These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Significance of slow synaptic potentials for transmission of excitation in guinea-pig myenteric plexus.
    Author: Morita K, North RA.
    Journal: Neuroscience; 1985 Feb; 14(2):661-72. PubMed ID: 2859550.
    Abstract:
    Intracellular recordings were made from neurones in myenteric ganglia of the guinea-pig ileum in vitro. Synaptic potentials were evoked by electrically stimulating presynaptic fibres as they entered the ganglion, using a small focal electrode. Slow synaptic depolarizations (excitatory postsynaptic potentials) were evoked in most myenteric neurones of both types. A single stimulus was more likely to evoke a slow excitatory postsynaptic potential in cells with nicotinic synaptic input (S cells; 50%) than in cells with long-lasting after-hyperpolarizations following the soma action potential (AH cells; 20%). Two pulses often evoked a slow excitatory postsynaptic potential in AH cells when one pulse was ineffective. The optimally effective time between the pulses was about 100 ms. Ten pulses resulted in slow excitatory postsynaptic potentials even when delivered at frequencies as low as 0.5 Hz. For the same frequency of presynaptic stimulation, the duration of the slow excitatory postsynaptic potential was greater in AH cells than in S cells and the amplitude of the slow excitatory postsynaptic potential was slightly greater in S than AH cells. Spontaneous depolarizations were observed which had time-courses and amplitudes similar to the evoked slow excitatory postsynaptic potential. They were not blocked by tetrodotoxin or atropine. The calcium-dependent after-hyperpolarization which follows one or more action potentials in AH cells was reduced or even abolished during the slow excitatory postsynaptic potential. Presynaptic nerve stimulation at intensities lower than those required to cause a slow excitatory postsynaptic potential caused a reduction in the calcium dependent after-hyperpolarization. It is concluded that the slow excitatory postsynaptic potential is generated by an intracellular intermediate process which is sensitive to the intracellular calcium concentration. The results suggest that the postsynaptic action of the synaptic transmitter is to interfere with the intracellular process which couples the entry of calcium to the increase in potassium conductance.
    [Abstract] [Full Text] [Related] [New Search]