ArticleThe Journal of physiology1997
Tachykinin-induced activation of non-specific cation conductance via NK3 neurokinin receptors in guinea-pig intracardiac neurones.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 51 citations in OpenAlex.
- Comparative specialization of intrinsic cardiac neurons in humans, mice and pigs.The Journal of physiology · 2025Article
- Comparative specialization of intrinsic cardiac neurons in humans, mice, and pigs.bioRxiv : the preprint server for biology · 2024Article
- Distribution and morphology of calcitonin gene-related peptide and substance P immunoreactive axons in the whole-mount atria of mice.Autonomic neuroscience : basic & clinical · 2014Article
- The role of substance p in ischaemic brain injury.Brain sciences · 2013Article
- Blocking neurogenic inflammation for the treatment of acute disorders of the central nervous system.International journal of inflammation · 2013Article
- Differential activation of guinea pig intrinsic cardiac neurons by the PAC1 agonists maxadilan and pituitary adenylate cyclase-activating polypeptide 27 (PACAP27).The Journal of pharmacology and experimental therapeutics · 2009Article
- Enhancement of Ih, but not inhibition of IM, is a key mechanism underlying the PACAP-induced increase in excitability of guinea pig intrinsic cardiac neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2009Article
- Identification of intracellular signaling cascades mediating the PACAP-induced increase in guinea pig cardiac neuron excitability.Journal of molecular neuroscience : MN · 2008Article
- Neurally released pituitary adenylate cyclase-activating polypeptide enhances guinea pig intrinsic cardiac neurone excitability.The Journal of physiology · 2007Article
- Pituitary adenylate cyclase-activating polypeptide expression and modulation of neuronal excitability in guinea pig cardiac ganglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. Whole mount preparations from guinea-pig hearts were used to characterize the receptors and ionic mechanisms mediating the substance P (SP)-induced depolarization of parasympathetic postganglionic neurones of the cardiac ganglion. 2. Measurement of the amplitude of depolarization in response to superfusion of different tachykinin agonists (neurokinins A (NKA) and B (NKB), SP, and senktide) gave a rank-order potency of NKB = senktide > NKA > SP, indicating involvement of an NK3 receptor. The use of the selective tachykinin receptor antagonists SR 140333, SR 48986, and SR 142801 demonstrated that only the NK3 receptor antagonist SR 142801 inhibited the SP-induced depolarization. 3. The SP-induced depolarization was not inhibited by Ba2+, TEA, or niflumic acid, or altered by reduced Cl- solutions, but was attenuated in reduced Na+ solutions. Single electrode voltage clamp studies demonstrated that the SP-induced inward current increased in amplitude at more negative potentials, had a reversal potential of approximately 0 mV, and was reduced in amplitude in reduced Na+ solutions. 4. We conclude that the SP-induced depolarization in guinea-pig postganglionic parasympathetic neurones of the cardiac ganglion is due to NK3-mediated activation of a non-selective cation conductance.
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