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ATP facilitates glutamatergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus.
Brain Res 2008; 1201:88-92BR

Abstract

Recent work has shown that adenosine 5'-triphosphate (ATP) plays an important role in modulating the activity of parasympathetic cardiac vagal neurons that dominate the neural control of heart rate. This study examined the mechanisms by which activation of ATP receptors modulates excitatory neurotransmission to cardiac vagal neurons. Glutamatergic activity to cardiac vagal neurons was isolated and examined using whole-cell patch-clamp recordings in an in vitro brain slice preparation in rats. ATP (100 microM) evoked increases in the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) in cardiac vagal neurons which were blocked by the broad P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 100 microM). Application of the selective P2X receptor agonist, alpha, beta-methylene ATP (100 microM), also increased glutamatergic mEPSCs neurotransmission to cardiac vagal neurons indicating P2X receptors enhance glutamatergic release to cardiac vagal neurons. The evoked increase in glutamatergic mEPSC was unaltered by the voltage-gated calcium channel blocker cadmium, and was abolished by the selective P2X receptor antagonist 2',3'-O-(2,4,6-Trinitrophenyl) adenosine 5'-triphosphate, TNP-ATP (100 microM). This work demonstrates that the ATP evoked facilitation of excitatory neurotransmission to cardiac vagal neurons is dependent upon activation of P2X receptors on glutamatergic presynaptic terminals.

Authors+Show Affiliations

Department of Pharmacology and Physiology, The George Washington University, 2300 Eye Street NW, Washington, DC 20037, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18295749

Citation

Jameson, Heather S., et al. "ATP Facilitates Glutamatergic Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus." Brain Research, vol. 1201, 2008, pp. 88-92.
Jameson HS, Pinol RA, Kamendi H, et al. ATP facilitates glutamatergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus. Brain Res. 2008;1201:88-92.
Jameson, H. S., Pinol, R. A., Kamendi, H., & Mendelowitz, D. (2008). ATP facilitates glutamatergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus. Brain Research, 1201, pp. 88-92. doi:10.1016/j.brainres.2008.01.065.
Jameson HS, et al. ATP Facilitates Glutamatergic Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus. Brain Res. 2008 Mar 27;1201:88-92. PubMed PMID: 18295749.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ATP facilitates glutamatergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus. AU - Jameson,Heather S, AU - Pinol,Ramon A, AU - Kamendi,Harriet, AU - Mendelowitz,David, Y1 - 2008/02/06/ PY - 2007/12/12/received PY - 2008/01/16/revised PY - 2008/01/21/accepted PY - 2008/2/26/pubmed PY - 2008/7/29/medline PY - 2008/2/26/entrez SP - 88 EP - 92 JF - Brain research JO - Brain Res. VL - 1201 N2 - Recent work has shown that adenosine 5'-triphosphate (ATP) plays an important role in modulating the activity of parasympathetic cardiac vagal neurons that dominate the neural control of heart rate. This study examined the mechanisms by which activation of ATP receptors modulates excitatory neurotransmission to cardiac vagal neurons. Glutamatergic activity to cardiac vagal neurons was isolated and examined using whole-cell patch-clamp recordings in an in vitro brain slice preparation in rats. ATP (100 microM) evoked increases in the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) in cardiac vagal neurons which were blocked by the broad P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 100 microM). Application of the selective P2X receptor agonist, alpha, beta-methylene ATP (100 microM), also increased glutamatergic mEPSCs neurotransmission to cardiac vagal neurons indicating P2X receptors enhance glutamatergic release to cardiac vagal neurons. The evoked increase in glutamatergic mEPSC was unaltered by the voltage-gated calcium channel blocker cadmium, and was abolished by the selective P2X receptor antagonist 2',3'-O-(2,4,6-Trinitrophenyl) adenosine 5'-triphosphate, TNP-ATP (100 microM). This work demonstrates that the ATP evoked facilitation of excitatory neurotransmission to cardiac vagal neurons is dependent upon activation of P2X receptors on glutamatergic presynaptic terminals. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/18295749/ATP_facilitates_glutamatergic_neurotransmission_to_cardiac_vagal_neurons_in_the_nucleus_ambiguus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)00239-4 DB - PRIME DP - Unbound Medicine ER -