Nicolas Vitale, Dominique Aunis, and Marie-France Bader. "Regulated Exocytosis in Chromaffin Cells." Journal of Biological Chemistry 273, no. 3 (January 16, 1998): 1373–79. http://dx.doi.org/10.1074/jbc.273.3.1373.

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Galas, Marie-Christine, J. Bernd Helms, Nicolas Vitale, Danièle Thiersé, Dominique Aunis, and Marie-France Bader. "Regulated Exocytosis in Chromaffin Cells." Journal of Biological Chemistry 272, no. 5 (January 31, 1997): 2788–93. http://dx.doi.org/10.1074/jbc.272.5.2788.

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Torres, M., P. Molina, and M. T. Miras-Portugal. "Adenosine transporters in chromaffin cells." FEBS Letters 201, no. 1 (May 26, 1986): 124–28. http://dx.doi.org/10.1016/0014-5793(86)80583-x.

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UNSICKER, K., and K. KRIEGLSTEIN. "Growth factors in chromaffin cells." Progress in Neurobiology 48, no. 4-5 (March 1996): 307–24. http://dx.doi.org/10.1016/0301-0082(95)00045-3.

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Nguyen, Tien T., and André De Léan. "Nonadrenergic modulation by clonidine of the cosecretion of catecholamines and enkephalins in adrenal chromaffin cells." Canadian Journal of Physiology and Pharmacology 65, no. 5 (May 1, 1987): 823–27. http://dx.doi.org/10.1139/y87-132.

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Cultured bovine chromaffin cells cosecrete catecholamines and enkephalins following cholinergic nicotinic stimulation. Initial reports on the inhibitory effect of clonidine on catecholamine secretion raised the possibility of a modulation of chromaffin cell function through a presynaptic adrenergic mechanism. The purpose of this work was to investigate the pharmacological characteristics of this inhibitory effect of clonidine on the cosecretion of catecholamines and enkephalins in 4-day-old cultured chromaffin cells. We observed that clonidine completely inhibits nicotine-stimulated secretion of both leucine-enkephalin and catecholamines with an IC50 of 34 μM. Treatment of chromaffin cells for 3 days with 100 nM reserpine leads to a 67% increase in nicotine-stimulated secretion of leucine-enkephalin without any effect on the IC50 of clonidine. In reserpine-treated chromaffin cells, norepinephrine (100 μM) inhibits only by 27% nicotine-stimulated secretion of leucine-enkephalin with an IC50 of 50 μM. Neither the alpha2-adrenergic antagonist yohimbine nor the alpha1-adrenergic antagonist prazosin could fully reverse the inhibitory effect of clonidine on leucine-enkephalin secretion at 10 nM. These results tend to rule out the role of alpha-adrenergic receptors in the mediation of clonidine inhibition of cosecretion in chromaffin cells.

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Trifaró, J. M., M. F. Bader, and J. P. Doucet. "Chromaffin cell cytoskeleton: its possible role in secretion." Canadian Journal of Biochemistry and Cell Biology 63, no. 6 (June 1, 1985): 661–79. http://dx.doi.org/10.1139/o85-084.

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Cytoskeleton proteins (actin, myosin, α-actinin, spectrin, tubulin, neurofilament subunits) and their regulatory proteins (calmodulin, gelsolin) have been isolated from adrenal chromaffin cells and characterized. Their physicochemical properties have been studied and their cell localizations have been revealed by biochemical, immunocytochemical, and ulstrastructural techniques. α-Actinin and spectrin are components of chromaffin granule membranes and some of the cell actin copurifies with these secretory granules. Myosin is not detected in the granules, but is present mainly in the cytosol and close to the cell surface. Trifluoperazine, a calmodulin antagonist, blocks stimulation-induced hormone release from chromaffin cells at a step distal from Ca2+ entry. High affinity calmodulin-binding sites have also been found in chromaffin granule membranes and their calmodulin-binding proteins have been characterized. Furthermore, microinjection of calmodulin antibodies into chromaffin cells blocks hormone output in response to stimulation. In view of the above findings, the possible roles of contractile proteins and calmodulin in chromaffin cell functions are discussed.

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Xie, Z., B. E. Herring, and A. P. Fox. "Excitatory and Inhibitory Actions of Isoflurane in Bovine Chromaffin Cells." Journal of Neurophysiology 96, no. 6 (December 2006): 3042–50. http://dx.doi.org/10.1152/jn.00571.2006.

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Isoflurane, a halogenated volatile anesthetic, is thought to produce anesthesia by depressing CNS function. Many anesthetics, including isoflurane, are thought to modulate and/or directly activate GABAA receptors. Chromaffin cells are known to express functional GABAA receptors. We previously showed that activation of the GABAA receptors, with specific agonists, leads to cellular excitation resulting from the depolarized anion equilibrium potential. In this study, our goal was to determine whether isoflurane mimicked this response and to explore the functional consequences of this activation. Furthermore, we sought to study the actions of isoflurane on nicotinic acetylcholine receptors (nAChRs) as they mediate the “sympathetic drive” in these cells. For these studies the Ca2+-indicator dye fura-2 was used to assay [Ca2+]i. Amperometric measurements were used to assay catecholamine release. We show that bovine adrenal chromaffin cells were excited by isoflurane at clinically relevant concentrations. Isoflurane directly activated GABAA receptors found in chromaffin cells, which depolarized the cells and elevated [Ca2+]i. Application of isoflurane directly to the chromaffin cells elicited catecholamine secretion from these cells. At the same time, isoflurane suppressed activation of nAChRs, which presumably blocks “sympathetic drive” to the chromaffin cells. These latter results may help explain why isoflurane produces the hypotension observed clinically.

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Nassar-Gentina, V., H. B. Pollard, and E. Rojas. "Electrical activity in chromaffin cells of intact mouse adrenal gland." American Journal of Physiology-Cell Physiology 254, no. 5 (May 1, 1988): C675—C683. http://dx.doi.org/10.1152/ajpcell.1988.254.5.c675.

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Membrane potentials of medullary chromaffin cells of the adrenal gland of the mouse were measured in situ. Resting potential (-54.3 +/- 8.8 mV) depended on extracellular [K+] as predicted by the constant-field equation with a permeability ratio, PNa/PK, of 0.09. Current-voltage (I-V) relationships showed that the current is rectified across the chromaffin cell membrane. A rectification ratio of 0.4 was calculated from the slopes of the I-V curves for positive (41 +/- 26 M omega) and negative (103 +/- M omega) currents. Because input resistance for a resting chromaffin cell in isolation is approximately 5 G omega, the chromaffin cells in situ behave as if they were electrically coupled. Most cells responded to depolarizing current pulses with repetitive action potentials, but only 50% of them showed spontaneous electrical activity. Spontaneous activity was often seen in the presence of tetrodotoxin (3 microM). Although the application of the K+-channel blockers tetraethylammonium and Ba2+ greatly increased the amplitude of the action potentials, only Ba2+ induced continuous electrical activity. Application of acetylcholine (ACh) always depolarized the cell membrane. This effect was blocked by atropine but not by D-tubocurarine, suggesting that ACh stimulation of chromaffin cells in the mouse involves activation of muscarinic receptors.

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Holz, Ronald W., and Ruth A. Senter. "Plasma Membrane and Chromaffin Granule Characteristics in Digitonin-Treated Chromaffin Cells." Journal of Neurochemistry 45, no. 5 (November 1985): 1548–57. http://dx.doi.org/10.1111/j.1471-4159.1985.tb07226.x.

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30

Michener, M. L., W. B. Dawson, and C. E. Creutz. "Phosphorylation of a chromaffin granule-binding protein in stimulated chromaffin cells." Journal of Biological Chemistry 261, no. 14 (May 1986): 6548–55. http://dx.doi.org/10.1016/s0021-9258(19)84597-0.

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31

Scheuner, D., C. D. Logsdon, and R. W. Holz. "Bovine chromaffin granule membranes undergo Ca(2+)-regulated exocytosis in frog oocytes." Journal of Cell Biology 116, no. 2 (January 15, 1992): 359–65. http://dx.doi.org/10.1083/jcb.116.2.359.

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We have devised a new method that permits the investigation of exogenous secretory vesicle function using frog oocytes and bovine chromaffin granules, the secretory vesicles from adrenal chromaffin cells. Highly purified chromaffin granule membranes were injected into Xenopus laevis oocytes. Exocytosis was detected by the appearance of dopamine-beta-hydroxylase of the chromaffin granule membrane in the oocyte plasma membrane. The appearance of dopamine-beta-hydroxylase on the oocyte surface was strongly Ca(2+)-dependent and was stimulated by coinjection of the chromaffin granule membranes with InsP3 or Ca2+/EGTA buffer (18 microM free Ca2+) or by incubation of the injected oocytes in medium containing the Ca2+ ionophore ionomycin. Similar experiments were performed with a subcellular fraction from cultured chromaffin cells enriched with [3H]norepinephrine-containing chromaffin granules. Because the release of [3H]norepinephrine was strongly correlated with the appearance of dopamine-beta-hydroxylase on the oocyte surface, it is likely that intact chromaffin granules and chromaffin granule membranes undergo exocytosis in the oocyte. Thus, the secretory vesicle membrane without normal vesicle contents is competent to undergo the sequence of events leading to exocytosis. Furthermore, the interchangeability of mammalian and amphibian components suggests substantial biochemical conservation of the regulated exocytotic pathway during the evolutionary progression from amphibians to mammals.

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Jousselin-Hosaja, M. "Effects of transplantation on mouse adrenal chromaffin cells." Journal of Endocrinology 116, no. 1 (January 1988): 149—NP. http://dx.doi.org/10.1677/joe.0.1160149.

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ABSTRACT The effects of long-term transplantation on the ultrastructure of adrenaline- and noradrenaline-storing cells from the adrenal medulla were determined using morphometric methods. Mouse adrenal medulla were freed from the adrenal cortex and grafted into the occipital cortex of the brain. Two types of chromaffin cells were identified by electron microscopy in grafts fixed with glutaraldehyde and osmium tetroxide. Noradrenaline-type cells were predominant and formed 70–80% of the surviving population of grafted chromaffin cells. A minority of the chromaffin cells contained medium-sized granules (140–210 nm in diameter) (medium granule cell; MGC) with finely granular moderately electron dense cores. Morphometric analysis of noradrenaline phenotype cells and MGC cells in transplants showed no significant differences compared with the noradrenaline-storing cells of normal adrenal glands. In contrast, noradrenaline-type cells and MGC cells in the grafts had areas of secretory vesicles which were significantly (P<0·01) larger and areas of rough endoplasmic reticulum which were significantly (P<0 ·01) smaller than those of the adrenaline-storing cells of normal adrenal glands. It was concluded that long-term transplantation caused no degenerative changes in the ultrastructure of mouse adrenal chromaffin cells. J. Endocr. (1988) 116, 149–153

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Bayley, Jean-Pierre, Heggert G. Rebel, Kimberly Scheurwater, Dominique Duesman, Juan Zhang, Francesca Schiavi, Esther Korpershoek, Jeroen C. Jansen, Abbey Schepers, and Peter Devilee. "Long-term in vitro 2D-culture of SDHB and SDHD-related human paragangliomas and pheochromocytomas." PLOS ONE 17, no. 9 (September 30, 2022): e0274478. http://dx.doi.org/10.1371/journal.pone.0274478.

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The neuroendocrine tumours paraganglioma and pheochromocytoma (PPGLs) are commonly associated with succinate dehydrogenase (SDH) gene variants, but no human SDH-related PPGL-derived cell line has been developed to date. The aim of this study was to systematically explore practical issues related to the classical 2D-culture of SDH-related human paragangliomas and pheochromocytomas, with the ultimate goal of identifying a viable tumour-derived cell line. PPGL tumour tissue/cells (chromaffin cells) were cultured in a variety of media formulations and supplements. Tumour explants and dissociated primary tumour cells were cultured and stained with a range of antibodies to identify markers suitable for use in human PPGL culture. We cultured 62 PPGLs, including tumours with confirmed SDHB, SDHC and SDHD variants, as well as several metastatic tumours. Testing a wide range of basic cell culture media and supplements, we noted a marked decline in chromaffin cell numbers over a 4–8 week period but the persistence of small numbers of synaptophysin/tyrosine hydroxylase-positive chromaffin cells for up to 99 weeks. In cell culture, immunohistochemical staining for chromogranin A and neuron-specific enolase was generally negative in chromaffin cells, while staining for synaptophysin and tyrosine hydroxylase was generally positive. GFAP showed the most consistent staining of type II sustentacular cells. Of the media tested, low serum or serum-free media best sustained relative chromaffin cell numbers, while lactate enhanced the survival of synaptophysin-positive cells. Synaptophysin-positive PPGL tumour cells persist in culture for long periods but show little evidence of proliferation. Synaptophysin was the most consistent cell marker for chromaffin cells and GFAP the best marker for sustentacular cells in human PPGL cultures.

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Jafferjee, Malika, Thairy Reyes Valero, Christine Marrero, Katie A. McCrink, Ava Brill, and Anastasios Lymperopoulos. "GRK2 Up-Regulation Creates a Positive Feedback Loop for Catecholamine Production in Chromaffin Cells." Molecular Endocrinology 30, no. 3 (March 1, 2016): 372–81. http://dx.doi.org/10.1210/me.2015-1305.

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Abstract Elevated sympathetic nervous system (SNS) activity aggravates several diseases, including heart failure. The molecular cause(s) underlying this SNS hyperactivity are not known. We have previously uncovered a neurohormonal mechanism, operating in adrenomedullary chromaffin cells, by which circulating catecholamine (CA) levels increase in heart failure: severe dysfunction of the adrenal α2-adrenergic receptors (ARs) due to the up-regulation of G protein-coupled receptor-kinase (GRK)-2, the kinase that desensitizes them. Herein we looked at the potential signaling mechanisms that bring about this GRK2 elevation in chromaffin cells. We found that chronic CA treatment of either PC12 or rat primary chromaffin cells can in itself result in GRK2 transcriptional up-regulation through α2ARs-Gi/o proteins-Src-ERK1/2. The resultant GRK2 increase severely enhances the α2AR desensitization/down-regulation elevating not only CA release but also CA biosynthesis, as evidenced by tyrosine hydroxylase up-regulation. Finally, GRK2 knockdown leads to enhanced apoptosis of PC12 cells, indicating an essential role for GRK2 in chromaffin cell homeostasis/survival. In conclusion, chromaffin cell GRK2 mediates a positive feedback loop that feeds into CA secretion, thereby enabling the adrenomedullary component of the SNS to turn itself on.

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García, Antonio G., Antonio M. García-De-Diego, Luis Gandía, Ricardo Borges, and Javier García-Sancho. "Calcium Signaling and Exocytosis in Adrenal Chromaffin Cells." Physiological Reviews 86, no. 4 (October 2006): 1093–131. http://dx.doi.org/10.1152/physrev.00039.2005.

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At a given cytosolic domain of a chromaffin cell, the rate and amplitude of the Ca2+ concentration ([Ca2+]c) depends on at least four efficient regulatory systems: 1) plasmalemmal calcium channels, 2) endoplasmic reticulum, 3) mitochondria, and 4) chromaffin vesicles. Different mammalian species express different levels of the L, N, P/Q, and R subtypes of high-voltage-activated calcium channels; in bovine and humans, P/Q channels predominate, whereas in felines and murine species, L-type channels predominate. The calcium channels in chromaffin cells are regulated by G proteins coupled to purinergic and opiate receptors, as well as by voltage and the local changes of [Ca2+]c. Chromaffin cells have been particularly useful in studying calcium channel current autoregulation by materials coreleased with catecholamines, such as ATP and opiates. Depending on the preparation (cultured cells, adrenal slices) and the stimulation pattern (action potentials, depolarizing pulses, high K+, acetylcholine), the role of each calcium channel in controlling catecholamine release can change drastically. Targeted aequorin and confocal microscopy shows that Ca2+ entry through calcium channels can refill the endoplasmic reticulum (ER) to nearly millimolar concentrations, and causes the release of Ca2+ (CICR). Depending on its degree of filling, the ER may act as a sink or source of Ca2+ that modulates catecholamine release. Targeted aequorins with different Ca2+ affinities show that mitochondria undergo surprisingly rapid millimolar Ca2+ transients, upon stimulation of chromaffin cells with ACh, high K+, or caffeine. Physiological stimuli generate [Ca2+]c microdomains in which the local subplasmalemmal [Ca2+]c rises abruptly from 0.1 to ∼50 μM, triggering CICR, mitochondrial Ca2+ uptake, and exocytosis at nearby secretory active sites. The fact that protonophores abolish mitochondrial Ca2+ uptake, and increase catecholamine release three- to fivefold, support the earlier observation. This increase is probably due to acceleration of vesicle transport from a reserve pool to a ready-release vesicle pool; this transport might be controlled by Ca2+ redistribution to the cytoskeleton, through CICR, and/or mitochondrial Ca2+ release. We propose that chromaffin cells have developed functional triads that are formed by calcium channels, the ER, and the mitochondria and locally control the [Ca2+]c that regulate the early and late steps of exocytosis.

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Wick, P. F., R. A. Senter, L. A. Parsels, M. D. Uhler, and R. W. Holz. "Transient transfection studies of secretion in bovine chromaffin cells and PC12 cells. Generation of kainate-sensitive chromaffin cells." Journal of Biological Chemistry 268, no. 15 (May 1993): 10983–89. http://dx.doi.org/10.1016/s0021-9258(18)82082-8.

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Langley, Keith, and Nancy J. Grant. "Do adrenergic chromaffin cells exocytose like noradrenergic cells." Trends in Neurosciences 18, no. 10 (October 1995): 440–41. http://dx.doi.org/10.1016/0166-2236(95)94492-n.

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Callewaert, G., R. G. Johnson, and M. Morad. "Regulation of the secretory response in bovine chromaffin cells." American Journal of Physiology-Cell Physiology 260, no. 4 (April 1, 1991): C851—C860. http://dx.doi.org/10.1152/ajpcell.1991.260.4.c851.

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The nicotine-induced current and the Ca2+ current were studied in cultured bovine chromaffin cells using the whole cell patch-clamp technique. The dose-response curve for the nicotinic current gave a dissociation constant of 53 microM and a Hill coefficient of 1.3. Desensitization of the nicotinic current was rapid, with time constants of 22 and 155 ms at 10 microM nicotine. At higher concentrations of nicotine, both time constants decreased somewhat, but the most prominent effect was on the ratio of the two components. Recovery from desensitization was fitted by a single exponential with a time constant of approximately 6 s. Ca2+ current and catecholamine secretion were highly sensitive to changes in extracellular H+ concentration ([H+]o), such that small increases in [H+]o markedly decreased both. The Ca2+ current measured in a chromaffin cell located within a cluster of cells, but not in a single isolated cell, was markedly suppressed when KCl or nicotine was used to induce secretion, suggesting possible local feedback of secretory agents. Among agents secreted by chromaffin cells, ATP, enkephalins, epinephrine, and protons, only protons significantly suppressed the Ca2+ current. Our findings suggest that the secretory response of chromaffin cells may be modulated by rapid desensitization of the nicotinic receptor and a secretion-dependent suppression of the Ca2+ current.

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Nakata, T., K. Sobue, and N. Hirokawa. "Conformational change and localization of calpactin I complex involved in exocytosis as revealed by quick-freeze, deep-etch electron microscopy and immunocytochemistry." Journal of Cell Biology 110, no. 1 (January 1, 1990): 13–25. http://dx.doi.org/10.1083/jcb.110.1.13.

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Calpactin I complex, a calcium-dependent phospholipid-binding protein, promotes aggregation of chromaffin vesicles at physiological micromolar calcium ion levels. Calpactin I complex was found to be a globular molecule with a diameter of 10.7 +/- 1.7 (SD) nm on mica. When liposomes were aggregated by calpactin, quick-freeze, deep-etching revealed fine thin strands (6.5 +/- 1.9 [SD] nm long) cross-linking opposing membranes in addition to the globules on the surface of liposomes. Similar fine strands were also observed between aggregated chromaffin vesicles when they were mixed with calpactin in the presence of Ca2+ ion. In cultured chromaffin cells, similar cross-linking short strands (6-10 nm) were found between chromaffin vesicles and the plasma membrane after stimulation with acetylcholine. Plasma membranes also revealed numerous globular structures approximately 10 nm in diameter on their cytoplasmic surface. Immunoelectron microscopy on frozen ultrathin sections showed that calpactin I was closely associated with the inner face of the plasma membranes and was especially conspicuous between plasma membranes and adjacent vesicles in chromaffin cells. These in vivo and in vitro data strongly suggest that calpactin I complex changes its conformation to cross-link vesicles and the plasma membrane after stimulation of cultured chromaffin cells.

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LEVINE, MARK. "Ascorbic Acid Enhancement of Norepinephrine Biosynthesis in Chromaffin Cells and Chromaffin Vesicles." Annals of the New York Academy of Sciences 493, no. 1 Cellular and (April 1987): 147–50. http://dx.doi.org/10.1111/j.1749-6632.1987.tb27194.x.

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41

Egger, Claudia, and Hans Winkler. "Bovine chromaffin cells: Studies on the biosynthesis of phospholipids in chromaffin granules." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1211, no. 3 (March 1994): 277–82. http://dx.doi.org/10.1016/0005-2760(94)90151-1.

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42

Wang, Jun Ming, Dirk Slembrouck, Junhui Tan, Lut Arckens, Frans H. H. Leenen, Pierre J. Courtoy, and Werner P. De Potter. "Presence of cellular renin-angiotensin system in chromaffin cells of bovine adrenal medulla." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 5 (November 1, 2002): H1811—H1818. http://dx.doi.org/10.1152/ajpheart.01092.2001.

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The presence of a local renin-angiotensin system has been established in organs that serve as angiotensin targets. In this study, the expression of angiotensinogen mRNA and subcellular localization of renin, angiotensin-converting enzyme, and angiotensin II were investigated in bovine adrenal medullary cells in primary culture. By light microscopy, expression of angiotensinogen mRNA, immunoreactive renin, angiotensin-converting enzyme, and angiotensin II were readily detectable only in the chromaffin cells. The density distribution of renin and angiotensin II in sucrose gradients suggested a concentration in chromaffin granules, a localization directly confirmed by immunoelectron microscopy. Reverse transcriptase-polymerase chain reaction and sequencing confirmed the expression of angiotensinogen in bovine chromaffin cells and the adrenal medulla. In addition, in vitro autoradiography indicated that both angiotensin-converting enzyme and angiotensin type 1 receptors were present in the adrenal medulla. These results provide the first direct evidence that chromaffin cells in the adrenal medulla are not only the target for angiotensin but should also be considered as potential local angiotensin-generating and -storing cells.

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Ehrhart-Bornstein, M., V. Vukicevic, K. F. Chung, and S. R. Bornstein. "Neuronal differentiation of chromaffin progenitor cells." Molecular Psychiatry 14, no. 1 (December 19, 2008): 1. http://dx.doi.org/10.1038/mp.2008.129.

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KIRSHNER, NORMAN, JAMES J. CORCORAN, BYRON CAUGHEY, and MIRA KORNER. "Chromaffin Vesicle Function in Intact Cells." Annals of the New York Academy of Sciences 493, no. 1 Cellular and (April 1987): 207–19. http://dx.doi.org/10.1111/j.1749-6632.1987.tb27202.x.

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MIRAS-PORTUGAL, M. T., J. PINTOR, P. ROTLLÁN, and M. TORRES. "Characterization of Ectonucleotidases in Chromaffin Cells." Annals of the New York Academy of Sciences 603, no. 1 Biological Ac (December 1990): 523–26. http://dx.doi.org/10.1111/j.1749-6632.1990.tb37726.x.

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EKBLOM, A. "Antinociceptive properties of adrenal chromaffin cells." Regional Anesthesia and Pain Medicine 22, no. 5 (September 1997): 486. http://dx.doi.org/10.1016/s1098-7339(97)80044-2.

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García, Antonio G., and Emilio Carbone. "Calcium-current facilitation in chromaffin cells." Trends in Neurosciences 19, no. 9 (January 1996): 383–84. http://dx.doi.org/10.1016/s0166-2236(96)20035-9.

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Delacruz, Joannalyn, Meng Huang, Joan Lenz, Manfred Lindau, and Shailendra Rathore. "Fusion Pore Selectivity in Chromaffin Cells." Biophysical Journal 112, no. 3 (February 2017): 396a. http://dx.doi.org/10.1016/j.bpj.2016.11.2148.

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OKA, Motoo, Kyoji MORITA, Masanori YOSHIZUMI, Hitoshi HOUCHI, Yasuko ISHIMURA, and Yutaka MASUDA. "Catecholamine secretion from adrenal chromaffin cells." Folia Pharmacologica Japonica 98, no. 3 (1991): 209–14. http://dx.doi.org/10.1254/fpj.98.3_209.

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Krause, Winfried, Norbert Michael, Carsten Lübke, Bruce G. Livett, and Peter Oehme. "Catecholamine release from fractionated chromaffin cells." European Journal of Pharmacology 302, no. 1-3 (April 1996): 223–28. http://dx.doi.org/10.1016/0014-2999(96)00103-3.

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