This review is focused on purinergic neurotransmission, i.e., ATP released from nerves as a transmitter or cotransmitter to act as an extracellular signaling molecule on both pre- and postjunctional membranes at neuroeffector junctions and synapses, as well as acting as a trophic factor during development and regeneration. Emphasis is placed on the physiology and pathophysiology of ATP, but extracellular roles of its breakdown product, adenosine, are also considered because of their intimate interactions. The early history of the involvement of ATP in autonomic and skeletal neuromuscular transmission and in activities in the central nervous system and ganglia is reviewed. Brief background information is given about the identification of receptor subtypes for purines and pyrimidines and about ATP storage, release, and ectoenzymatic breakdown. Evidence that ATP is a cotransmitter in most, if not all, peripheral and central neurons is presented, as well as full accounts of neurotransmission and neuromodulation in autonomic and sensory ganglia and in the brain and spinal cord. There is coverage of neuron-glia interactions and of purinergic neuroeffector transmission to nonmuscular cells. To establish the primitive and widespread nature of purinergic neurotransmission, both the ontogeny and phylogeny of purinergic signaling are considered. Finally, the pathophysiology of purinergic neurotransmission in both peripheral and central nervous systems is reviewed, and speculations are made about future developments.

/pdf/physiology-and-pathophysiology-of-purinergic-1z94g2hz0f.pdf

Physiology and Pathophysiology of Purinergic Neurotransmission

Types of nerves in the enteric nervous system

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1476-5381.1965.tb02093.x

Observations on an isolated, innervated preparation of rat urinary bladder

1 High concentrations of adenosine 5'-triphosphate (ATP, 100 to 1000 micrometer) were required to cause contraction of the rat urinary bladder, while adenosine and adenosine 5'monophosphate (AMP, 1 to 50 micrometer) produced relaxation. 2 One hundred fold lower concentrations of beta-gamma-methylene ATP, which is resistant to degradation to AMP and adenosine, caused dose-dependent, phasic contractions which mimicked atropine-resistant responses to nerve stimulation. 3 Adenosine and AMP caused dose-dependent inhibition of carbachol-induced contractions; theophylline competitively antagonized this inhibition but not the contractile responses to beta-gamma-methylene ATP, ATP or atropine-resistant nerve stimulation. 4 These results suggest that the insensitivity of the rat bladder to ATP is due to its rapid degradation to AMP and adenosine and support the hypothesis that the bladder receives a purinergic excitatory innervation.

Effects of adenosine 5'-triphosphate (ATP) and beta-gamma-methylene ATP on the rat urinary bladder.

The effect of atropine on plasma gastrin response to feeding.

The well known fact that atropine susceptibility is not an infallible criterion of cholinergic transmission is discussed in some detail. Various examples of atropine-resistant nerve effects have been considered, and the following types of atropine-resistance can be distinguished:

1) Apparent resistance which is due to destruction of atropine in the animal. This occurs in a proportion of rabbits, in which atropinesterase is present in the blood and in some tissues. The effect of atropine is then very brief and may erroneously be thought to be absent.

2) Atropine-resistance in cholinergic neuro-effector systems, as for example in intestinal preparations from some species, and possibly in the bladder. In the intestine corroborative evidence provided by anticholinesterases and by botulinum toxin strongly suggests that the nerve endings concerned are cholinergic, and therefore supports the theory put forward by Dale and Gaddum that this type of atropine-resistance is due to "proximity" of the nerve endings to the effector cells. It is pointed out that the classification of intestinomotor drugs by means of atropine is influenced by these considerations.

3) The secondary formation of an atropine-resistant pharmacological agent, e.g., of bradykinin in the salivary glands. Acetylcholine or chorda stimulation lead to the extrusion of a proteolytic enzyme capable of forming bradykinin from serum proteins.

4) Atropine-resistance due to non-cholinergic transmission. Two examples of this are considered: (a) antidromic trigeminal pupillary constriction; and (b) antidromic vasodilatation in the rabbit's ear. Confirmatory evidence from other sources indicates the non-cholinergic nature of these effects.

5) Several nicotinic actions of acetylcholine are relatively resistant to atropine, but can nevertheless be blocked by the alkaloid in appropriate concentrations.

The use and limitations of atropine for pharmacological studies on autonomic effectors

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The use and limitations of atropine for pharmacological studies on autonomic effectors