EPSP = Excitatory postsynaptic potential

The AMPA receptors for glutamate, the nicotinic acetylcholine receptor and the 5-HT3-receptor for serotonin are cation channels (Table 1). When they open, the major consequence is a sudden entry of Na+, depolarization and an excitatory postsynaptic potential (EPSP Fig. 1). 

Figure 1.4 Ionic basis for excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Resting membrane potential ( — 70 mV) is maintained by Na+ influx and K+ efflux. Varying degrees of depolarisation, shown by different sized EPSPs (a and b), are caused by increasing influx of Na. When the membrane potential moves towards threshold potential (60-65 mV) an action potential is initiated (c). The IPSPs (a b ) are produced by an influx of Cl. Coincidence of an EPSP (b) and IPSP (a ) reduces the size of the EPSP (d)...

Figure 5.2 Temporal summation. Multiple excitatory postsynaptic potentials (EPSPs) produced by a single presynaptic neuron in close sequence may add together to depolarize the postsynaptic neuron to threshold and generate an action potential.

Figure 5.3 Spatial summation. Multiple excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs) produced by many presynaptic neurons simultaneously may add together to alter the membrane potential of the postsynaptic neuron. Sufficient excitatory input (A and B) will depolarize the membrane to threshold and generate an action potential. The simultaneous arrival of excitatory and inhibitory inputs (A and C) may cancel each other out so that the membrane potential does not change.

Both NMDA and AMPA receptor components of excitatory postsynaptic potentials (EPSPs) are produced by the brief (1 ms) appearance of free transmitter in the synaptic cleft (Fig 15-10A). Synaptically released glutamate thus... 

Excitatory postsynaptic potentials (EPSPs), spikes from, 172... 

Activation of ionotropic mechanisms creates postsynaptic potentials. An influx of cations or efflux of anions depolarizes the neuron, creating an excitatory-postsynaptic potential (EPSP). Conversely, an influx of anions or efflux of cations hyperpolarizes the neuron, creating an inhibitory-postsynaptic potential (IPSP). Postsynaptic potentials are summated both... 

When receptors are directly linked to ion channels, fast excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs) occur. However, it is well established that slow potential changes also occur and that such changes are due to the receptor being linked to the ion channel indirectly via a second messenger system. 

B. Long-term potentiation in the dentate gyrus recorded in vivo. The graph plots the early rising slope of the field excitatory postsynaptic potential (EPSP) in response to low frequency stimulation (700 pA, 100 ms, 0.05 Hz). Four trains of high frequency stimulation (700 pA, 82.5 ms, 400 Hz) were dehvered at time 0. This produced an immediate increase in the EPSP slope (post-tetanic potentiation) and a sustained relatively constant enhancement that lasted for at least 60 minutes. Representative traces are included below the graph. Note the obvious increase in size of the superimposed population spike (downward deflection). 

When an excitatory pathway is stimulated, a small depolarization or excitatory postsynaptic potential (EPSP) is recorded. This potential is due to the excitatory transmitter acting on an ionotropic receptor, causing an increase in cation permeability. Changing the stimulus intensity to the pathway, and therefore the number of presynaptic fibers activated, results in a graded change in the size of the depolarization. When a sufficient number of excitatory fibers are activated, the excitatory postsynaptic potential depolarizes the postsynaptic cell to threshold, and an all-or-none action potential is generated. 

Neurotransmitters can be classified as excitatory or inhibitory, depending on the nature of the action they elicit. Stimulation of excitatory neurons causes a movement of ions that results in a depolarization of the postsynaptic membrane. These excitatory postsynaptic potentials (EPSP) are generated by the following (1) Stimulation of an excitatory neuron causes the release of neurotransmitter molecules, such as norepinephrine or acetylcholine, which bind to receptors on the postsynaptic cell membrane. This causes a transient increase in the permeability of sodium (Na+) ions. (2) The influx of Na+ causes a weak depolarization or excitatory postsynaptic potential (EPSP). (3) If the number of excitatory fibers stimulated increases, more excitatory neurotransmitter is released, finally causing the EPSP depolarization of the postsynaptic cell to pass a threshold, and an all-or-none action potential is generated. [Note The generation of a nerve impulse typically reflects the activation of synaptic receptors by thousands of excitatory neurotransmitter molecules released from many nerve fibers.] (See Figure 8.2 for an example of an excitatory pathway.)... 

Combination of the transmitter with postjunctional receptors and production of the postjunctional potential. The released transmitter diffuses across the synaptic or junctional cleft and combines with specialized receptors on the postjunctional membrane this often results in a localized increase in the ionic permeability, or conductance, of the membrane. With certain exceptions (noted below), one of three types of permeabdity change can occur (a) a generalized increase in the permeabdity to cations (notably Na+ but occasionady Ca +), resulting in a localized depolarization of the membrane, i.e., an excitatory postsynaptic potential (EPSP) (b) a selective increase in permeabdity to anions, usually Q, resulting in stabdization or hyperpolarization of the membrane (an inhibitory postsynaptic potential or IPSP) or (c) an increased permeability to K+ (the K+ gradient is directed outward thus, hyperpolarization results, i.e., an IPSP). 

ACh interacts with the nicotinic ACh receptor to initiate an end-plate potential (EPP) in muscle or an excitatory postsynaptic potential (EPSP) in peripheral ganglia (Chapter 6). The nicotinic receptor of vertebrate skeletal muscle is a pentamer composed of 4 distinct subunits a, /3, y, and S) in the stoichiometric ratio of 2 1 1 1, respectively. In mature, innervated muscle end plates, the y subunit is replaced by the closely related e subunit. The nicotinic receptor is prototypical of other pen-tameric ligand-gated ion channels, which include the receptors for the inhibitory amino acids (y-aminobutyric acid [GABA] and glycine) and S-HT serotonin receptors (Figure 9-1). 

Nicotinic mechanism The mechanism of nicotinic action has been clearly defined. The ACh receptor is located on a channel protein that is selective for sodium and potassium. When the receptor is activated, the channel opens and depolarization of the cell (an excitatory postsynaptic potential EPSP) occurs as a direct result of the influx of sodium. These ACh receptors are present on ganglion cells (both sympathetic and parasympathetic) and the neuromuscular end plate. If large enough, the EPSP evokes a propagated action potential in the surrounding membrane. 

Role of the ion current carried by the channel Excitatory postsynaptic potentials (EPSPs) are usually generated by the opening of sodium or calcium channels. In some... 

Activation of chloride or potassium ion channels often generates inhibitory postsynaptic potentials (IPSPs) and inhibits nerve membranes. Activation of sodium and inhibition of potassium ion channels generate excitatory postsynaptic potentials (EPSPs). The answer is (A). 

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