Neuronal potentials inhibitory postsynaptic

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 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... 

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

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. 

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-... 

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]).

Ge S, Niesen CE. Beta-hydroxybutyrate potentiates GABA-A mediated inhibitory postsynaptic potentials in immature hippocampal CAl neurons. Epilepsia 1998 39 (Suppl 61 135. 

Fig. 3.18. Existence of two types of periodic behaviour in thalamic neurons. Starting from a stable membrane potential, a slight hyperpolarization gives rise to oscillations characterized by a frequency of 6 Hz, whereas depolarization produces oscillations of 10 Hz frequency. The occurrence of these two types of oscillations is linked to the existence of a high threshold (H.T.) and a low threshold (L.T.) characterizing the excitability of these neurons, i.p.s.p., inhibitory postsynaptic potential (Jahnsen Llinas, 1984b).

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