Ultrastructural analysis of choline acetyltransferase-immunoreactive sympathetic preganglionic neurons and their dendritic bundles in rat thoracic spinal cord

Synapse ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 299-312 ◽  
Author(s):  
Jeffrey A. Markham ◽  
James E. Vaughn
1995 ◽  
Vol 354 (2) ◽  
pp. 193-208 ◽  
Author(s):  
Ida J. Llewellyn-Smith ◽  
Paul Pilowsky ◽  
Jane B. Minson ◽  
John Chalmers

1992 ◽  
Vol 70 (S1) ◽  
pp. S92-S97 ◽  
Author(s):  
Hiroe Inokuchi ◽  
Megumu Yoshimura ◽  
Canio Polosa ◽  
Syogoro Nishi

Intracellular recordings were made from 168 sympathetic preganglionic neurons in the slice of the second or third thoracic spinal-cord segment of the adult cat to study the actions of noradrenaline on these neurons. Noradrenaline, applied by superfusion (0.5–50 μM), produced membrane depolarization in 73 neurons and membrane hyperpolarization in 39 neurons. In 26 neurons noradrenaline produced a biphasic response (depolarization–hyperpolarization or vice versa). The depolarization was blocked by prazosin, while the hyperpolarization was blocked by yohimbine. The noradrenaline-induced depolarization was associated with an increase in neuron input resistance, while the noradrenaline-induced hyperpolarization was associated with a decrease in neuron input resistance. Both responses decreased in amplitude with membrane hyperpolarization and were nullified at around the potassium equilibrium potential EK. The null potential of both responses became more and less negative with a decrease and an increase, respectively, in the extracellular potassium concentration. When the membrane potential was made more negative than EK, the noradrenaline-induced hyperpolarization reversed to depolarization in all cases, whereas in only 4 of 12 cases did the noradrenaline-induced depolarization reverse to hyperpolarization. These data suggest that the noradrenaline-induced depolarization is a result of a decrease, while the noradrenaline-induced hyperpolarization is a result of an increase in K+ conductance. Cobalt (2 mM), low calcium – high magnesium, and intracellular EGTA markedly reduced or abolished the noradrenaline-induced depolarization but had no significant effect on the noradrenaline-induced hyperpolarization. Barium (2 mM) depressed both responses. Tetraethylammonium (10–30 mM), 4-aminopyridine (3 mM), and cesium (2 mM) had no effect on either response. These data suggest that the noradrenaline-induced depolarization is a result of an inactivation of a background calcium-sensitive K+ conductance, while the noradrenaline-induced hyperpolarization is due to activation of a calcium-insensitive potassium conductance.Key words: K+ conductances, catecholamines, Ca2+ dependent, K+ current, spinal cord.


1992 ◽  
Vol 581 (1) ◽  
pp. 67-80 ◽  
Author(s):  
I.J. Llewellyn-Smith ◽  
K.D. Phend ◽  
J.B. Minson ◽  
P.M. Pilowsky ◽  
J.P. Chalmers

1967 ◽  
Vol 45 (6) ◽  
pp. 1033-1045 ◽  
Author(s):  
Canio Polosa

The behavior of single sympathetic preganglionic neurons, during and after repetitive antidromic driving, was studied with extracellular microelectrodes in the cat's spinal cord. It was found that repetitive antidromic excitation of spontaneously active units could produce a subsequent, long-lasting inactivity or "silent period". A similar silent period could be produced by antidromic excitation of units in the acutely isolated and deafferentated, upper thoracic, spinal cord. It occurred whenever the neuron soma had been involved in high-frequency activity. It is concluded that the silent period of sympathetic preganglionic neurons is generated in the spinal cord and is due to accumulation of post-activation depression by the cell bodies of the affected units.


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