Editing Inhibitory postsynaptic potential (section)

{{short description|Electrical signal inhibiting a neuron from firing}}

An '''inhibitory postsynaptic potential''' ('''IPSP''') is a kind of [[synaptic potential]] that makes a [[Chemical synapse|postsynaptic neuron]] less likely to generate an [[action potential]].<ref name="neurobook">Purves et al. Neuroscience. 4th ed. Sunderland (MA): Sinauer Associates, Incorporated; 2008.</ref> The opposite of an inhibitory postsynaptic potential is an [[excitatory postsynaptic potential]] (EPSP), which is a synaptic potential that makes a postsynaptic neuron ''more'' likely to generate an action potential.  IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell-to-cell signalling. EPSPs and IPSPs compete with each other at numerous synapses of a neuron. This determines whether an action potential occurring at the presynaptic terminal produces an action potential at the postsynaptic membrane.  Some common neurotransmitters involved in IPSPs are [[GABA]] and [[glycine]]. 

Inhibitory presynaptic neurons release neurotransmitters that then bind to the [[Neurotransmitter receptor|postsynaptic receptors]]; this induces a change in the permeability of the [[Chemical synapse|postsynaptic neuronal membrane]] to particular ions. An electric current that changes the postsynaptic membrane potential to create a more negative [[postsynaptic potential]] is generated, i.e. the postsynaptic membrane potential becomes more negative than the resting membrane potential, and this is called [[Hyperpolarization (biology)|hyperpolarisation]]. To generate an action potential, the postsynaptic membrane must [[depolarisation|depolarize]]—the membrane potential must reach a voltage threshold more positive than the resting membrane potential. Therefore, hyperpolarisation of the postsynaptic membrane makes it less likely for depolarisation to sufficiently occur to generate an action potential in the postsynaptic neuron.

[[Depolarization]] can also occur due to an IPSP if the reverse potential is between the resting threshold and the [[action potential]] threshold.  Another way to look at inhibitory postsynaptic potentials is that they are also a chloride conductance change in the neuronal cell because it decreases the driving force.<ref name="Thompson">{{cite journal | vauthors = Thompson SM, Gähwiler BH | title = Activity-dependent disinhibition. I. Repetitive stimulation reduces IPSP driving force and conductance in the hippocampus in vitro | journal = Journal of Neurophysiology | volume = 61 | issue = 3 | pages = 501–11 | date = March 1989 | pmid = 2709096 | doi = 10.1152/jn.1989.61.3.501 }}</ref> This is because, if the neurotransmitter released into the [[Chemical synapse#Structure|synaptic cleft]] causes an increase in the [[Cell membrane#Permeability|permeability]] of the postsynaptic membrane to [[Chloride|chloride ions]] by binding to [[Ligand-gated ion channel|ligand-gated]] [[Chloride channel|chloride ion channels]] and causing them to open, then chloride ions, which are in greater concentration in the synaptic cleft, diffuse into the postsynaptic neuron. As these are negatively charged ions, hyperpolarisation results, making it less likely for an action potential to be generated in the postsynaptic neuron. [[Microelectrodes]] can be used to measure postsynaptic potentials at either excitatory or inhibitory synapses.

In general, a postsynaptic potential is dependent on the type and combination of receptor channel, reverse potential of the postsynaptic potential, [[action potential]] threshold voltage, ionic permeability of the ion channel, as well as the concentrations of the ions in and out of the cell; this determines if it is excitatory or inhibitory.  IPSPs always tend to keep the membrane potential more negative than the action potential threshold and can be seen as a "transient hyperpolarization".<ref>{{cite book | first1 = Matthew | last1 = Levy | first2 = Bruce | last2 = Koeppen | first3 = Bruce | last3 = Stanton | name-list-style = vanc |title=Berne & Levy principles of physiology |publisher=Elsevier Mosby |isbn=978-0-8089-2321-3 |edition=4th | date = 2005 }}</ref>

IPSPs were first investigated in motorneurons by David P. C. Lloyd, [[John Eccles (neurophysiologist)|John Eccles]] and [[Rodolfo Llinás]] in the 1950s and 1960s.<ref>{{cite journal | vauthors = Coombs JS, Eccles JC, Fatt P | title = The specific ionic conductances and the ionic movements across the motoneuronal membrane that produce the inhibitory post-synaptic potential | journal = The Journal of Physiology | volume = 130 | issue = 2 | pages = 326–74 | date = November 1955 | pmid = 13278905 | pmc = 1363415 | doi = 10.1113/jphysiol.1955.sp005412 }}</ref><ref>{{cite journal | vauthors = Llinas R, Terzuolo CA | title = Mechanisms of Supraspinal Actions Upon Spinal Cord Activities. Reticular Inhibitory Mechanisms Upon Flexor Motoneurons | journal = Journal of Neurophysiology | volume = 28 | issue = 2 | pages = 413–22 | date = March 1965 | pmid = 14283063 | doi = 10.1152/jn.1965.28.2.413 }}</ref>

[[Image:IPSPflowchart.jpg|thumb|540px|Flowchart describing how an inhibitory postsynaptic potential works from neurotransmitter release to summation]]