ArticleBrain research2008
ATP facilitates glutamatergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus.
Article in Brain research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Neural Control of Tissue Perfusion: Emerging Evidence and Beyond.Current hypertension reports · 2026Review
- Evidence that BDNF regulates heart rate by a mechanism involving increased brainstem parasympathetic neuron excitability.Journal of neurochemistry · 2014Article
- Glutamate transporter type 3 knockout leads to decreased heart rate possibly via parasympathetic mechanism.Transgenic research · 2013Article
- Purinergic P2X receptors facilitate inhibitory GABAergic and glycinergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus.Brain research · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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.
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