Action potentials generation

Psychostimulants. Figure 2 Dopamine molecules have two different possible targets. Both ways are initially increased by DAT inhibition caused by methylphenidate pre- and postsynaptic dopamine receptors. Stimulation of postsynaptic receptors results in inhibition of presynaptic action potential generation. On the other hand, presynaptic receptor stimulation leads to a transmission inhibition of action potentials. Therefore, both mechanisms are responsible for a decrease in vesicular depletion of dopamine into the synaptic cleft (adapted from [2]). 

There is no single underlying cause for the myotonia seen in the muscles of myotonic patients. The typical myotonic response is a train of action potentials generated in a muscle fiber in response to a single stimulus. Experimental work has shown that such a response can be generated in normal muscle fibers in which chloride conductance is suppressed, and this may be the cause of the myotonia of Thomsen s disease (see Barchi, 1988 for examples). It is almost certainly not the cause of myotonia in myotonic dystrophy in which there is an associated fall in... 

The membranes of nerve cells contain well-studied ion channels that are responsible for the action potentials generated across the membrane. The activity of some of these channels is controlled by neurotransmitters hence, channel activity can be regulated. One ion can regulate the activity of the channel of another ion. For example, a decrease of Ca + concentration in the extracellular fluid increases membrane permeability and increases the diffusion of Na+. This depolarizes the membrane and triggers nerve discharge, which may explain the numbness, tinghng, and muscle cramps symptomatic of a low level of plasma Ca. ... 

As discussed previously, the neurohypophysis has a direct anatomical connection to the hypothalamus. Therefore, the hypothalamus regulates the release of hormones from the neurohypophysis by way of neuronal signals. Action potentials generated by the neurosecretory cells originating in the hypothalamus are transmitted down the neuronal axons to the nerve terminals in the neurohypophysis and stimulate the release of the hormones into the blood. The tracts formed by these axons are referred to as hypothalamic-hypophyseal tracts (see Figure 10.2). The action potentials are initiated by various forms of sensory input to the hypothalamus. Specific forms of sensory input that regulate the release of ADH and oxytocin are described in subsequent sections in this chapter. 

Compare and contrast the action potentials generated by the SA node and ventricular muscle cells... 

The action potential generated in the ventricular muscle is very different from that originating in the SA node. The resting membrane potential is not only stable it is much more negative than that of the SA node. Second, the slope of the depolarization phase of the action potential is much steeper. Finally, there is a lengthy plateau phase of the action potential in which the muscle cells remain depolarized for approximately 300 msec. The physiological significance of this sustained depolarization is that it leads to sustained contraction (also about 300 msec), which facilitates ejection of blood. These disparities in the action potentials are explained by differences in ion channel activity in ventricular muscle compared to the SA node. 

Figure 14.1 Effect of autonomic nervous system stimulation on action potentials of the sinoatrial (SA) node. A normal action potential generated by the SA node under resting conditions is represented by the solid line the positive chronotropic effect (increased heart rate) of norepinephrine released from sympathetic nerve fibers is illustrated by the short dashed line and the negative chronotropic effect (decreased heart rate) of acetylcholine released from parasympathetic nerve fibers is illustrated by the long dashed line.

Frequency of action potential generation and duration of this electrical activity to the motor neurons, and therefore the muscles of inspiration and expiration, which determines the depth of breathing, or the tidal volume (as the frequency and duration of stimulation increase, the tidal volume increases)... 

This pathway provides several amplification steps between odorant binding and signal generation. Due to the electrically compact structure of the cell, it is possible for the activation of only a few tens of channels to drive the membrane to the threshold for action-potential generation. Thus, it is theoretically possible that the limit of olfactory detection is a single molecule, although this has not yet been conclusively demonstrated. 

Hirst I m convinced that it s clipping action potential generation and release. Alison is not sure what the action potentials are doing, but she agrees they are an essential part of the response. 

Once you get an action potential generated, it will flow down the neuronal axon. Remember that an action potential is a sequence of membrane depolarization and repolarization events mediated by voltage-gated sodium ion and potassium ion channels. The basic idea is provided in figure 21.3. The initial depolarization will spread to adjacent voltage-gated ion channels, which will open, ions will flow, and so forth. Thus, the wave of depolarization moves down the axon. It is the means by... 

The rapid removal of transmitter is essential to the exquisite control of neurotransmission. As a consequence of rapid removal, the magnitude and duration of effect produced by acetylcholine are directly related to the frequency of transmitter release, that is, to the frequency of action potentials generated in the neuron. 

In the mammalian CNS powerful inhibitory systems function continually to slow the number of action potentials generated. The effects of stimulating an excitatory pathway can appear to be exaggerated if normal inhibitory influences to that region are diminished. Correspondingly, an inhibitory pathway will appear exaggerated if part of the excitatory influence to that system has been removed. 

Action potentials generated by neurons convey information in their rate—how many occur in a given period of time, which can be up to a few himdred per second—and sometimes in their timing relative to one another. Networks of neurons process sensory information, control movement, and create the still mysterious nature of consciousness by... 

Schematic diagram of a primary afferent neuron mediating pain, its synapse with a secondary afferent in the spinal cord, and the targets for local pain control. The primary afferent neuron cell body is not shown. At least three nociceptors are recognized acid, injury, and heat receptors. The nerve ending also bears opioid receptors, which can inhibit action potential generation. The axon bears sodium channels and potassium channels (not shown), which are essential for action potential propagation. Synaptic transmission involves release of substance P, a neuropeptide (NP) and glutamate and activation of their receptors on the secondary neuron. Alpha2 adrenoceptors and opioid receptors modulate the transmission process.

Because sodium influx plays an important role during action potential generation during phase 0 of... 

Figure 7.47. Effect of incubation at 30°C on the rate of action potential generation by a mechanoreceptor nerve bundle for four congeners of Petrolisthes. (Unpublished data of J. Knape and G.N. Somero.)...

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