Expression and physiological actions of neuropeptide Y in guinea pig parasympathetic cardiac ganglia

Kennedy, Audra L.; Harakall, Susan A.; Lynch, Sarah; Braas, Karen M.; Hardwick, Jean C.; Mawe, Gary M.; Parsons, Rodney L.

doi:10.1016/s0165-1838(98)00072-1

Cited by 29 publications

(31 citation statements)

References 19 publications

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“…Previous studies of the intrinsic cardiac plexus have shown evidence for adrenergic regulation of intracardiac neurons (5,26,38,41). Norepinephrine directly affected ϳ70% of guinea pig intrinsic neurons.…”

Section: R1396 Adrenergic Muscarinic and Ang II Modulation Of Intramentioning

confidence: 80%

“…Previous studies have shown that intracardiac neurons possess receptors for a variety of putative neuromodulators, including muscarinic receptors (7,24,38), adrenergic receptors (22,33), neuropeptides (11,17), and locally produced chemicals (34). Studies on the direct interactions between the sympathetic and parasympathetic neurons in this plexus are few (26), although the importance of this balance is integral to the normal function of the organism. For example, surgical disruption of the right atrial ganglionated plexus in dogs prevents parasympathetically mediated bradycardia, while maintaining parasympathetically induced suppression of sympathetic inputs modulating chronotropic function (30,35).…”

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Angiotensin II potentiates adrenergic and muscarinic modulation of guinea pig intracardiac neurons

Girasole

Palmer

Corrado

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Girasole AE, Palmer CP, Corrado SL, Southerland EM, Ardell JL, Hardwick JC. Angiotensin II potentiates adrenergic and muscarinic modulation of guinea pig intracardiac neurons. Am J Physiol Regul Integr Comp Physiol 301: R1391-R1399, 2011. First published August 24, 2011 doi:10.1152/ajpregu.00145.2011The intrinsic cardiac plexus represents a major peripheral integration site for neuronal, hormonal, and locally produced neuromodulators controlling efferent neuronal output to the heart. This study examined the interdependence of norepinephrine, muscarinic agonists, and ANG II, to modulate intrinsic cardiac neuronal activity. Intracellular voltage recordings from whole-mount preparations of the guinea pig cardiac plexus were used to determine changes in active and passive electrical properties of individual intrinsic cardiac neurons. Application of either adrenergic or muscarinic agonists induced changes in neuronal resting membrane potentials, decreased afterhyperpolarization duration of single action potentials, and increased neuronal excitability. Adrenergic responses were inhibited by removal of extracellular calcium ions, while muscarinic responses were inhibited by application of TEA. The adrenergic responses were heterogeneous, responding to a variety of receptor-specific agonists (phenylephrine, clonidine, dobutamine, and terbutaline), although ␣-receptor agonists produced the most frequent responses. Application of ANG II alone produced a significant increase in excitability, while application of ANG II in combination with either adrenergic or muscarinic agonists produced a much larger potentiation of excitability. The ANG IIinduced modulation of firing was blocked by the angiotensin type 2 (AT 2) receptor inhibitor PD 123319 and was mimicked by the AT2 receptor agonist CGP-42112A. AT1 receptor blockade with telmasartin did not alter neuronal responses to ANG II. These data demonstrate that ANG II potentiates both muscarinically and adrenergically mediated activation of intrinsic cardiac neurons, doing so primarily via AT2 receptor-dependent mechanisms. These neurohumoral interactions may be fundamental to regulation of neuronal excitability within the intrinsic cardiac nervous system.

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Section: R1396 Adrenergic Muscarinic and Ang II Modulation Of Intramentioning

confidence: 80%

mentioning

confidence: 99%

Angiotensin II potentiates adrenergic and muscarinic modulation of guinea pig intracardiac neurons

Girasole

Palmer

Corrado

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The number of cardiac neurons in each preparation was determined by counting ChAT-IR or PGP-9.5-IR cells (Mawe et al, 1996;Braas et al, 1998;Kennedy et al, 1998;Lynch et al, 1999;Calupca et al, 2000;Braas et al, 2004,Parsons et al, 2006. PGP-95-IR neurons) X 100 = %].…”

Section: Quantification Of Peptide-ir Cardiac Neuronsmentioning

confidence: 99%

Regulation of neuronal pituitary adenylate cyclase-activating polypeptide expression during culture of guinea-pig cardiac ganglia

et al. 2007

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The trophic neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) increases in many different neuron types following injury; a response postulated to support cell survival and regeneration. In acutely isolated cardiac ganglia, approximately 1% of the cardiac neurons exhibited PACAP immunoreactivity whereas after 72 hours in culture, ~25% of the neurons were PACAP immunoreactive. In contrast, there was no increase in vasoactive intestinal polypeptide (VIP)-immunoreactive (IR) cells. Using a combination of immunocytochemical and molecular techniques, we have quantified PACAP expression, during explant culture of guinea pig cardiac ganglia. Using real time PCR, PACAP transcript levels increased progressively up to 48 hours in culture with no further increase after 72 hours. PACAP transcript levels were reduced by neurturin at 48 hours in culture but not after 24 or 72 hours in culture. In addition, neurturin partially suppressed the percentage of PACAP-IR neurons after 72 hours in culture, an effect mediated by activation of the phosphatidylinositol 3-kinase and mitogen activated protein kinase signaling pathways. The addition of different known regulatory molecules, including CNTF, Il-1β, TNFα, bFGF, TGF βand NGF did not increase the percentage of PACAP-IR neurons after 24 hours in culture; a result indicating that the generation and secretion of these factors did not stimulate PACAP expression. The presence of 20 nM PACAP or 10 μM forskolin increased the percentage of PACAP-IR cardiac neurons in 24 hour cultures, but not in 72 hour cultures. Neither treatment enhanced the number of VIP-IR neurons. The addition of the PAC 1 receptor antagonist, M65 (100 nM) suppressed the 20 nM PACAP-induced increase in percentage of PACAP-IR cells in 24 hour cultures indicating the effect of PACAP was mediated through the PAC 1 receptor. However, 100 nM M65 had no effect on the percentage of PACAP-IR cells in either 24 or 48 hour cultures not treated with exogenous PACAP, suggesting that endogenous release of PACAP likely did not contribute to the enhanced peptide expression. We postulate that the enhanced PACAP expression, which occurs in response to injury is facilitated in the explant cultured cardiac ganglia by the loss of a target-derived inhibitory factor, very likely neurturin. In intact tissues the presence of neurturin would normally suppress PACAP expression. Lastly, our results indicate that many common trophic factors do not enhance PACAP expression in the cultured cardiac neurons. However, the stimulatory role of an, as yet, unidentified factor can not be excluded. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content...

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“…Both SP and PACAP depolarize guinea pig cardiac neurons (Konishi et al, 1985;Hardwick et al, 1995Hardwick et al, , 1997Braas et al, 1998). The SP-induced depolarization of guinea pig intracardiac neurons is mediated by activation of an NK 3 tachykinin receptor coupled to a nonselective cationic conductance (Hardwick et al, 1997).…”

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TRPC6 immunoreactivity is colocalized with neuronal nitric oxide synthase in extrinsic fibers innervating guinea pig intrinsic cardiac ganglia

Calupca

Locknar

Parsons

2002

J of Comparative Neurology

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Tachykinins depolarize guinea pig intracardiac neurons by activating nonselective cationic channels. Recently, members of the transient receptor potential family of membrane channels (TRPC) have been implicated in the generation of G protein-coupled receptor-activated nonselective cationic currents. We have investigated whether guinea pig cardiac neurons exhibit immunoreactivity to TRPC. Our results showed that nerve fibers within guinea pig intrinsic cardiac ganglia exhibited immunoreactivity to TRPC6. After culture of cardiac ganglia whole-mount explants for 72 hours, the TRPC6-IR fiber networks were absent. Therefore, the TRPC6-IR fibers were derived from sources extrinsic to the heart. A small percentage ( approximately 3%) of intracardiac neurons also exhibited TRPC6 immunoreactivity in control preparations, and the percentage of cells exhibiting TRPC6 immunoreactivity was not changed following explant culture for 72 hours. The few intrinsic TRPC6-IR neurons also exhibited nitric oxide synthase (NOS) immunoreactivity, indicating that they were nitrergic as well. We compared the immunohistochemical staining patterns of TRPC6-IR fibers with the staining patterns of a number of other neurotransmitters or neurotransmitter synthetic enzymes that mark specific extrinsic inputs to the intrinsic cardiac ganglia. The TRPC6-IR fibers were not immunoreactive for choline acetyltransferase, tyrosine hydroxylase, or substance P. However, the TRPC6-IR fibers exhibited immunoreactivity to neuronal NOS. Therefore, we propose that the TRPC6-IR fibers within the guinea pig intrinsic cardiac ganglia are vagal sensory fibers that also contain NOS. We found, in support of this conclusion, that TRPC6-IR cells were also present in sections of nodose ganglia.

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Expression and physiological actions of neuropeptide Y in guinea pig parasympathetic cardiac ganglia

Cited by 29 publications

References 19 publications

Angiotensin II potentiates adrenergic and muscarinic modulation of guinea pig intracardiac neurons

Angiotensin II potentiates adrenergic and muscarinic modulation of guinea pig intracardiac neurons

Regulation of neuronal pituitary adenylate cyclase-activating polypeptide expression during culture of guinea-pig cardiac ganglia

TRPC6 immunoreactivity is colocalized with neuronal nitric oxide synthase in extrinsic fibers innervating guinea pig intrinsic cardiac ganglia

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