scholarly journals Rapid vesicle replenishment after the immediately releasable pool exocytosis is tightly linked to fast endocytosis, and depends on basal calcium and cortical actin in chromaffin cells

2021 ◽  
Author(s):  
Mauricio Montenegro ◽  
Lucas Bayonés ◽  
José Moya‐Díaz ◽  
Cecilia Borassi ◽  
Andrés Martín Toscani ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Cortical Actin ◽  
Releasable Pool

scholarly journals Cortical F-Actin, the Exocytic Mode, and Neuropeptide Release in Mouse Chromaffin Cells Is Regulated by Myristoylated Alanine-rich C-Kinase Substrate and Myosin II

2009 ◽  
Vol 20 (13) ◽  
pp. 3142-3154 ◽  
Author(s):  
Bryan W. Doreian ◽  
Tiberiu G. Fulop ◽  
Robert L. Meklemburg ◽  
Corey B. Smith
Keyword(s):  
Chromaffin Cells ◽  
Myosin Ii ◽  
Splanchnic Nerve ◽  
Cortical Actin ◽  
Kinase Substrate ◽  
Actin Cortex ◽  
Collapse Mode ◽  
Associated Proteins ◽  
Intact Cortex ◽  
Activity Dependent

Adrenal medullary chromaffin cells are innervated by the sympathetic splanchnic nerve and translate graded sympathetic firing into a differential hormonal exocytosis. Basal sympathetic firing elicits a transient kiss-and-run mode of exocytosis and modest catecholamine release, whereas elevated firing under the sympathetic stress response results in full granule collapse to release catecholamine and peptide transmitters into the circulation. Previous studies have shown that rearrangement of the cell actin cortex regulates the mode of exocytosis. An intact cortex favors kiss-and-run exocytosis, whereas disrupting the cortex favors the full granule collapse mode. Here, we investigate the specific roles of two actin-associated proteins, myosin II and myristoylated alanine-rich C-kinase substrate (MARCKS) in this process. Our data demonstrate that MARCKS phosphorylation under elevated cell firing is required for cortical actin disruption but is not sufficient to elicit peptide transmitter exocytosis. Our data also demonstrate that myosin II is phospho-activated under high stimulation conditions. Inhibiting myosin II activity prevented disruption of the actin cortex, full granule collapse, and peptide transmitter release. These results suggest that phosphorylation of both MARCKS and myosin II lead to disruption of the actin cortex. However, myosin II, but not MARCKS, is required for the activity-dependent exocytosis of the peptide transmitters.

Adrenal Chromaffin Cells Exhibit Impaired Granule Trafficking in NCAM Knockout Mice

2005 ◽  
Vol 94 (2) ◽  
pp. 1037-1047 ◽  
Author(s):  
Shyue-An Chan ◽  
Luis Polo-Parada ◽  
Lynn T. Landmesser ◽  
Corey Smith
Keyword(s):  
Neuromuscular Junction ◽  
Knockout Mice ◽  
Transmitter Release ◽  
Chromaffin Cells ◽  
Vesicle Trafficking ◽  
Catecholamine Release ◽  
Neuroendocrine Cells ◽  
Release Mechanism ◽  
General Role ◽  
Releasable Pool

Neural cell adhesion molecule (NCAM) plays several critical roles in neuron path-finding and intercellular communication during development. In the clinical setting, serum NCAM levels are altered in both schizophrenic and autistic patients. NCAM knockout mice have been shown to exhibit deficits in neuronal functions including impaired hippocampal long term potentiation and motor coordination. Recent studies in NCAM null mice have indicated that synaptic vesicle trafficking and active zone targeting are impaired, resulting in periodic synaptic transmission failure under repetitive physiological stimulation. In this study, we tested whether NCAM plays a role in vesicle trafficking that is limited to the neuromuscular junction or whether it may also play a more general role in transmitter release from other cell systems. We tested catecholamine release from neuroendocrine chromaffin cells in the mouse adrenal tissue slice preparation. We utilize electrophysiological and electrochemical measures to assay granule recruitment and targeting in wild-type and NCAM −/− mice. Our data show that NCAM −/− mice exhibit deficits in normal granule trafficking between the readily releasable pool and the highly release-competent immediately releasable pool. This defect results in a decreased rate of granule fusion and thus catecholamine release under physiological stimulation. Our data indicate that NCAM plays a basic role in the transmitter release mechanism in neuroendocrine cells through mediation of granule recruitment and is not limited to the neuromuscular junction and central synapse active zones.

scholarly journals Huntingtin-associated protein 1 regulates exocytosis, vesicle docking, readily releasable pool size and fusion pore stability in mouse chromaffin cells

2014 ◽  
Vol 592 (7) ◽  
pp. 1505-1518 ◽  
Author(s):  
Kimberly D. Mackenzie ◽  
Michael D. Duffield ◽  
Heshan Peiris ◽  
Lucy Phillips ◽  
Mark P. Zanin ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Pool Size ◽  
Fusion Pore ◽  
Vesicle Docking ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Pore Stability

P/Q Ca2+ channels are functionally coupled to exocytosis of the immediately releasable pool in mouse chromaffin cells

Cell Calcium ◽  
2008 ◽  
Vol 43 (2) ◽  
pp. 155-164 ◽  
Author(s):  
Yanina D. Álvarez ◽  
Lorena I. Ibañez ◽  
Osvaldo D. Uchitel ◽  
Fernando D. Marengo
Keyword(s):  
Chromaffin Cells ◽  
Releasable Pool ◽  
Ca2 Channels

Morphological Observations on the Granule Types in Rabbit Extra-Adrenal Chromaffin Cells.

1975 ◽  
Vol 33 ◽  
pp. 318-319
Author(s):  
Joe A. Mascorro ◽  
Robert D. Yates
Keyword(s):  
Chromaffin Cells ◽  
Sodium Phosphate ◽  
Ganglion Cells ◽  
Ultrastructural Level ◽  
Osmic Acid ◽  
Adrenal Chromaffin Cells ◽  
Potassium Iodate ◽  
Perfusion Fluid ◽  
New Zealand White Rabbits ◽  
Adrenal Chromaffin

Extra-adrenal chromaffin organs (abdominal paraganglia) constitute rich sources of catecholamines. It is believed that these bodies contain norepinephrine exclusively. However, the present workers recently observed epinephrine type granules in para- ganglion cells. This report investigates catecholamine containing granules in rabbit paraganglia at the ultrastructural level.New Zealand white rabbits (150-170 grams) were anesthetized with 50 mg/kg Nembutal (IP) and perfused with 3% glutaraldehyde buffered with 0.2M sodium phosphate, pH 7.3. The retroperitoneal tissue blocks were removed and placed in perfusion fluid for 4 hours. The abdominal paraganglia were dissected from the blocks, diced, washed in phosphate buffer and fixed in 1% osmic acid buffered with phosphate. In other animals, the glutaraldehyde perfused tissue blocks were immersed for 1 hour in 3% glutaraldehyde/2.5% potassium iodate buffered as before. The paraganglia were then diced, separated into two vials and washed in the buffer. A portion of this tissue received osmic acid fixation.

Alleviation of pain and depression by specific neural transplants: Fine structural correlates

1992 ◽  
Vol 50 (2) ◽  
pp. 1066-1067
Author(s):  
George D. Pappas ◽  
Jacqueline Sagen
Keyword(s):  
Opioid Peptides ◽  
Chromaffin Cells ◽  
Pain Sensitivity ◽  
Opioid Peptide ◽  
Local Source ◽  
Pain Models ◽  
Neural Transplants ◽  
Adrenergic Antagonists ◽  
Csf Levels ◽  
Donor Source

We have been interested in the use of neural transplants mainly as a local source of neuroactive substances, rather than as a replacement for damaged neural circuities. In particular, we have been exploring the possibilities of reducing pain by transplants of opioid peptide producing cells, and reducing depression by transplants of monoamine-producing cells. For the past several years, work in our laboratory has demonstrated in both acute and chronic pain models that transplantation of adrenal medullary tissue or isolated chromaffin cells into CNS pain modulatory regions can reduce pain sensitivity in rodents. Chromaffin cells were chosen as donor source since they produce high levels of both opioid peptides and catecholamines, substances which independently, and probably synergistically, reduce pain sensitivity when injected locally into the spinal cord. The analgesia produced by these transplants most likely results from the release of both opioid peptides and catecholamines, since it can be blocked or attenuated by opiate or adrenergic antagonists, respectively. Furthermore, CSF levels of met-enkephalin and catecholamines are increased by the transplants.

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