Inhibitory/excitatory postsynaptic potentials

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 5.3 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.

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. 

Interaction of excitatory and inhibitory synapses. On the left, a suprathreshold stimulus is given to an excitatory pathway (E) and an action potential is evoked. On the right, this same stimulus is given shortly after activating an inhibitory pathway (I), which results in an inhibitory postsynaptic potential (IPSP) that prevents the excitatory potential from reaching threshold. 

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). 

Postsynaptic receptors, including two types of muscarinic receptors and at least one type of peptidergic receptor, have been found in ganglionic synapses, where nicotinic transmission is primary. These receptors may facilitate or inhibit transmission by evoking slow excitatory or inhibitory postsynaptic potentials (EPSPs or IPSPs). 

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). 

The excitatory postsynaptic potential is a depolarization potential, because the equilibrium potential of Na" and (reversal potential) is at the level of -20-0 mV whereas the resting potential of the postsynaptic membrane in most nerve and muscle is about -80—100 mV in a typical physiological environment. On the other hand the inhibitory postsynaptic potential can also be evoked by another type of chemical transmitter which acts by hyperpolariz-ing the membrane in this case the receptor responsible for production of the... 

Figure 44. Excitatory and inhibitory synaptic actions in cat brain cells. Synaptic potential and currents are shown in the figures. EPSP—excitatory postsynaptic potential IPSP—inhibitory postsynaptic potential (after ref. 213).

Concentrations of ammonia equivalent to those reported in the brain in HE are known to cause deleterious effects on the CNS functions by both direct and indirect mechanisms (Szerb and Butterworth, 1992, review). Direct effects of the NH/ ion on both inhibitory and excitatory neurotransmission have been reported. Millimolar concentrations of ammonia impair postsynaptic inhibition in the brain by inactivation of the extrusion of Cl" from neurons (Raabe, 1987). This inactivation of Cl extrusion abolishes the concentration gradient for Cl across the neuronal membrane. Consequently, the opening of CT channels by the inhibitory neurotransmitter no longer takes place and the inhibitory postsynaptic potential (IPSP) is abolished. It has been demonstrated that brain ammonia concentrations as low as 0.5 mM may exert this adverse effect on inhibitory neurotransmission. 

The EEG is produced by electrical dipoles in the outer brain cortex. The waveform is too low in frequency to be the summed result of fast action potential events. Instead, the electric signal is believed to be attributable to the aggregate of excitatory and inhibitory postsynaptic potentials (EPSPs/IPSPs). 

Such clear postsynaptic potentials can be recorded intracellularly with microelectrodes in large quiescent neurons after appropriate activation but may be somewhat artificial. In practice a neuron receives a large number of excitatory and inhibitory inputs and its bombardment by mixed inputs means that its potential is continuously changing and may only move towards the threshold for depolarisation if inhibition fails or is overcome by a sudden increase in excitatory input. 

Since the orexin receptors are Gq protein-coupled (Alexander et al. 2006), one may assume that this also holds true for the presynaptic orexin receptor(s), but so far no data are available. Nonetheless, the six studies carried out in central nervous preparations permit some conclusions on the post-G protein mechanisms. In all instances, the orexins increased the frequency of spontaneous inhibitory or excitatory postsynaptic potentials or currents. The results differed, however, with respect to the influence of tetrodotoxin. In the medial and lateral hypothalamus (van den Pol et al. 1998 Li et al. 2002), dorsal vagal complex (Davis et al. 2003), and caudal nucleus tractus solitarii (Smith et al. 2002), orexins increased the frequency of the miniature potentials or currents also in the presence of tetrodotoxin, suggesting that they directly influenced the vesicle release machinery (references in italics in Table 5). On the other hand, in the prefrontal cortex (Lambe and Aghajanian 2003) and lat-erodorsal tegmentum (Burlet et al. 2002), the orexins did not retain their facilitatory effect in the presence of tetrodotoxin, suggesting an effect further upstream e.g., on Ca2+ and/or K+ channels. 

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