Review lecture. Neurotransmitters and trophic factors in the autonomic nervous system.

Burnstock, Geoffrey

doi:10.1113/jphysiol.1981.sp013648

Cited by 372 publications

(149 citation statements)

References 153 publications

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“…The classical view of autonomic innervation is that the junction between nerve terminals and smooth and cardiac muscle is not a well defined structure (Burnstock, 1981). Instead some investigators have suggested that transmitter is released en passage as action potentials conduct down axons, and innervation is defined by the volume through which a transmitter can diffuse and still reach postjunctional receptors at an effective concentration.…”

Section: Discussionmentioning

confidence: 99%

“…With the present study we have provided morphological and functional data supporting the hypothesis that cholinergic neurotransmission depends to a significant degree on synaptic junctions between motor neurons and specific classes of ICC in gastrointestinal muscles. Cholinergic neuromuscular transmission in autonomically innervated muscles, such as the GI tract, has been thought to occur via release of ACh, diffusion of the transmitter through a loosely defined postjunctional volume, and binding and activation of muscarinic receptors expressed by smooth muscle cells (Burnstock, 1981). The postjunctional responses (EJPs) elicited in smooth muscle cells exposed to sufficient amounts of ACh were thought to elicit depolarization responses in neighboring, possibly noninnervated, smooth muscle cells via gap junctions.…”

Section: Discussionmentioning

confidence: 99%

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Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

et al. 2000

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Interstitial cells of Cajal (ICC) are interposed between enteric neurons and smooth muscle cells in gastrointestinal muscles. The role of intramuscular ICC (IC-IM) in mediating enteric excitatory neural inputs was studied using gastric fundus muscles of wild-type animals and W/W v mutant mice, which lack IC-IM. Excitatory motor neurons, labeled with antibodies to vesicular acetylcholine transporter or substance-P, were closely associated with IC-IM. Immunocytochemistry showed close contacts between enteric neurons and IC-IM. IC-IM also formed gap junctions with smooth muscle cells. Electrical field stimulation yielded fast excitatory junction potentials in the smooth muscle that were blocked by atropine. Neural responses were greatly reduced in muscles of W/W v animals. Loss of cholinergic responses in W/W v muscles seemed to be caused by the loss of close synaptic contacts between motor neurons and IC-IM, because these muscles were not less responsive to exogenous acetylcholine than were wild-type muscles. W/W v muscles also responded to excitatory nerve stimulation when the breakdown of acetylcholine was blocked by neostigmine. The density of cholinergic nerve bundles within the muscles was not significantly different in wild-type and W/W v muscles, and similar amounts of 14 [C]choline were released from preloaded wildtype and W/W v muscles in response to nerve stimulation. The impact of losing IC-IM on gastric compliance was also evaluated in intact stomachs. Pressure increased as a function of fluid volume and infusion rate in wild-type animals, but W/W v animals showed little basal tone and minimal increases in pressure with fluid infusions. These data suggest that IC-IM play a major role in receiving cholinergic excitatory inputs from the enteric nervous system in the murine fundus.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

et al. 2000

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“…In particular adenosine 5'-triphodifferent regions of the intestine (Costa et al, 1986; Manzini et sphate (ATP) (Burnstock et al, 1970;Burnstock, 1981;, and that different mechanisms regulate the release of Vladimirova & Shuba, 1984;Zagorodnyuk & Shuba, 1986; different NANC inhibitory transmitters (Zagorodnyuk & Crist et al, 1992). Vasoactive intestinal peptide (VIP) (Grider Maggi, 1994;Bridgewater et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

The possible role of ATP and PACAP as mediators of apamin‐sensitive NANC inhibitory junction potentials in circular muscle of guinea‐pig colon

Zagorodnyuk

Santicioli

Maggi

et al. 1996

British J Pharmacology

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Bogomoletz Institute of Physiology, Kiev, Ukraine 1 In the presence of atropine (1 gM), guanethidine (3 gM), indomethacin (3 Mm), nifedipine (1 MM), Lnitroarginine (L-NOARG, 100 pM), and the selective tachykinin NK, and NK2 receptor antagonists, SR 140,333 and GR 94,800, respectively (0.1 gM each), a single pulse of electrical field stimulation (EFS) produced a monophasic non-adrenergic non-cholinergic (NANC) inhibitory junction potential (ij.p., about 10 mV in amplitude) in the circular muscle of guinea-pig proximal colon, recorded by the modified single sucrose gap technique.2 The P2 purinoceptor agonist, a,# methylene ATP (cz,1 mATP, 100 gM) and the pituitary adenylyl cyclase activating peptide (PACAP, 1 gM) both produced hyperpolarization (11 + 0.8 mV, n = 14 and 10.2+0.8 mV, n= 19, respectively) and relaxation (1.1+0.2 mV, n= 14 and 1.5+0.2 mN, n= 19, respectively) of the circular muscle.3 Apamin (0.1 Mm) nearly abolished (about 90% inhibition) the NANC i.j.p. and the a,f3 mATPinduced hyperpolarization, markedly reduced the a,,B mATP-induced relaxation (73% inhibition) and the PACAP-induced hyperpolarization (65% inhibition), while the PACAP-induced relaxation was unaffected. 4 Tetraethylammonium (TEA, 10 mM) increased the EFS-evoked ij.p. and revealed an excitatory junction potential (ej.p.). In the presence of TEA, o,fl mATP induced a biphasic response: transient depolarization and contraction followed by hyperpolarization and relaxation. The hyperpolarization to PACAP was reduced by TEA (45% inhibition) but the relaxation was unaffected. 5 The combined application of apamin (0.1 Mm) and TEA (10 mM) abolished the ij.p. and single pulse EFS evoked a pure ej.p. with latency three times longer than that of the ij.p. In the majority of strips tested, a,,B mATP and PACAP elicited a biphasic response : depolarization and small contraction followed by hyperpolarization and relaxation. 6 The P2 purinoceptor antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) inhibited the NANC ij.p. in concentration-dependent manner and inhibited the a,f mATP-induced hyperpolarization and relaxation, without affecting the hyperpolarization and relaxation induced by PACAP. On the other hand, the P2 purinoceptor antagonist, suramin (100 gM) inhibited to a similar extent (60-80%) the NANC ij.p. and the hyperpolarization and relaxation induced by ci,fl mATP or PACAP. 7 PPADS and suramin reduced the NANC ej.p. evoked by a single pulse EFS in the presence of apamin and TEA (100 Mm of PPADS and 300 gM of suramin inhibited the ej.p. by about 40%).8 We conclude that ATP, but not PACAP, mediates the apamin-sensitive NANC ij.p. in the circular muscle of the guinea-pig colon. After blockade of the NANC ij.p., ATP may act as an excitatory transmitter by activating excitatory P2 purinoceptors. The subtypes of P2 purinoceptor involved in the inhibitory and excitatory responses remain to be established. The data suggest that excitatory P2 purinoceptors may be located extrajunctionally.

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“…However, the exact nature of the inhibitory neurotransmitter released by inhibitory NANC neurones still remains controversial. Depending on the tissue and/or species studied, mainly vasoactive intestinal polypeptide (VIP) (Goyal & Rattan, 1980;Grider et al, 1985) or adenosine 5'-triphosphate (ATP) (Burnstock, 1972;1981) have been suggested as the putative NANC neurotransmitter. Previously, we demonstrated the presence of an inhibitory NANC innervation in the canine terminal ileum and ileocolonic junction; stimulation of NANC neurones either by electrical impulses or by nicotinic receptor stimulation resulted in relaxations resistant to adrenoceptor and cholinoceptor blockade (Pelckmans et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Evidence for nitric oxide as mediator of non‐adrenergic, non‐cholinergic relaxations induced by ATP and GABA in the canine gut

Boeckxstaens

Pelckmans

Bult

et al. 1991

British J Pharmacology

120

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Review lecture. Neurotransmitters and trophic factors in the autonomic nervous system.

Cited by 372 publications

References 153 publications

Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

The possible role of ATP and PACAP as mediators of apamin‐sensitive NANC inhibitory junction potentials in circular muscle of guinea‐pig colon

Evidence for nitric oxide as mediator of non‐adrenergic, non‐cholinergic relaxations induced by ATP and GABA in the canine gut

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