IPSP = Inhibitory postsynaptic potential

An inhibitory input increases the influx of Cl to make the inside of the neuron more negative. This hyperpolarisation, the inhibitory postsynaptic potential (IPSP), takes the membrane potential further away from threshold and firing. It is the mirror-image of the EPSP and will reduce the chance of an EPSP reaching threshold voltage. 

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 11.5 Chloride distribution and the GABAa response. The change in membrane voltage (Fm) that results from an increase in chloride conductance following activation of GABAa receptors is determined by the resting membrane potential and the chloride equilibrium potential (Fci)- (a) Immature neurons accumulate CF via NKCC, while mature neurons possess a Cl -extruding transporter (KCC2). (b) In immature neurons GABAa receptor activation leads to CF exit and membrane depolarisation while in mature neurons the principal response is CF entry and h5q)erpolarisation. This is the classic inhibitory postsynaptic potential (IPSP)...

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. 

Stimulation of inhibitory neurons causes movement of ions that results in a hyperpolarization of the postsynaptic membrane. These inhibitory postsynaptic potentials (IPSP) are generated by the following (1) Stimulation of inhibitory neurons releases neurotransmitter molecules, such as Y-aminobutyric acid (GABA) or glycine, which bind to receptors on the postsynaptic cell membrane. This causes a transient increase in the permeability of specific ions, such as, potassium and chloride ions. (2) The influx of chloride (Cl ) and efflux of potassium (K+) cause a weak hyperpolarization or inhibitory post-... 

Figures. The blocking action of lOOpM CGP35348 on the late inhibitory postsynaptic potential (IPSP) recorded intracellularly from a rat CA1 pyramidal neuron. (Reproduced with permission of authors and editor of [26]).

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). 

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. 

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