Potentials, electric postsynaptic

I.3. Synaptic Potential. A postsynaptic membrane may be considered as a chemosensory membrane. The signal transmissions through most synaptic regions (the region where one nerve ending terminates at a dendrite of another nerve cell) are mediated by chemical transmitters released from the nerve end upon the arrival of an action potential (Table 25). In some synapses, the two membranes are so closely adhered that the electrical impulse (action current) will directly initiate a synaptic potential at the second cell (i.e., an electrical synapse (Fig. 43A)). However, in a chemical synpase, the chemical transmitters released from the presynaptic terminal diffuse and react at a certain part of the dendrite membrane (postsynaptic membrane) where chemical receptors are located. The chemical transmitters react with the... 

Imon, H., Ito, K., Dauphin, L. McCarley, R. W. (1996). Electrical stimulation of the cholinergic laterodorsal tegmental nucleus elicits scopolamine-sensitive excitatory postsynaptic potentials in medial pontine reticular formation neurons. Neuroscience 74, 393-401. 

A variety of methods have been developed to study exocytosis. Neurotransmitter and hormone release can be measured by the electrical effects of released neurotransmitter or hormone on postsynaptic membrane receptors, such as the neuromuscular junction (NMJ see below), and directly by biochemical assay. Another direct measure of exocytosis is the increase in membrane area due to the incorporation of the secretory granule or vesicle membrane into the plasma membrane. This can be measured by increases in membrane capacitance (Cm). Cm is directly proportional to membrane area and is defined as Cm = QAJV, where Cm is the membrane capacitance in farads (F), Q is the charge across the membrane in coulombs (C), V is voltage (V) and Am is the area of the plasma membrane (cm2). The specific capacitance, Q/V, is the amount of charge that must be deposited across 1 cm2 of membrane to change the potential by IV. The specific capacitance, mainly determined by the thickness and dielectric constant of the phospholipid bilayer membrane, is approximately 1 pF/cm2 for intracellular organelles and the plasma membrane. Therefore, the increase in plasma membrane area due to exocytosis is proportional to the increase in Cm. 

Stimulation of the motoneuron releases acetylcholine onto the muscle endplate and results in contraction of the muscle fiber. Contraction and associated electrical events can be produced by intra-arterial injection of ACh close to the muscle. Since skeletal muscle does not possess inherent myogenic tone, the tone of apparently resting muscle is maintained by spontaneous and intermittent release of ACh. The consequences of spontaneous release at the motor endplate of skeletal muscle are small depolarizations from the quantized release of ACh, termed miniature endplate potentials (MEPPs) [15] (seeCh. 10). Decay times for the MEPPs range between l and 2 ms, a duration similar to the mean channel open time seen with ACh stimulation of individual receptor molecules. Stimulation of the motoneuron results in the release of several hundred quanta of ACh. The summation of MEPPs gives rise to a postsynaptic excitatory potential (PSEP),... 

FIG. 5. Ca2+ sparks drive electrical activity in myocytes. In contrast to the traditional concept of electrical activity deriving from descending neural control via postsynaptic responses, spontaneous Ca2+ release results in electrical activity in smooth muscle. The figure shows a Ca2+ spark activating sarcolemmal Ca2+-activated Cl- channels and spontaneous transient inward currents (STICs) (current trace above). Whether Ca2+ sparks activate outward STOCs (Ca2+-activated K+ currents) or STICs will depend on the proportion of channels expressed and the resting potential of the myocyte. 

During a laboratory demonstration to depict the complexity of neurotransmission in autonomic ganglia, Professor Smith sets up an anesthetized mammalian preparation in which she is recording postsynaptic events following the electrical stimulation of preganglionic sympathetic nerves. This demonstrates a complex action potential that consists of a fast EPSP followed by a slow IPSP followed by a slow EPSP and finally by a late very slow EPSP. 

Early researchers thought of two means by which synaptic transmission could occur. Action potentials could jump the gap by some electrical mechanism such as induction—this is the same process by which an electrical current in one coil of a transformer induces a current in the other coil, even though the coils are not in contact. Another possible mechanism of synaptic transmission involves the use of a chemical intermediate. Suppose an action potential caused molecules of a certain chemical to be released at the tip of the axon. These molecules would diffuse across the gap, reaching the other side in a short period of time. But researchers were imsure what effect these molecules could have on the postsynaptic neuron that receives the message. (The transmitting neuron is known as the presynaptic neuron.) In 1906, the British researchers Thomas Elliot (1877-1961) and John Eangley (1852-1925) considered the idea of a receptor on the postsynaptic neuron, on which the chemical might dock and exert its effects. 

Postictal inhibition has been demonstrated after bilateral ECS through ear-clip electrodes as well as after direct electrical stimulation of specific brain areas [for review, see Krauss and Fisher 1993]. TMS might exert anticonvulsive effects by stimulation of brain areas that are responsible for seizure inhibition. Alternatively, TMS might inhibit by direct inhibition of neural excitability in brain regions that are responsible for seizure initiation and spreading. Indeed, the TMS-induced decrease in postsynaptic action potentials hints that TMS might generate direct inhibitory mechanisms on neural excitability. 

Once the electrical signal has arrived at a chemical synapse (see Fig 4.2) a cascade of events is triggered with the arrival of an electrical impulse (an action potential), a chemical compound known as a neurotransmitter is released from the presynaptic side into the synaptic cleft. The released neurotransmitter then reaches the membrane of the second cell (postsynaptic membrane) where it interacts with a macromolecule, a so-called receptor. It is this neurotransmitter receptor interaction that triggers another cascade of (chemical) reactions within the second cell and this ultimately leads to the generation of an electrical signal within this cell. This signal then is transferred along this second cell s axon towards another synapse. 

Once a neurotransmitter is bound to the postsynaptieally located receptor a change in the electrical potential of the postsynaptic membrane occurs. Depending on both the type of transmitter and the properties of the postsynaptic receptor involved, the membrane potential of the second cell is... 

In the presynaptic cell, the neurotransmitters are stored in vesicles. On arrival of an electrical signal (action potential, see 16.2), an influx of Ca takes place into the presynaptic cell as voltage-gated Ca channels are opened. The increase in Ca concentration leads to fusion of the vesicles with the membrane of the postsynaptic cell. The neurotransmitters are released into the synaptic cleft and diffuse to a corresponding receptor on the surface of the postsynaptic cell. Binding of the nemotransmitter to the receptor induces opening of an ion channel that is a component of the receptor. The type of ions that can enter depends on the selectivity of the ion channel. There are Na K, Ca and Cf specific ion channels. The ion flux creates an electric signal in the post-... 

Each of their receptors transmits its signal across the plasma membrane by increasing transmembrane conductance of the relevant ion and thereby altering the electrical potential across the membrane. For example, acetylcholine causes the opening of the ion channel in the nicotinic acetylcholine receptor (AChR), which allows Na+ to flow down its concentration gradient into cells, producing a localized excitatory postsynaptic potential—a depolarization. 

In most instances the arrival of a nerve signal at the presynaptic end of a neuron causes the release of a transmitter substance (neurohormone). Tire transmitter passes across the 10-50 nm (typically 20 nm) synaptic cleft between the two cells and induces a change in the electrical potential of the postsynaptic membrane of the next neuron (Fig. 30-10).149 401 Excitatory transmitters usually cause depolarization of the membrane. By this we mean that the membrane potential, which in a resting neuron is -50 to -70 mv (Chapter 8), falls to nearly zero often as a consequence of an increased permeability to Na+ and a resultant inflow of sodium ions. The resulting postsynaptic... 

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.

Gap junctions provide in the nervous system the structural correlate of one class of electrical synapses, characterized by very close apposition between the presynaptic and postsynaptic membranes. It should be noted, in this respect, that different junctional specializations can mediate different forms of electrical transmission between neurons (Bennett, 1997). Electrical synapses transmit preferentially, but not exclusively, low-frequency stimuli, that allow the rapid transfer of a presynaptic impulse into an electrical excitatory potential in the postjunctional cells. Electrical transmission, via the intercellular channels, can be bidirectional. The widely held opinion that electrical transmission is characteristic of lower vertebrates probably derives from the large cell systems in which electrical synapses were identified in the initial period of intracellular recording (reviewed by Bennett, 1997). Contradicting this view, electrotonic coupling between neurons has now been demonstrated in many areas of the mammalian central nervous system and has been implicated in neuronal synchronization. Gap junctional intercellular communication can occur between glial cells, glia and neurons, as well as between neurons. 

The process of information flow between neurons is termed synaptic transmission, and in its most basic form it is characterized by unidirectional communication from the presynaptic to postsynaptic neuron. The process begins with the initiation of an electrical impulse in the axon of the presynaptic neuron. This electrical signal—the action potential—propagates to the axon terminal, which thereby stimulates the fusion of a transmitter-fllled synaptic vesicle with the presynaptic terminal membrane. The process of synaptic vesicle fusion is highly regulated and involves numerous biochemical reactions it culminates in the release of chemical neurotransmitter into the synaptic cleft. The released neurotransmitter diffuses across the cleft and binds to and activates receptors on the postsynaptic site, which thereby completes the process of synaptic transmission. 

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