An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential.[1] 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 postsynaptic receptors; this induces a change in the permeability of the 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 hyperpolarisation. To generate an action potential, the postsynaptic membrane must 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.[2] This is because, if the neurotransmitter released into the synaptic cleft causes an increase in the permeability of the postsynaptic membrane to chloride ions by binding to ligand-gated 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".[3]
IPSPs were first investigated in motorneurons by David P. C. Lloyd, John Eccles and Rodolfo Llinás in the 1950s and 1960s.[4][5]
Flowchart describing how an inhibitory postsynaptic potential works from neurotransmitter release to summation
^Thompson SM, Gähwiler BH (March 1989). "Activity-dependent disinhibition. I. Repetitive stimulation reduces IPSP driving force and conductance in the hippocampus in vitro". Journal of Neurophysiology. 61 (3): 501–11. doi:10.1152/jn.1989.61.3.501. PMID 2709096.
^Levy M, Koeppen B, Stanton B (2005). Berne & Levy principles of physiology (4th ed.). Elsevier Mosby. ISBN 978-0-8089-2321-3.
^Coombs JS, Eccles JC, Fatt P (November 1955). "The specific ionic conductances and the ionic movements across the motoneuronal membrane that produce the inhibitory post-synaptic potential". The Journal of Physiology. 130 (2): 326–74. doi:10.1113/jphysiol.1955.sp005412. PMC 1363415. PMID 13278905.
^Llinas R, Terzuolo CA (March 1965). "Mechanisms of Supraspinal Actions Upon Spinal Cord Activities. Reticular Inhibitory Mechanisms Upon Flexor Motoneurons". Journal of Neurophysiology. 28 (2): 413–22. doi:10.1152/jn.1965.28.2.413. PMID 14283063.
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