The Significance of Brain Acetylcholine

1953 ◽  
Vol 99 (415) ◽  
pp. 247-251 ◽  
Author(s):  
J. Crossland

Until a few years ago there existed a sharp dichotomy of opinion between the pharmacologists, who, on the basis of their experiments, assigned to acetylcholine the role of universal synaptic transmitter, and the electrophysiologists, who denied that this substance could effect the transfer of excitation from one conducting element to another. It is, however, now generally agreed that, certainly at the neuromuscular junction, and probably also at ganglionic and some—but not all—central synapses, acetylcholine does indeed exert a primary transmitter action. It must be added that recognition of this fundamental action has been hastened as a result of recent experiments by those very electrophysiologists (such as Eccles and his colleagues) who previously supported exclusively electrical hypotheses of nervous transmission. For this reason the assumption which is implicit throughout this paper that the acetylcholine in brain is concerned in maintaining central synaptic transmission is likely to go unchallenged and requires no detailed justification here.

1976 ◽  
Vol 4 (3) ◽  
pp. 199-202 ◽  
Author(s):  
T. A. Torda ◽  
P. W. Gage

Thiopentone and pentobarbitone reduce the time constant of decay of miniature end-plate currents when applied in anaesthetic concentrations to the neuromuscular junction. Such an effect at central synapses would lead to failure of synaptic transmission in the central nervous system and may reflect a common mode of action of many anaesthetic drugs.


Synapse ◽  
2017 ◽  
Vol 71 (5) ◽  
pp. e21964 ◽  
Author(s):  
Filippo Weisz ◽  
Sonia Piccinin ◽  
Dalila Mango ◽  
Richard Teke Ngomba ◽  
Nicola B. Mercuri ◽  
...  

Synapse ◽  
2005 ◽  
Vol 58 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Maksim V. Storozhuk ◽  
Svetlana Y. Ivanova ◽  
Pavel M. Balaban ◽  
Platon G. Kostyuk

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Xinyan Gao ◽  
Yongfa Qiao ◽  
Baohui Jia ◽  
Xianghong Jing ◽  
Bin Cheng ◽  
...  

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.


2013 ◽  
Vol 49 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Hiroshi Nishimune ◽  
John A. Stanford ◽  
Yasuo Mori

Cell Calcium ◽  
2021 ◽  
pp. 102420
Author(s):  
Filip de Souza Polli ◽  
Vincenzo Roncace ◽  
Anton Maximov
Keyword(s):  

1971 ◽  
Vol 177 (1049) ◽  
pp. 509-539 ◽  

Synaptic transmission has been analysed in parasympathetic nerve cells that lie in the transparent interatrial septum of the heart of the frog. Using Nomarski interference optics, one can see much cellular detail, including synaptic boutons in living preparations. 1. On each ganglion cell, the 10 to 20 synaptic boutons are usually derived from a single vagal nerve fibre. These fibres branch extensively to innervate a number of septal ganglion cells. 2. The chemical transmitter, acetylcholine (ACh), liberated by a presynaptic impulse survives for up to 40 ms, setting up an excitatory postsynaptic potential (e.p.s.p.) which triggers one and sometimes two action potentials in the postsynaptic cell. The e.p.s.p. is made up of quantal components, as at the neuromuscular junction. 3. Nerve-evoked e.p.s.p.s can be well matched in amplitude and time course by iontophoretic application of ACh to selected areas of the neuronal membrane. In particular, the miniature e.p.s.p., which is due to the focal release of a small quantity of transmitter, was accurately mimicked by iontophoretic application of ACh. By grading the amount of ACh released from an electrode one could also duplicate the wide variety of nerve-evoked postsynaptic discharges of ganglion cells. 4. The permeability changes initiated in the postsynaptic membrane by applied ACh and the synaptic transmitter appear identical, since the ionic fluxes for both responses have the same equilibrium potential. Also, the receptors which react with the synaptic transmitter are desensitized by applied ACh. 5. Cholinesterase inhibitors (Tensilon and Eserine) have a variable action on different cells, with respect both to nerve-evoked and Ach evoked potentials. The reasons for this variation are unclear, and need further study. 6. Miniature e.p.s.p.s resemble analogous potentials at nerve-muscle junctions and other synapses. A significant proportion of the min e.p.s.p.s is released as multiple units. This proportion is increased in high Ca2+, while single units alone occur in a low Ca2+-high Mg2+ environment. 7. The experiments provide information about the release of ACh from nerve terminals and its action on the postsynaptic membrane of neurons. They are in good agreement with analogous studies on skeletal neuromuscular junctions


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