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Neurons resting potential

Figure 1.6 Presynaptic inhibition of the form seen in the dorsal horn of the spinal cord, (a) The axon terminal (i) of a local neuron is shown making an axo-axonal contact with a primary afferent excitatory input (ii). (b) A schematic enlargement of the synapse, (c) Depolarisation of the afferent terminal (ii) at its normal resting potential by an arriving action potential leads to the optimal release of neurotransmitter, (d) When the afferent terminal (ii) is already partially depolarised by the neurotransmitter released onto it by (i) the arriving acting potential releases less transmitter and so the input is less effective... Figure 1.6 Presynaptic inhibition of the form seen in the dorsal horn of the spinal cord, (a) The axon terminal (i) of a local neuron is shown making an axo-axonal contact with a primary afferent excitatory input (ii). (b) A schematic enlargement of the synapse, (c) Depolarisation of the afferent terminal (ii) at its normal resting potential by an arriving action potential leads to the optimal release of neurotransmitter, (d) When the afferent terminal (ii) is already partially depolarised by the neurotransmitter released onto it by (i) the arriving acting potential releases less transmitter and so the input is less effective...
SKca and M channels are not the only K+ channels regulated by transmitters. As noted above, transmitters can also close, or open, other K+ channels that do not directly regulate excitability but instead determine the resting potential of the neuron, and hence depolarise or hyperpolarise the neuron. [Pg.45]

Investigations of the cellular effects of radiofrequency radiation provide evidence of damage to various types of avian and mammalian cells. These effects involve radiofrequency interactions with cell membranes, especially the plasma membrane. Effects include alterations in membrane cation transport, Na+/K+-ATPase activity, protein kinase activity, neutrophil precursor membrane receptors, firing rates and resting potentials of neurons, brain cell metabolism, DNA and RNA synthesis in glioma cells, and mitogenic effects on human lymphocytes (Cleary 1990). [Pg.1699]

In a resting state, neurons maintain a negatively charged potential, referred to as the resting potential, that is actively maintained by energy-... [Pg.43]

There is one last, important point. The unequal distribution of ions across the plasma membrane of the neuron leads to a net negative charge on the inside of the neuron and a net positive charge on the outside. This separation of charge creates a potential difference, or voltage, across the neuronal plasma membrane. For a neuron at rest, this potential difference amounts to about 65 millivolts (mV), with the inside negative. By convention, we say that the resting potential of the neuron is -65 mV. [Pg.289]

Most cells possess an electrical potential across then-plasma membrane, which is positive on the external surface. This is known as the resting potential. The neurone is no exception it has a potential of between 50 and 75 millivolts (mV). The resting potential arises from the following ... [Pg.310]

The transient change in the transmembrane potential upon excitation. An action potential cycle consists of a transient depolarization of the cell membrane of an excitable cell (such as a neuron) as a result of increased permeability of ions across the membrane, followed by repolarization, hyperpolarization, and finally a return to the resting potential. This cycle typically lasts 1-2 milliseconds and travels along the axon from the cell body (or, axon hillock) to the axonal terminus at a rate of 1-100 meters per second. See Membrane Potential... [Pg.25]

Fig. 2. Electrophysiological trace from a prefrontal layer V showing the rapid onset of spEPSCs in response to puff application (1 s) of 5-HT. Note the increase in spEP-SCs begins within approx 3-4 s. The neuron is voltage-clamped close to its resting potential and is not directly depolarized by the application of 5-HT. Fig. 2. Electrophysiological trace from a prefrontal layer V showing the rapid onset of spEPSCs in response to puff application (1 s) of 5-HT. Note the increase in spEP-SCs begins within approx 3-4 s. The neuron is voltage-clamped close to its resting potential and is not directly depolarized by the application of 5-HT.
Fig. 4. Electrophysiological traces from a prefrontal layer V showing the response to nearby electrical stimulation of corticocortical afferents. Stimulus artifact appears as a vertical line. (1) The fast evoked excitatory postsynaptic current (evEPSC) follows immediately, as depicted by the arrow. Under normal conditions, stimulation at 0.1 Hz evokes only a fast evEPSC. (2) However, after the application of a psychedelic hallucinogen (3 pMDOI, 15 min), stimulation at this frequency almost always evokes both a fast evEPSC and a late evEPSC, as depicted by the arrows. The neuron is voltage-clamped close to its resting potential and was not directly depolarized by DOI. It is not known what type of glutamate release accounts for the late evEPSC. Traces are averages of 10 sweeps taken during each of the conditions. Fig. 4. Electrophysiological traces from a prefrontal layer V showing the response to nearby electrical stimulation of corticocortical afferents. Stimulus artifact appears as a vertical line. (1) The fast evoked excitatory postsynaptic current (evEPSC) follows immediately, as depicted by the arrow. Under normal conditions, stimulation at 0.1 Hz evokes only a fast evEPSC. (2) However, after the application of a psychedelic hallucinogen (3 pMDOI, 15 min), stimulation at this frequency almost always evokes both a fast evEPSC and a late evEPSC, as depicted by the arrows. The neuron is voltage-clamped close to its resting potential and was not directly depolarized by DOI. It is not known what type of glutamate release accounts for the late evEPSC. Traces are averages of 10 sweeps taken during each of the conditions.

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See also in sourсe #XX -- [ Pg.89 , Pg.92 ]




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