Inhibitory postsynaptic potential
n., [ɪnˈhɪbɪtərɪ ˌpəʊstsɪˈnæptɪk pəˈtɛnʃəl]
Definition: a postsynaptic potential wherein the binding of neurotransmitters with the postsynaptic receptors leads to hyperpolarization.
Table of Contents
Inhibitory Postsynaptic Potential Definition
An inhibitory postsynaptic potential is a type of synaptic potential. It is responsible for reducing the chances of a postsynaptic neuron generating an action potential. In the 1950s, IPSP was examined for the first time in motor neurons.
How about excitatory postsynaptic potential? Let us define it to understand how it is different from an inhibitory postsynaptic potential. An excitatory postsynaptic potential (EPSP) is a postsynaptic potential that increases the likelihood of a postsynaptic neuron initiating the action potential. IPSPs or inhibitory postsynaptic potentials can occur at any chemical synapses that communicate via neurotransmitter release.
What causes an IPSP? At the postsynaptic membrane, there is temporary hyperpolarization which is due to the flow of negative ions. An IPSP is generated when the inhibitory presynaptic cell gets connected to the dendrite and fires an action potential.
What is an inhibitory presynaptic potential?
Presynaptic inhibitory neurons are responsible for releasing certain neurotransmitters. Postsynaptic receptors are attached to neurons. As a result, the postsynaptic neuronal membrane’s sensitivity to certain ions will be altered.
What is the primary goal of an inhibitory postsynaptic potential?
The main goal and function of IPSP are not only to counteract but also to cancel out the excitatory state of EPSP.
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The inhibitory postsynaptic potential is a type of postsynaptic potential where the binding of neurotransmitters with the postsynaptic receptors causes the opening of ion channels. This results in hyperpolarization (or the net gain of negative charge across the membrane) and so, the firing of an action potential from the postsynaptic cell is less likely. In general, the resting potential of a neuron is about -70mV, and the firing threshold of an action potential is about -50mV. When there is a net gain of negative charge across the membrane of a postsynaptic neuron, the potential moves further to zero or away from the firing threshold. Hence, the postsynaptic potential is inhibitory as the probability to fire an action potential is reduced.
See also: excitatory postsynaptic potential
Hyperpolarization takes place when the current is created that alters the postsynaptic membrane potential to a greater negative value. Comparing the potential of the postsynaptic membrane and resting membrane it’s found that the postsynaptic membrane has a more negative charge as compared to the resting membrane.
An action potential can only be generated by depolarizing the postsynaptic membrane. It means the membrane potential must exceed the resting membrane potential by a voltage threshold. As a result, the IPSP hyperpolarizing currents of the postsynaptic membrane decrease the likelihood of adequate depolarization occurring to trigger an action potential in the postsynaptic neuron.
Depolarization is induced by IPSP and this can happen in between the resting threshold and action potential threshold due to the existence of reverse potential.
When there is the release of neurotransmitters into the synaptic cleft, it will increase the absorption of chloride ions. There is also the opening and binding of ligand-gated chloride ion channels and thus the chloride ion oozes out into the postsynaptic neuron. As these ions have a negative charge so hyperpolarisation occurs, decreasing the likelihood of a postsynaptic neuron generating an action potential. Microelectrodes can be used to monitor excitatory or inhibitory synapses’ postsynaptic potentials.
In general, an IPSP is inhibitory because it has a different combination and type of channel receptors on the postsynaptic reverse potential.
The excited or inhibition state of the action potential is dependent on:
- The threshold voltage of action potential
- The ion concentrations within and outside the cell
- The permeability of ionic channels
IPSPs try to maintain the potential of the membrane more negative in comparison to the action potential threshold, which is referred to as “transient hyperpolarization”. IPSPs and EPSPs contend with one another at a neuron’s multiple synapses. This parameter controls whether the action potential generated at the presynaptic terminal regenerates at the postsynaptic membrane. Gamma-aminobutyric acid and glycine are two neurotransmitters that are frequently involved in IPSPs.
IPSPs from this system can be temporally added to suprathreshold or subthreshold EPSPs. This is done to lower the magnitude of the final postsynaptic potential. When IPSPs (negative) and EPSPs (positive) are equivalent and get sum together, they will cancel the effect of each other. The equilibrium state of IPSPs and EPSPs is critical for the incorporation of excitatory and inhibitory synaptic information.
Inhibitory postsynaptic potential gets affected by the size of the neuron. Smaller neurons use simple temporal summation of postsynaptic potentials. A greater number of ionotropic receptors, synapses, and a greater distance between the synapse is the requirement of larger neurons. The soma allows for the extension of neural connections.
GABA is one of the prevalent neurotransmitters that are present in the adult mammalian retina and brain. It is involved in inhibitory postsynaptic potential. The receptors of GABA are pentamers. They are composed of three distinct subunits (α, β, γ). They are also some other additional subunits (δ, ε, θ, π, ρ) and forms are present. The open channels are porous to potassium and chloride ions selectively and allow their movement across the membrane.
Inhibitory receptors are classified into two types:
- Ionotropic receptors
- Metabotropic receptors
The activation of IPSP must have ionotropic receptors. In extracellular sites, the neurotransmitters are attached and help to activate the passage of ions. It permits the ions to pass through the postsynaptic cell membrane and it is composed of a membrane-spanning domain. Such type of receptor initiates postsynaptic activities within a few milliseconds of receiving an action potential from the presynaptic terminal. These channels affect the overall time and amplitude of postsynaptic potentials. Ionotropic receptors of GABA are involved in the binding of a variety of medicines. Additionally, alcohol also shows significant effects on ionotropic receptors of GABA.
G protein-coupled receptors are a type of metabotropic receptor which are used for the production of intracellular metabolites by transmitter binding mechanism. The binding of the G protein-coupled receptors with transmitters causes a configurational change in the receptor body. The three different proteins that make up the G protein-coupled receptor are activated by these configurational changes. The subunits of G protein alter the ion channels, significant reduction or increase in the activity of enzymes causes the production of intracellular messengers that activate the kinase’s activity. The important neurotransmitters such as glutamate, 5-HTT, and ACH, are used to stimulate the metabotropic receptors. The function of these neurotransmitters is also to activate the ionotropic receptors. The mammalian proteins stimulate metabotropic receptors.
IPSP has a wide range of applications in the real world. Postsynaptic neurons use a variety of receptors, G-proteins, and ion channels to communicate with one other. Drugs that modify neurotransmitter activities can cure neurological and psychological diseases.
For instance, investigations on opioid-mediated receptor desensitization of the brain’s locus coeruleus are being conducted. When an agonist is injected at a greater concentration for an extended period, hyperpolarization spikes and then diminishes. The more opioids required to treat pain, the greater the patient’s tolerance. The investigations are critical as they enable us to gain a better understanding of how to manage pain and also the responses to various medications used which are used to treat pain. By examining the pain tolerance, more effective pain treatments can be made.
Additionally, in the ventral tegmental region of dopamine neurons, research has been conducted and found these neurons are responsible for reward as well as movement and motivation. Dopamine neurons are highly excitable, resulting in a wide range of metabolic processes. Opioids decrease the release of GABA, reducing inhibition and allowing neurons to activate freely. Morphine and opioids are associated with IPSP as they stimulate dopamine neurons to disinhibit.
The input-output character and features of an inhibitory forebrain synapse are investigated by IPSPs. It also examines the learned behavior. The results demonstrate an excess of GABAergic activity in the thalamus. This is crucial because accurate sound localization requires exact spike timing in the ascending auditory pathways.
Additionally, basal ganglia of amphibians are examined by inhibitory postsynaptic potential. This is done to find out how motor performance is controlled by the striatum’s inhibitory outputs to the tectum and tegmentum. According to a study, visually directed behaviors may be controlled by the inhibitory striatal-tegmental circuit observed in frogs. In amphibians, the basal ganglia are critical for receiving olfactory, visual, mechanosensory, and auditory inputs. The disinhibitory striate-protecto-tectal circuit is critical for amphibians’ prey catching activities.
IPSP can be repressed by themselves in cerebellar Purkinje cells and CA1 pyramidal cells via a signaling pathway dubbed depolarized-induced suppression of inhibition (DSI). In the laboratory, step depolarizations of the soma have been utilized to generate DSIs, although synaptically generated depolarization of the dendrites can also be employed. DSIs can significantly reduce dendritic IPSP via direct depolarization.
Thus, IPSPs are advantageous for communication between the olfactory bulb and cortex. EPSPs are enhanced in exterior tufted cells by continuous sodium ion conductance. Low-voltage triggered calcium ion conductance increases the magnitude of EPSPs even further. The nonselective cation conductance induced by hyperpolarization lowers EPSP duration and summation and also converts inhibitory inputs to postsynaptic excitement. IPSPs enter when the membranes of tufted cells are depolarized, and IPSPs are then inhibited. IPSPs trigger action potentials at the resting threshold. GABA is required for the IPSPs to do the majority of their function in the exterior tufted cells.
In synaptic transmission, excitatory neurotransmitter glutamate is linked with EPSP. However, a study reveals that glutamate may also be employed for IPSP in neurons. This elucidates how metabotropic glutamate receptors trigger phosphoinositide hydrolysis in dopamine neurons via activated G proteins. Through calcium ion channels, the resulting products attach to inositol triphosphate (IP3) receptors. Calcium is derived from reserves and activates potassium conductance, resulting in the complete inhibition of dopamine cells. The fluctuating quantities of synaptically produced glutamate cause an excitement by activating ionotropic glutamate receptors, followed by suppression of metabotropic glutamate receptors.
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- The neuron and nervous system. (2022) Retrieved 22 April, 2022, from https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/the-synapse
- Techlab.bu.edu. (2022). EPSP IPSP. Retrieved 22 April, 2022, from http://techlab.bu.edu/resources/software_view/epsp_ipsp/index.html#:~:text=An%20inhibitory%20postsynaptic%20potentials%20(IPSP,dendrite%2C%20fires%20an%20action%20potential
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