biology

Kainate receptor

Kainate receptor is a biology topic covered in the lgStudy science library. This page brings together a partial reference excerpt, illustrations, worked examples, real-world applications and a short study plan, so you can understand Kainate receptor rather than just read about it. In short: Kainate receptors, or kainic acid receptors (KARs), are ionotropic receptors that respond to the neurotransmitter glutamate. They were first identified as a distinct receptor type through their selective activation by the agonist kainate, a drug first isolated from the algae Digenea simplex.

Key takeaways

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Reproduce the core statement of Kainate receptor from memory before moving on to harder problems.

Reference excerpt

Kainate receptors, or kainic acid receptors (KARs), are ionotropic receptors that respond to the neurotransmitter glutamate. They were first identified as a distinct receptor type through their selective activation by the agonist kainate, a drug first isolated from the algae Digenea simplex. They have been traditionally classified as a non-NMDA-type receptor, along with the AMPA receptor. KARs are less understood than AMPA and NMDA receptors, the other ionotropic glutamate receptors. Postsynaptic kainate receptors are involved in excitatory neurotransmission. Presynaptic kainate receptors have been implicated in inhibitory neurotransmission by modulating release of the inhibitory neurotransmitter GABA through a presynaptic mechanism.

Structure There are five types of kainate receptor subunits, GluR5 (GRIK1), GluR6 (GRIK2), GluR7 (GRIK3), KA1 (GRIK4) and KA2 (GRIK5), which are similar to AMPA and NMDA receptor subunits and can be arranged in different ways to form a tetramer, a four subunit receptor. GluR5-7 can form homomers (ex. a receptor composed entirely of GluR5) and heteromers (ex. a receptor composed of both GluR5 and GluR6), however, KA1 and KA2 can only form functional receptors by combining with one of the GluR5-7 subunits. Since 2009 the kainate receptor subunits have been renamed to correspond with their gene name. Hence GluR5-7 are now GluK1-3 and KA1 and KA2 are GluK4 and GluK5, respectively. Each KAR subunit begins with a 400-residue extracellular N-terminal domain, which plays a key role in assembly, followed by the first segment of the neurotransmitter-binding cleft, called S1. This segment then passes through the cell membrane, forming the first of three membrane-spanning regions, M1. The M2 segment then begins on the cytoplasmic face of the membrane, pushes into the cell membrane about halfway, and then dips back out to the cytoplasm. This segment, termed the "p loop," determines the calcium permeability of the receptor. M2 turns into M3, another transmembrane segment which emerges on the extracellular face to complete the neurotransmitter binding site (a portion called S2). M4 begins extracellularly, and passes again through the membrane into the cytoplasm, forming the C-terminal of the protein. Differences in the ligand binding pocket allow for the development of moderately subunit-selective kainate receptor agonists and antagonists.

Conductance The ion channel formed by kainate receptors is permeable to sodium and potassium ions. The single channel conductance of kainate receptor channels is similar to that of AMPA channels, at about 20 pS. However, rise and decay times for postsynaptic potentials generated by KARs are slower than for AMPA postsynaptic potentials. Their permeability to Ca2+ is usually very slight but varies with subunits and RNA editing at the tip of the p loop.

Heteromers Many kainate receptors appear to exist as heteromers. The 'high-affinity' subunits GluK4 and GluK5 can only form functional channels as heteromers with 'low-affinity' subunits (GluK1-3).

Roles Kainate receptors have both presynaptic and postsynaptic actions. They have a somewhat more limited distribution in the brain than AMPA and NMDA receptors, and their function is less well defined. The convulsant kainic acid induces seizures, in part, by activation of kainate receptors containing the GluK2 subunit and also probably via AMPA receptors Activation of kainate receptors containing the GluK1 subunit can also induce seizures but deletion of this subunit does not reduce seizure susceptibility to kainate or in other seizure models. Deletion of either GluK1 or GluK2 does not alter kindling epileptogenesis or the expression of kindled seizures. Recent investigation through voltage clamping has shown that kainate receptors have more than just an ionotropic (or directly changing a membrane's conductivity) role in neurons. The metabotropic (or indirect through secondary protein pathways) effect has been verified through many accessory proteins and sustained current through G-protein cascades. The specific link of this pathway remains to be found, as well as the explanation for why the polarization and distribution of KARs varies so much across neurons and brain regions. The proteins have been shown to pace the receptors and help explain KAR's role in maturation of neural circuits during development. One of the larger connections and roles that kainate receptors have been shown to have is to several neurological diseases and conditions. KAR expression and distribution has shown a linkage to schizophrenia, depression, autism, Huntington's, bipolar disorder, and epilepsy among others. Most come through mutations of GluK1-5. The causation is unclear and the subject of further investigation.

Plasticity Unlike AMPA receptors, kainate receptors play only a minor role in signaling at synapses. Kainate receptors have a subtle role in synaptic plasticity, affecting the likelihood that the postsynaptic cell will fire in response to future stimulation. Activating kainate receptors in the presynaptic cell can affect the amount of neurotransmitters that are released This effect may occur quickly and last for a long time, and the effects of repetitive stimulation of KARs can be additive over time.

Ligands

Agonists 5-Iodowillardiine ATPA Domoic acid Glutamic acid (glutamate) – the endogenous agonist Kainic acid – the agonist after which the receptor is named LY-339,434 SYM-2081

Antagonists CNQX DNQX Ethanol – non-selective NS102 Kynurenic acid – endogenous ligand Tezampanel – also an AMPAR antagonist UBP-302 UBP-310 UBP-316 (ACET) Theanine

See also NMDA receptor AMPA receptor Long term potentiation

References

External links Kainate+Receptor at the U.S. National Library of Medicine Medical Subject Headings (MeSH)

Illustrations

Worked examples

Example 1 — a first encounter with Kainate receptor

Start with the simplest possible case. Write down what Kainate receptor claims or describes in one sentence, then invent the smallest concrete situation in which that sentence is true. In biology, the smallest case is usually a single object, a single equation or a single measurement. Check that every symbol or term in your sentence has a meaning in that case.

Example 2 — changing one variable

Take the situation from Example 1 and change exactly one quantity: double it, halve it, or set it to zero. Predict what should happen to Kainate receptor before you calculate. Comparing your prediction with the result is the fastest way to find out whether you understand the idea or only the words.

Example 3 — an exam-style question

Typical questions about Kainate receptor ask you to (a) state it precisely, (b) apply it to given data, and (c) explain a limitation. Practise writing all three answers in under five minutes; the third part is what separates a full-mark answer from an average one.

Applications of Kainate receptor

In research: Kainate receptor appears in biology research whenever the underlying quantities have to be modelled precisely. Papers usually cite it as a starting assumption and then explore where it breaks down.
In technology and industry: Engineering practice reuses Kainate receptor in design rules, simulations and safety margins. Knowing the idea lets you read a specification sheet and understand why the numbers look the way they do.
In the classroom: Kainate receptor is common in secondary-school and first-year university syllabi. It links to neighbouring topics Cell signaling, Glutamate (neurotransmitter), Ionotropic glutamate receptors, so understanding it makes those chapters shorter.
In everyday life: Look for Kainate receptor outside the textbook — in sport, cooking, traffic, electronics or the sky above you. An example you found yourself is remembered far longer than one you were given.

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How to study Kainate receptor in 20 minutes

Read the reference excerpt below once, without taking notes.
Close the page and write down what Kainate receptor means in your own words.
Compare your version with the excerpt and mark what you missed.
Work through the three examples above with pen and paper.
Explain Kainate receptor out loud to somebody else — or to Teacher Smith in the lgStudy chat.

Frequently asked questions

What is Kainate receptor in simple terms?

Why does Kainate receptor matter?

Because it connects several biology ideas at once: it gives you a definition you can apply, a quantity you can calculate, and a way to check whether a result is plausible.

How should I study Kainate receptor?

Read the excerpt, restate it from memory, then work through the examples and applications listed on this page. The five-step study plan above takes about twenty minutes.

What does this page cover?

It gives you a compact reference excerpt plus original lgStudy explanations, examples, applications and study material on Kainate receptor.