Synaptic Mechanisms for Long-Term Potentiation in Sympathetic Ganglia

1987 ◽  
pp. 211-224
Author(s):  
Donald A. McAfee ◽  
Clark A. Briggs ◽  
Richard E. McCaman ◽  
David G. McKenna
Keyword(s):  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Term Potentiation ◽  
Synaptic Mechanisms

Temporally distinct pre- and post-synaptic mechanisms maintain long-term potentiation

Nature ◽  
1989 ◽  
Vol 338 (6215) ◽  
pp. 500-503 ◽  
Author(s):  
Stephen N. Davies ◽  
Robin A. J. Lester ◽  
Klaus G. Reymann ◽  
Graham L. Collingridge
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation ◽  
Synaptic Mechanisms

Synaptic plasticity in sympathetic ganglia from acquired and inherited forms of ouabain-dependent hypertension

2001 ◽  
Vol 281 (2) ◽  
pp. R635-R644 ◽  
Author(s):  
Azeez A. Aileru ◽  
Aline De Albuquerque ◽  
John M. Hamlyn ◽  
Paolo Manunta ◽  
Jui R. Shah ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Neurons ◽  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Term Potentiation ◽  
Compound Action Potentials ◽  
Cervical Ganglia

Altered sympathetic nervous system activity has been implicated often in hypertension. We examined short-term potentiation [posttetanic potentiation (PTP)] and long-term potentiation (LTP) in the isolated superior cervical ganglia (SCG) from Sprague-Dawley (SD) rats given vehicle, digoxin, or ouabain by subcutaneous implants as well as in animals with ouabain-induced hypertension (OHR), and inbred Baltimore ouabain-resistant (BOR) and Baltimore ouabain-sensitive (BOS) strains of rats. Postganglionic compound action potentials (CAP) were used to determine PTP and LTP following a tetanic stimulus (20 Hz, 20 s). Baseline CAP magnitude was greater in ganglia from OHR than in vehicle-treated SD rats before tetanus, but the decay time constant of PTP was significantly decreased in OHR and in rats infused with digoxin that were normotensive. In hypertensive BOS and OHR, the time constants for the decay of both PTP and LTP ( t L) were increased and correlated with blood pressure (slope = 0.15 min/mmHg, r = 0.52, P < 0.047 and 6.7 min/mmHg, r = 0.906, P < 0.0001, respectively). In BOS and OHR, t L (minutes) was 492 ± 40 ( n = 7) and 539 ± 41 ( n = 5), respectively, and differed ( P < 0.05) from BOR (257 ± 48, n = 4), SD vehicle rats (240 ± 18, n = 4), and captopril-treated OHR (370 ± 52, n = 5). After the tetanus, the CAP at 90 min in BOS and OHR SCG declined less rapidly vs. SD vehicle rats or BOR. Captopril normalized blood pressure and t L in OHR. We conclude that the duration of ganglionic LTP and blood pressure are tightly linked in ouabain-dependent hypertension. Our results favor the possibility that enhanced duration of LTP in sympathetic neurons contributes to the increase in sympathetic nerve activity in ouabain-dependent hypertension and suggest that a captopril-sensitive step mediates the link of ouabain with LTP.

scholarly journals Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

1986 ◽  
Vol 87 (5) ◽  
pp. 775-793 ◽  
Author(s):  
E Kumamoto ◽  
K Kuba
Keyword(s):  
Transmitter Release ◽  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Presynaptic Terminal ◽  
Synaptic Delay ◽  
K Channel ◽  
Term Potentiation ◽  
Relative Change ◽  
Theoretical Considerations

A mechanism of the long-term potentiation of transmitter release induced by adrenaline (ALTP) was studied by recording intracellularly the fast excitatory postsynaptic potentials (fast EPSPs). The ALTP was produced during the blockade of K+ channels at the presynaptic terminals by tetraethylammonium (TEA). The synaptic delay, possibly reflecting a relative change in the duration of an action potential at the presynaptic terminal, was not changed during the course of the ALTP. By contrast, it was significantly lengthened by TEA and other K+ channel inhibitors (4-aminopyridine and Cs+) that markedly enhanced the evoked release of transmitter. The magnitude of facilitation of the fast EPSP, induced by a conditional stimulus to the preganglionic nerve, was decreased during the generation of the ALTP, but was unchanged during the potentiation of transmitter release caused by TEA. These results, together with theoretical considerations applying the residual Ca2+ hypothesis to the facilitation, suggest that the enhancement of transmitter release during the ALTP is not caused by an increased Ca2+ influx during a presynaptic impulse owing to the blockade of K+ channel or the modulation of Ca2+ channel, but presumably is induced by a rise in the basal level of free Ca2+ in the presynaptic terminal.

Psychosocial stress-induced hypertension results from in vivo expression of long-term potentiation in rat sympathetic ganglia

2005 ◽  
Vol 20 (3) ◽  
pp. 849-857 ◽  
Author(s):  
Karim A. Alkadhi ◽  
Karem H. Alzoubi ◽  
Abdulaziz M. Aleisa ◽  
Felicia L. Tanner ◽  
Ayad S. Nimer
Keyword(s):  
Psychosocial Stress ◽  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Term Potentiation ◽  
Induced Hypertension ◽  
In Vivo Expression
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