Inhibitory postsynaptic potentials

An inhibitory postsynaptic potential is a local hypetpo-larizing potential at a postsynaptic membrane, which is elicited by the release of an inhibitory neurotransmitter via an inhibitory postsynaptic current. 

The GABAA-receptor and the glycine receptor are Cl-channels (Table 1). When they open at a resting membrane potential of about -60 mV, the consequence is an entry of Cl-, hyperpolarization and an inhibitory postsynaptic potential (DPSP Fig. 1). 

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.

HD HIV HMG hpp IL-2 IPSP hydroxydanaidal human immunodeficiency virus hydroxymethylglutaryl hours postparasitization interleukin 2 inhibitory postsynaptic potential... 

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. 

Fiorillo CD, Williams JT (1998) Glutamate mediates an inhibitory postsynaptic potential in dopamine neurons. Nature 394 78-82... 

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. 

GABA receptors are divided into two main types GABAa and GABAB. inhibitory postsynaptic potentials in many areas of the brain have a fast and slow component. The fast component is mediated by GABAa receptors and the slow component by GABAB receptors. The difference in kinetics stems from the differences in coupling of the receptors to ion channels. GABAa... 

Spinal sites of opioid action. Mu (v), delta (5), and kappa ( ) agonists reduce transmitter release from presynaptic terminals of nociceptive primary afferents. Mu-agonists also hyperpolarize second-order pain transmission neurons by increasing K+ conductance, evoking an inhibitory postsynaptic potential. 

Bobker DH, Williams JT. The serotonergic inhibitory postsynaptic potential in prepositus hypoglossi is mediated by two potassium currents. J Neurosci. 1995 15 223-229. 

Yoshimura M, Higashi H. 5-Hydroxytryptamine mediates inhibitory postsynaptic potentials in rat dorsal raphe neurons. Neurosci Lett 1985 53 69-74. 

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-... 

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