Non‐additive interaction between nicotinic cholinergic and P2X purine receptors in guinea‐pig enteric neurons in culture

Zhou, Xiaoping; Galligan, James J.

doi:10.1111/j.1469-7793.1998.685ba.x

Cited by 102 publications

(107 citation statements)

References 32 publications

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“…Studies have shown that there is a functional interaction between P2X and nicotinic acetylcholine receptors [68][69][70]. P2X receptors are co-expressed in at least 67% of b Left Depolarization to pressure application of DMPP (1 μM).…”

Section: Interactions Between P2x Receptors and Other Ligand-gated Iomentioning

confidence: 99%

Purinergic receptors and synaptic transmission in enteric neurons

Ren

Bertrand

2007

Purinergic Signalling

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Purines such as ATP and adenosine participate in synaptic transmission in the enteric nervous system as neurotransmitters or neuromodulators. Purinergic receptors are localized on the cell bodies or nerve terminals of different functional classes of enteric neurons and, with other receptors, form unique receptor complements. Activation of purinergic receptors can regulate neuronal activity by depolarization, by regulating intracellular calcium, or by modulating second messenger pathways. Purinergic signaling between enteric neurons plays an important role in regulating specific enteric reflexes and overall gastrointestinal function. In the present article, we review evidence for purine receptors in the enteric nervous system, including P1 (adenosine) receptors and P2 (ATP) receptors. We will explore the role they play in mediating fast and slow synaptic transmission and in presynaptic inhibition of transmission. Finally, we will examine the molecular properties of the native receptors, their signaling mechanisms, and their role in gastrointestinal pathology. Keywords

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Section: Interactions Between P2x Receptors and Other Ligand-gated Iomentioning

confidence: 99%

Purinergic receptors and synaptic transmission in enteric neurons

Ren

Bertrand

2007

Purinergic Signalling

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“…Functional cross-inhibition between receptors activated by ATP and either acetylcholine or GABA has been reported lately in neurons or transfected cells (21)(22)(23)(24)(25), and we recently demonstrated that a physical interaction between P2X and 5-HT 3 receptors leads to an activity-dependent cross inhibition between the two cationic channels (26). We decided to explore the possibility that ligandgated chloride channels may also interact with P2X ATP-gated channels through similar mechanisms.…”

mentioning

confidence: 99%

Cross-talk and Co-trafficking between ρ1/GABA Receptors and ATP-gated Channels

Boué‐Grabot

Émerit

Toulmé

et al. 2004

Journal of Biological Chemistry

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␥-Aminobutyric-acid (GABA) and ATP ionotropic receptors represent two structurally and functionally different classes of neurotransmitter-gated channels involved in fast synaptic transmission. We demonstrate here that, when the inhibitory 1/GABA and the excitatory P2X 2 receptor channels are co-expressed in Xenopus oocytes, activation of one channel reduces the currents mediated by the other one. This reciprocal inhibitory cross-talk is a receptor-mediated phenomenon independent of agonist cross-modulation, membrane potential, direction of ionic flux, or channel densities. Functional interaction is disrupted when the cytoplasmic C-terminal domain of P2X 2 is deleted or in competition experiments with minigenes coding for the Cterminal domain of P2X 2 or the main intracellular loop of 1 subunits. We also show a physical interaction between P2X 2 and 1 receptors expressed in oocytes and the co-clustering of these receptors in transfected hippocampal neurons. Co-expression with P2X 2 induces retargeting and recruitment of mainly intracellular 1/ GABA receptors to surface clusters. Therefore, molecular and functional cross-talk between inhibitory and excitatory ligand-gated channels may regulate synaptic strength both by activity-dependent current occlusion and synaptic receptors co-trafficking.Neuronal activity is regulated by a number of transmitters acting on different receptor types (1). Fast neurotransmission is achieved through different classes of transmitter-gated channels, including the P2X and nicotinic receptor superfamilies (1, 2). The family of P2X ATP-gated cation channels is composed of seven genes coding for subunits with two transmembrane domains, intracellular N and C termini, and a large extracellular loop (2). The nicotinic superfamily includes the GABA-gated 1 channels along with the acetylcholine, 5-HT 3 , and glycine receptors that share several structural features, including a large extracellular N-terminal domain, four hydrophobic transmembrane domains (M1-M4), and a long cytoplasmic loop connecting M3 and M4 (1). GABA receptor channels have been classified into two subtypes based on their pharmacological properties. GABA A receptors are inhibited by bicuculline, whereas GABA C receptors are insensitive to this antagonist (1). Diversity of GABA A receptors is achieved by pentameric assembly of multiple subunits, including ␣1-6, ␤1-3, ␥1-3, ␦, , and ⑀. GABA C receptors are composed of 1-3 subunits that can assemble into homo-oligomers (3, 4). Recent data suggest that a 1 subunit could co-assemble with a GABA A subunit (5, 6). Neuronal ATP and GABA C ionotropic receptors are involved in fast excitatory and inhibitory synaptic transmission, respectively, and display overlapping distribution in many regions of the nervous system, including DRG, dorsal horn of the spinal cord (7, 8), retina (9 -13), hippocampus (14 -15), cerebellum (14, 16), and anterior pituitary (17, 18).Recently, Jo and co-workers described ATP and GABA corelease from the same axon terminals into the dorsal horn of the spinal ...

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“…It is known that co-activation of nicotinic and P2X 2 purinergic receptors inhibits the functions of both ion channels through direct protein-protein interaction on the neuronal cell membrane (Nakazawa 1994;Barajas-Lopez et al 1998;Zhou and Galligan 1998;Khakh et al 2000Khakh et al , 2005. Similar interaction between nicotinic and purinergic receptors in rat urinary bladder smooth muscle has been recently described (Jenes et al 2012).…”

Section: Introductionmentioning

confidence: 82%

“…Previous experiments gave evidence on cholinergic and purinergic interaction between neuronal nicotinic and P2X 2 purinergic receptors in sympathetic ganglia (Nakazawa 1994), hippocampal neurons (Khakh et al 2005), and myenteric neurons (Barajas-Lopez et al 1998;Zhou and Galligan 1998;Brown and Galligan 2003). In these systems, co-application of a nicotinic and a purinergic agonist produced Figure 4.…”

Section: Cholinergic and Purinergic Receptor Activation Of Human Urinmentioning

confidence: 99%

Nicotine interferes with purinergic signaling in smooth muscle cells isolated from urinary bladders of patients with lower urinary tract symptoms

Jenes¹,

Szigeti²,

Ruzsnavszky³

et al. 2014

gpb

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Abstract. In patients with outlet obstruction, the contraction of the base is reduced compared to that of healthy individuals, while the contraction of the dome is not affected. Here, we investigated the cellular mechanisms that might be responsible for cholinergic effects blocking non-adrenergic non-cholinergic contractions in the base of the urinary bladder.Smooth muscle cells either from the base or from the dome of human urinary bladders were cultured to determine the contribution of cholinergic and purinergic mechanisms to their Ca 2+ homeostasis.While ATP evoked Ca 2+ transients in all the cells, nicotine and carbachol induced Ca 2+ transients only in 56% and 44% of the cells, respectively. When ATP was administered together with nicotine or carbachol, the amplitudes of the Ca 2+ transients recorded from cells prepared from the base of bladders were significantly smaller (42 ± 6% with nicotine and 56 ± 9% with carbachol) than those evoked by ATP alone. This inhibition was much less apparent in the dome of bladders.The inhibition between the cholinergic and purinergic signaling pathways reported in this work may decrease the strength of the contraction of the base of the urinary bladder in patients with outlet obstruction during voiding.

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Non‐additive interaction between nicotinic cholinergic and P2X purine receptors in guinea‐pig enteric neurons in culture

Cited by 102 publications

References 32 publications

Purinergic receptors and synaptic transmission in enteric neurons

Purinergic receptors and synaptic transmission in enteric neurons

Cross-talk and Co-trafficking between ρ1/GABA Receptors and ATP-gated Channels

Nicotine interferes with purinergic signaling in smooth muscle cells isolated from urinary bladders of patients with lower urinary tract symptoms

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