About: Synaptic potential is a research topic. Over the lifetime, 776 publications have been published within this topic receiving 56161 citations. The topic is also known as: synaptic potentials.
TL;DR: This chapter presents some solutions to problems encountered on attempting to depolarize cat motoneurons sufficiently to reverse Ia excitatory postsynaptic potentials (EPSPs).
Abstract: Publisher Summary This chapter presents some solutions to problems encountered on attempting to depolarize cat motoneurons sufficiently to reverse Ia excitatory postsynaptic potentials (EPSPs). The polarization of motoneurons by injected current is limited by the active and passive membrane properties. The sodium conductance increases, leading to action potential generation and repetitive firing, which shows little tendency to adaptation or depolarization block. The potassium conductance underlying delayed rectification and the afterhyperpolarization of the action potential increases dramatically, short-circuiting the membrane, preventing further depolarization, and shunting out both EPSPs and inhibitory postsynaptic potentials (IPSPs). It is found that if the electrode polarized and/or rectified, it would be impossible to assess the true membrane potential during the massive current injection needed to depolarize the cell. The rastered records of the EPSP and conductance pulse pairs, taken before and during the current ramp show that these potentials were obscured during the repetitive firing whereas later, spikes or local responses can be seen to be fired by the EPSPs.
TL;DR: The object of the simulation has been to determine the magnitude of a chloride conductance required to reduce transmitter release, for various diameters of synaptic boutons, connected to axons with diameters in the range 0.1-1.0 microns.
Abstract: 1. During presynaptic inhibition, an increased conductance in the membrane of the presynaptic bouton is presumed to reduce the action potential, thereby reducing transmitter release. The object of ...
TL;DR: In most experiments the preparations were not in as good condition and only a synaptic potential was recorded from the post-fibre, so it is difficult to assign a value to the delay between pre-spike and synaptic response.
Abstract: MICROELECTRODES have been inserted into both pre- and post-junctional elements of certain one-way synapses in the abdominal nerve-cord of the crayfish (Astacus fluviatilis). The pre-synaptic fibres are giant axons (lateral and medial) which run through the length of the cord. The post-fibre is, in each case, the largest of the motor axons which leave the ganglion in the third root. Fig. 1 shows an example of nerve-impulse transmission across such a synapse. The pre-junctional axon was stimulated with external electrodes; and its action potential, recorded intra-cellularly close to the synapse, is shown on the upper trace. The ensuing post-synaptic response, also recorded intracellularly from the junctional region, is shown on the lower beam. The magnitudes of the pre- and post-spikes were 92 and 70 mV., respectively. The post-spike was initiated when the synaptic potential exceeded about 20 mV. In most experiments the preparations were not in as good condition and only a synaptic potential was recorded from the post-fibre. It is difficult to assign a value to the delay between pre-spike and synaptic response. Both potentials seem to arise at about the same time but at different rates. When a test for antidromic transmission is made, it is found that a spike in the post-fibre usually gives rise to no detectable potential change in the pre-axon.
TL;DR: The pyloric 1 (p1) muscle of the stomach of the lobster, Homarus americanus, is studied, showing that as the muscle fibers increased in length, the spacing between the terminal innervation increased proportionally, so the number of synaptic contact regions/muscle fiber did not change.
TL;DR: The locations of the cell bodies of axons responsible for synaptic potentials evoked in neurochemically identified submucous neurons of the guinea-pig small intestine were investigated using a combination of intracellular recording, immunohistochemical and lesioning techniques.
Abstract: The locations of the cell bodies of axons responsible for synaptic potentials evoked in neurochemically identified submucous neurons of the guinea-pig small intestine were investigated using a combination of intracellular recording, immunohistochemical and lesioning techniques. The myenteric plexus was removed from an 8–15 mm wide ring of small intestine in 15 anaesthetized guinea-pigs. After the operations, the animals were allowed to recover for 3–7 days so that nerve terminals that were disconnected from their cell bodies would degenerate. Preparations of submucous plexus were then made from the region under the lesion. Submucous neurons were impaled with electrodes containing a mixture of KC1 and the fluorescent dye, Lucifer yellow CH, and their electrophysiological properties determined. They were then filled with the dye for subsequent reidentification after processing for immunohistochemical localization of vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY). The synaptic inputs to 33 neurons were characterized: 19 of these were found to be VIP-reactive, 7 were NPY-reactive and 7 were negative for both VIP and NPY. These results were compared to those obtained from 43 neurons in control preparations: 25 VIP-reactive, 9 NPY-reactive and 9 negative for both VIP and NPY. Removal of the myenteric plexus caused a significant reduction in the number of inputs providing fast excitatory synaptic potentials to each of the neurochemically defined classes of neurons. The lesions also caused a significant reduction in the number of VIP-reactive neurons that exhibited slow excitatory synaptic potentials (other neurochemical types do not normally exhibit such responses). In contrast, the number of neurons in which inhibitory synaptic potentials could be evoked was unchanged. It is concluded that many of the excitatory synaptic terminals on submucous neurons originate from cell bodies in the myenteric plexus.