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Article: Serotonin and the serotonin transporter in the adrenal gland.

Bauer, Mary Beth / Currie, Kevin P M

2023 Volume 124, Page(s) 39–78

Abstract: The adrenal glands are key components of the mammalian endocrine system, helping maintain physiological homeostasis and the coordinated response to stress. Each adrenal gland has two morphologically and functionally distinct regions, the outer cortex and ...

Abstract	The adrenal glands are key components of the mammalian endocrine system, helping maintain physiological homeostasis and the coordinated response to stress. Each adrenal gland has two morphologically and functionally distinct regions, the outer cortex and inner medulla. The cortex is organized into three concentric zones which secrete steroid hormones, including aldosterone and cortisol. Neural crest-derived chromaffin cells in the medulla are innervated by preganglionic sympathetic neurons and secrete catecholamines (epinephrine, norepinephrine) and neuropeptides into the bloodstream, thereby functioning as the neuroendocrine arm of the sympathetic nervous system. In this article we review serotonin (5-HT) and the serotonin transporter (SERT; SLC6A4) in the adrenal gland. In the adrenal cortex, 5-HT, primarily sourced from resident mast cells, acts as a paracrine signal to stimulate aldosterone and cortisol secretion through 5-HT
MeSH term(s)	Animals ; Humans ; Serotonin/metabolism ; Serotonin Plasma Membrane Transport Proteins/genetics ; Serotonin Plasma Membrane Transport Proteins/metabolism ; Aldosterone/metabolism ; Hydrocortisone ; Adrenal Glands ; Mammals
Chemical Substances	Serotonin (333DO1RDJY) ; Serotonin Plasma Membrane Transport Proteins ; Aldosterone (4964P6T9RB) ; Hydrocortisone (WI4X0X7BPJ) ; SLC6A4 protein, human
Language	English
Publishing date	2023-07-18
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	201161-x
ISSN	2162-2620 ; 0083-6729
ISSN (online)	2162-2620
ISSN	0083-6729
DOI	10.1016/bs.vh.2023.06.002
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Article ; Online: NaV-igating the MAP from PACAP to excitement. Focus on "Activation of MEK/ERK signaling contributes to the PACAP-induced increase in guinea pig cardiac neuron excitability".

Currie, Kevin P M

American journal of physiology. Cell physiology

2016 Volume 311, Issue 4, Page(s) C641–C642

MeSH term(s)	Animals ; Guinea Pigs ; Heart ; Neurons ; Pituitary Adenylate Cyclase-Activating Polypeptide ; Signal Transduction
Chemical Substances	Pituitary Adenylate Cyclase-Activating Polypeptide
Language	English
Publishing date	2016-09-21
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00270.2016
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Article ; Online: Phospholipase C-ε defines a PACAP-stimulated pathway for secretion in the chromaffin cell.

Chen, Xiaohuan / Coffman, Breanna L / Brindley, Rebecca L / Galpin, Jason D / Ahern, Christopher A / Currie, Kevin P M / Smrcka, Alan V / Axelrod, Daniel / Anantharam, Arun

Journal of neuroendocrinology

2023 Volume 35, Issue 11, Page(s) e13255

Abstract: Adrenomedullary chromaffin cells respond to splanchnic (sympathetic) nerve stimulation by releasing stress hormones into the circulation. The signal for hormone secretion is encoded in the neurotransmitters - especially acetylcholine (ACh) and pituitary ... ...

Abstract	Adrenomedullary chromaffin cells respond to splanchnic (sympathetic) nerve stimulation by releasing stress hormones into the circulation. The signal for hormone secretion is encoded in the neurotransmitters - especially acetylcholine (ACh) and pituitary adenylate cyclase activating polypeptide (PACAP) - that are released into the splanchnic-chromaffin cell synapse. However, functional differences in the effects of ACh and PACAP on the chromaffin cell secretory response are not well defined. Here, selective agonists of PACAP receptors or nicotinic and muscarinic acetylcholine receptors were applied to chromaffin cells. The major differences in the effects of these agents were not on exocytosis, per se, but rather on the steps upstream of exocytosis. In almost every respect, the properties of individual fusion events triggered by PACAP and cholinergic agonists were similar. On the other hand, the properties of the Ca
MeSH term(s)	Acetylcholine/metabolism ; Catecholamines/metabolism ; Catecholamines/pharmacology ; Cholinergic Agonists/metabolism ; Cholinergic Agonists/pharmacology ; Chromaffin Cells/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Hormones ; Pituitary Adenylate Cyclase-Activating Polypeptide/metabolism ; Animals ; Mice ; Receptors, Cholinergic/metabolism
Chemical Substances	Acetylcholine (N9YNS0M02X) ; Catecholamines ; Cholinergic Agonists ; Guanine Nucleotide Exchange Factors ; Hormones ; Pituitary Adenylate Cyclase-Activating Polypeptide ; phospholipase C epsilon (EC 3.1.4.11) ; Receptors, Cholinergic
Language	English
Publishing date	2023-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1007517-3
ISSN	1365-2826 ; 0953-8194
ISSN (online)	1365-2826
ISSN	0953-8194
DOI	10.1111/jne.13255
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Article ; Online: Joint Injury, Osteoarthritis, and Cardiovascular Disease Risk Factors in Former National Football League Athletes: An NFL-LONG Study.

Kuenze, Christopher / Pietrosimone, Brian / Currie, Katharine D / Walton, Samuel R / Kerr, Zachary Y / Brett, Benjamin L / Chandran, Avinash / DeFreese, J D / Mannix, Rebekah / Echemendia, Ruben J / McCrea, Michael / Guskiewicz, Kevin M / Meehan, William P

Journal of athletic training

2023 Volume 58, Issue 6, Page(s) 528–535

Abstract: Context: Individuals with lower extremity osteoarthritis (OA) have a 25% greater risk of cardiovascular disease (CVD) than those without OA. The prevalence of traumatic joint injuries among National Football League (NFL) players exposes these athletes ... ...

Abstract	Context: Individuals with lower extremity osteoarthritis (OA) have a 25% greater risk of cardiovascular disease (CVD) than those without OA. The prevalence of traumatic joint injuries among National Football League (NFL) players exposes these athletes to an elevated risk for OA and potentially a greater risk of cardiovascular risk factors (CRFs) and CVD. Objectives: To examine the associations between a history of lower extremity joint injury, lower extremity OA, and the prevalence of CRFs and CVD among former NFL athletes. Design: Cross-sectional study. Patients or other participants: Former NFL players completed a comprehensive health questionnaire that was used in an ongoing study, the Neurologic Function Across the Lifespan: A Prospective, Longitudinal, and Translational Study for Former NFL Players (NFL-LONG). A subsample of 1738 former players reported lifetime medical diagnoses including CVD or CRFs. Main outcome measure(s): Crude and adjusted prevalence ratios (PRsadj) characterized the associations between CVD or CRFs and injury, OA diagnosis, or both among athletes who reported (1) no history of lower extremity joint injury or surgery and no diagnosed OA, (2) a history of lower extremity joint injury or surgery and no diagnosed OA, and (3) a history of lower extremity joint injury or surgery and diagnosed OA. Results: Neither a history of lower extremity joint injury (PRadj = 1.34; 95% CI = 0.86, 2.07) nor a history of lower extremity joint injury and diagnosed OA (PRadj = 1.41; 95% CI = 0.89, 2.25) was significantly associated with CVD. However, CRFs were 30% and 53% more prevalent in former players with lower extremity joint injury and no diagnosed OA (PRadj = 1.30; 95% CI = 1.12, 1.50) and those with lower extremity joint injury and diagnosed OA (PRadj = 1.53; 95% CI = 1.31, 1.78), respectively, versus athletes with no history of either condition. Conclusions: The prevalence of CRFs was highest among former NFL athletes with a history of lower extremity joint injury and diagnosed OA. These findings provide insight regarding the potential pathways to chronic diseases that may be initiated by joint injury early in life.
MeSH term(s)	Humans ; Football/injuries ; Cross-Sectional Studies ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/complications ; Prospective Studies ; Osteoarthritis/epidemiology ; Osteoarthritis/etiology ; Athletes ; Heart Disease Risk Factors
Language	English
Publishing date	2023-01-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2070051-9
ISSN	1938-162X ; 1062-6050
ISSN (online)	1938-162X
ISSN	1062-6050
DOI	10.4085/1062-6050-0437.22
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Article ; Online: Jedi-1 deficiency increases sensory neuron excitability through a non-cell autonomous mechanism.

Trevisan, Alexandra J / Bauer, Mary Beth / Brindley, Rebecca L / Currie, Kevin P M / Carter, Bruce D

Scientific reports

2020 Volume 10, Issue 1, Page(s) 1300

Abstract: The dorsal root ganglia (DRG) house the primary afferent neurons responsible for somatosensation, including pain. We previously identified Jedi-1 (PEAR1/MEGF12) as a phagocytic receptor expressed by satellite glia in the DRG involved in clearing ... ...

Abstract	The dorsal root ganglia (DRG) house the primary afferent neurons responsible for somatosensation, including pain. We previously identified Jedi-1 (PEAR1/MEGF12) as a phagocytic receptor expressed by satellite glia in the DRG involved in clearing apoptotic neurons during development. Here, we further investigated the function of this receptor in vivo using Jedi-1 null mice. In addition to satellite glia, we found Jedi-1 expression in perineurial glia and endothelial cells, but not in sensory neurons. We did not detect any morphological or functional changes in the glial cells or vasculature of Jedi-1 knockout mice. Surprisingly, we did observe changes in DRG neuron activity. In neurons from Jedi-1 knockout (KO) mice, there was an increase in the fraction of capsaicin-sensitive cells relative to wild type (WT) controls. Patch-clamp electrophysiology revealed an increase in excitability, with a shift from phasic to tonic action potential firing patterns in KO neurons. We also found alterations in the properties of voltage-gated sodium channel currents in Jedi-1 null neurons. These results provide new insight into the expression pattern of Jedi-1 in the peripheral nervous system and indicate that loss of Jedi-1 alters DRG neuron activity indirectly through an intercellular interaction between non-neuronal cells and sensory neurons.
MeSH term(s)	Action Potentials ; Animals ; Biomarkers ; Cell Line ; Ganglia, Spinal/cytology ; Ganglia, Spinal/metabolism ; Humans ; Immunohistochemistry ; Mice ; Mice, Knockout ; Mice, Transgenic ; Neuroglia/metabolism ; Neuroglia/ultrastructure ; Patch-Clamp Techniques ; Receptors, Cell Surface/deficiency ; Sensory Receptor Cells/metabolism ; Sensory Receptor Cells/ultrastructure
Chemical Substances	Biomarkers ; PEAR1 protein, mouse ; Receptors, Cell Surface
Language	English
Publishing date	2020-01-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-57971-2
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Article: Sampling related individuals within ponds biases estimates of population structure in a pond-breeding amphibian.

O'Connell, Kyle A / Mulder, Kevin P / Maldonado, Jose / Currie, Kathleen L / Ferraro, Dennis M

Ecology and evolution

2019 Volume 9, Issue 6, Page(s) 3620–3636

Abstract: Effective conservation and management of pond-breeding amphibians depends on the accurate estimation of population structure, demographic parameters, and the influence of landscape features on breeding-site connectivity. Population-level studies of pond- ... ...

Abstract	Effective conservation and management of pond-breeding amphibians depends on the accurate estimation of population structure, demographic parameters, and the influence of landscape features on breeding-site connectivity. Population-level studies of pond-breeding amphibians typically sample larval life stages because they are easily captured and can be sampled nondestructively. These studies often identify high levels of relatedness between individuals from the same pond, which can be exacerbated by sampling the larval stage. Yet, the effect of these related individuals on population genetic studies using genomic data is not yet fully understood. Here, we assess the effect of within-pond relatedness on population and landscape genetic analyses by focusing on the barred tiger salamanders (
Language	English
Publishing date	2019-03-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2635675-2
ISSN	2045-7758
ISSN	2045-7758
DOI	10.1002/ece3.4994
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Article ; Online: G protein modulation of CaV2 voltage-gated calcium channels.

Currie, Kevin P M

Channels (Austin, Tex.)

2010 Volume 4, Issue 6, Page(s) 497–509

Abstract: ... by CaV2.1 (P/Q-type) and CaV2.2 (N-type) channels. It is well established that G protein coupled receptors ...

Abstract	Voltage-gated Ca(2+) channels translate the electrical inputs of excitable cells into biochemical outputs by controlling influx of the ubiquitous second messenger Ca(2+) . As such the channels play pivotal roles in many cellular functions including the triggering of neurotransmitter and hormone release by CaV2.1 (P/Q-type) and CaV2.2 (N-type) channels. It is well established that G protein coupled receptors (GPCRs) orchestrate precise regulation neurotransmitter and hormone release through inhibition of CaV2 channels. Although the GPCRs recruit a number of different pathways, perhaps the most prominent, and certainly most studied among these is the so-called voltage-dependent inhibition mediated by direct binding of Gβγ to the α1 subunit of CaV2 channels. This article will review the basics of Ca(2+) -channels and G protein signaling, and the functional impact of this now classical inhibitory mechanism on channel function. It will also provide an update on more recent developments in the field, both related to functional effects and crosstalk with other signaling pathways, and advances made toward understanding the molecular interactions that underlie binding of Gβγ to the channel and the voltage-dependence that is a signature characteristic of this mechanism.
MeSH term(s)	Animals ; Calcium Channels/chemistry ; Calcium Channels/metabolism ; Calcium Channels, L-Type/metabolism ; Calcium Channels, P-Type/metabolism ; Calcium Channels, Q-Type/metabolism ; Calcium Signaling ; GTP-Binding Protein beta Subunits/chemistry ; GTP-Binding Protein beta Subunits/metabolism ; GTP-Binding Protein gamma Subunits/chemistry ; GTP-Binding Protein gamma Subunits/metabolism ; Humans ; Ion Channel Gating ; Membrane Potentials ; Models, Molecular ; Protein Conformation ; Receptors, G-Protein-Coupled/metabolism ; Structure-Activity Relationship
Chemical Substances	Calcium Channels ; Calcium Channels, L-Type ; Calcium Channels, P-Type ; Calcium Channels, Q-Type ; G-protein Beta gamma ; GTP-Binding Protein beta Subunits ; GTP-Binding Protein gamma Subunits ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2010-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2262854-X
ISSN	1933-6969 ; 1933-6969
ISSN (online)	1933-6969
ISSN	1933-6969
DOI	10.4161/chan.4.6.12871
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Article ; Online: Inhibition of Ca2+ channels and adrenal catecholamine release by G protein coupled receptors.

Currie, Kevin P M

Cellular and molecular neurobiology

2010 Volume 30, Issue 8, Page(s) 1201–1208

Abstract: Catecholamines and other transmitters released from adrenal chromaffin cells play central roles in the "fight-or-flight" response and exert profound effects on cardiovascular, endocrine, immune, and nervous system function. As such, precise regulation of ...

Abstract	Catecholamines and other transmitters released from adrenal chromaffin cells play central roles in the "fight-or-flight" response and exert profound effects on cardiovascular, endocrine, immune, and nervous system function. As such, precise regulation of chromaffin cell exocytosis is key to maintaining normal physiological function and appropriate responsiveness to acute stress. Chromaffin cells express a number of different G protein coupled receptors (GPCRs) that sense the local environment and orchestrate this precise control of transmitter release. The primary trigger for catecholamine release is Ca2+ entry through voltage-gated Ca2+ channels, so it makes sense that these channels are subject to complex regulation by GPCRs. In particular G protein βγ heterodimers (Gbc) bind to and inhibit Ca2+ channels. Here I review the mechanisms by which GPCRs inhibit Ca2+ channels in chromaffin cells and how this might be altered by cellular context. This is related to the potent autocrine inhibition of Ca2+ entry and transmitter release seen in chromaffin cells. Recent data that implicate an additional inhibitory target of Gβγ on the exocytotic machinery and how this might fine tune neuroendocrine secretion are also discussed.
MeSH term(s)	Adrenal Glands/cytology ; Adrenal Glands/metabolism ; Animals ; Calcium Channels/metabolism ; Catecholamines/metabolism ; Chromaffin Cells/metabolism ; GTP-Binding Protein beta Subunits/metabolism ; GTP-Binding Protein gamma Subunits/metabolism ; Humans ; Receptors, G-Protein-Coupled/metabolism
Chemical Substances	Calcium Channels ; Catecholamines ; G-protein Beta gamma ; GTP-Binding Protein beta Subunits ; GTP-Binding Protein gamma Subunits ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2010-11-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-010-9596-7
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Article ; Online: "Slow" Voltage-Dependent Inactivation of CaV2.2 Calcium Channels Is Modulated by the PKC Activator Phorbol 12-Myristate 13-Acetate (PMA).

Zhu, Lei / McDavid, Sarah / Currie, Kevin P M

PloS one

2015 Volume 10, Issue 7, Page(s) e0134117

Abstract: CaV2.2 (N-type) voltage-gated calcium channels (Ca2+ channels) play key roles in neurons and neuroendocrine cells including the control of cellular excitability, neurotransmitter / hormone secretion, and gene expression. Calcium entry is precisely ... ...

Abstract	CaV2.2 (N-type) voltage-gated calcium channels (Ca2+ channels) play key roles in neurons and neuroendocrine cells including the control of cellular excitability, neurotransmitter / hormone secretion, and gene expression. Calcium entry is precisely controlled by channel gating properties including multiple forms of inactivation. "Fast" voltage-dependent inactivation is relatively well-characterized and occurs over the tens-to- hundreds of milliseconds timeframe. Superimposed on this is the molecularly distinct, but poorly understood process of "slow" voltage-dependent inactivation, which develops / recovers over seconds-to-minutes. Protein kinases can modulate "slow" inactivation of sodium channels, but little is known about if/how second messengers control "slow" inactivation of Ca2+ channels. We investigated this using recombinant CaV2.2 channels expressed in HEK293 cells and native CaV2 channels endogenously expressed in adrenal chromaffin cells. The PKC activator phorbol 12-myristate 13-acetate (PMA) dramatically prolonged recovery from "slow" inactivation, but an inactive control (4α-PMA) had no effect. This effect of PMA was prevented by calphostin C, which targets the C1-domain on PKC, but only partially reduced by inhibitors that target the catalytic domain of PKC. The subtype of the channel β-subunit altered the kinetics of inactivation but not the magnitude of slowing produced by PMA. Intracellular GDP-β-S reduced the effect of PMA suggesting a role for G proteins in modulating "slow" inactivation. We postulate that the kinetics of recovery from "slow" inactivation could provide a molecular memory of recent cellular activity and help control CaV2 channel availability, electrical excitability, and neurotransmission in the seconds-to-minutes timeframe.
MeSH term(s)	Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channels, N-Type/chemistry ; Calcium Channels, N-Type/genetics ; Calcium Channels, N-Type/metabolism ; Calcium Signaling/drug effects ; Cattle ; Cells, Cultured ; Chromaffin Cells/drug effects ; Chromaffin Cells/metabolism ; Enzyme Activation/drug effects ; Guanosine Diphosphate/analogs & derivatives ; Guanosine Diphosphate/metabolism ; HEK293 Cells ; Humans ; Kinetics ; Patch-Clamp Techniques ; Protein Kinase C/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Thionucleotides/metabolism
Chemical Substances	CACNA1B protein, human ; Calcium Channel Blockers ; Calcium Channels, N-Type ; Recombinant Proteins ; Thionucleotides ; Guanosine Diphosphate (146-91-8) ; guanosine 5'-O-(2-thiodiphosphate) (71376-97-1) ; Protein Kinase C (EC 2.7.11.13) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0134117
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Article ; Online: PACAP and acetylcholine cause distinct Ca2+ signals and secretory responses in chromaffin cells.

Morales, Alina / Mohan, Ramkumar / Chen, Xiaohuan / Coffman, Breanna L / Bendahmane, Mounir / Watch, Lester / West, Joshua L / Bakshi, Shreeya / Traynor, John R / Giovannucci, David R / Kammermeier, Paul J / Axelrod, Daniel / Currie, Kevin P M / Smrcka, Alan V / Anantharam, Arun

The Journal of general physiology

2022 Volume 155, Issue 2

Abstract: The adrenomedullary chromaffin cell transduces chemical messages into outputs that regulate end organ function throughout the periphery. At least two important neurotransmitters are released by innervating preganglionic neurons to stimulate exocytosis in ...

Abstract	The adrenomedullary chromaffin cell transduces chemical messages into outputs that regulate end organ function throughout the periphery. At least two important neurotransmitters are released by innervating preganglionic neurons to stimulate exocytosis in the chromaffin cell-acetylcholine (ACh) and pituitary adenylate cyclase activating polypeptide (PACAP). Although PACAP is widely acknowledged as an important secretagogue in this system, the pathway coupling PACAP stimulation to chromaffin cell secretion is poorly understood. The goal of this study is to address this knowledge gap. Here, it is shown that PACAP activates a Gαs-coupled pathway that must signal through phospholipase C ε (PLCε) to drive Ca2+ entry and exocytosis. PACAP stimulation causes a complex pattern of Ca2+ signals in chromaffin cells, leading to a sustained secretory response that is kinetically distinct from the form stimulated by ACh. Exocytosis caused by PACAP is associated with slower release of peptide cargo than exocytosis stimulated by ACh. Importantly, only the secretory response to PACAP, not ACh, is eliminated in cells lacking PLCε expression. The data show that ACh and PACAP, acting through distinct signaling pathways, enable nuanced and variable secretory outputs from chromaffin cells.
MeSH term(s)	Pituitary Adenylate Cyclase-Activating Polypeptide/pharmacology ; Pituitary Adenylate Cyclase-Activating Polypeptide/metabolism ; Acetylcholine/pharmacology ; Acetylcholine/metabolism ; Calcium/metabolism ; Catecholamines/metabolism ; Chromaffin Cells/metabolism
Chemical Substances	Pituitary Adenylate Cyclase-Activating Polypeptide ; Acetylcholine (N9YNS0M02X) ; Calcium (SY7Q814VUP) ; Catecholamines
Language	English
Publishing date	2022-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3118-5
ISSN	1540-7748 ; 0022-1295
ISSN (online)	1540-7748
ISSN	0022-1295
DOI	10.1085/jgp.202213180
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