Properties of the slow excitatory postsynaptic potential in mammalian sympathetic ganglion cells

1982 ◽  
Vol 13 (4) ◽  
pp. 278-284
Author(s):  
A Ya Ivanov ◽  
V. I. Skok
2004 ◽  
Vol 21 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Jozsef Vigh ◽  
Paul Witkovsky

We obtained intracellular recordings from transient, On–Off amacrine and ganglion cells of the turtle retina. We tested the ability of neurotransmitter agonists and antagonists to modify the responses to light stimuli. The metabotropic glutamate agonist, 2-amino-phosphonobutyric acid (APB), selectively blocked On responses, whereas the amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) receptor antagonist, GYKI, blocked both On and Off responses. Although GYKI appeared to block excitation completely, suggesting an absence of N-methyl-d-aspartate (NMDA)-mediated responses, it was found that in the presence of ionotropic gamma-aminobutyric acid (GABA) blockers, the excitatory postsynaptic potential (EPSP) was prolonged. The late component of the EPSP was blocked by the NMDA antagonist, D-2-amino-5-phosphopentanoic acid (D-AP5). Picrotoxin (PTX) and bicuculline (BCC) induced a mean hyperpolarization of −6.4 mV, suggesting a direct effect of GABA on transient amacrine and ganglion cells, since antagonism of a GABA-mediated inhibition of release of glutamate by bipolars would depolarize third-order neurons. The acetylcholine agonist, carbachol, or the nicotinic agonist, epibatidine, depolarized all On–Off neurons. This action was blocked by d-tubocurarine. Cholinergic inputs to On–Off neurons increase their excitability without altering the pattern of light responsiveness.


Author(s):  
J. Quatacker ◽  
W. De Potter

Mucopolysaccharides have been demonstrated biochemically in catecholamine-containing subcellular particles in different rat, cat and ox tissues. As catecholamine-containing granules seem to arise from the Golgi apparatus and some also from the axoplasmic reticulum we examined wether carbohydrate macromolecules could be detected in the small and large dense core vesicles and in structures related to them. To this purpose superior cervical ganglia and irises from rabbit and cat and coeliac ganglia and their axons from dog were subjected to the chromaffin reaction to show the distribution of catecholamine-containing granules. Some material was also embedded in glycolmethacrylate (GMA) and stained with phosphotungstic acid (PTA) at low pH for the detection of carbohydrate macromolecules.The chromaffin reaction in the perikarya reveals mainly large dense core vesicles, but in the axon hillock, the axons and the terminals, the small dense core vesicles are more prominent. In the axons the small granules are sometimes seen inside a reticular network (fig. 1).


2002 ◽  
Vol 99 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Kengo Funakoshi ◽  
Yoshitoshi Atobe ◽  
Tatsuya Hisajima ◽  
Masato Nakano ◽  
Tetsuo Kadota ◽  
...  

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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