GABA receptor: Difference between revisions
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== Function == | == Function == | ||
It has been found that GABAB receptors provide an inhibitory function through the coupling to G-proteins and the recruitment of second messengers (Bettler, 2004). Presynaptic GABAB receptors effectively repress the influx of calcium ions (Ca2+) via the inhibition of voltage gated Ca2+ channels through the activation of Gβγ subunits (Bettler, 2004). Postsynaptic GABAB receptors then activate the opening of potassium ion (K+) channels, again through the activation of Gβγ subunits (Bettler, 2004). The efflux of potassium ions results in the hyperpolarization of the neuronal membrane due to the greatly negative Nernst value of potassium in cerebrospinal fluid. This hyperpolarization of the neuronal membrane causes the neuron’s membrane potential to move away from threshold, thus inhibiting the gaba neuronal function (Bettler, 2004). This functions in opposition of the GABAA receptor to control and slow the inhibitory postsynaptic potentials (Cryan, 2005). Aside from the interaction with ion channels, GABAB receptors also inhibit adenylyl cyclase through the Giα/Goα subunits and activate adenylyl cyclase through Gβγ subunits (Bettler, 2004). It has been found that the Giα/Goα subunits inhibit adenylyl cyclase types I, III, V, and VI (Bettler, 2004). Additionally, the Gβγ subunits stimulates adenylyl cyclase types II, IV, and VII (Bettler, 2004). This control of adenylyl cyclase is expected to control neuronal function for a longer period of time compared to the control via ion channels (Geng, 2013). The GABAB1 sushi domains are axonal trafficking signals that help to localize the receptors to glutmatergic terminals (Cryan 2005). | |||
== Disease == | == Disease == |
Revision as of 22:03, 9 November 2015
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GABA receptors are proteins utilized for the primary inhibitory neurotransmitter in vertebrate central nervous systems, gamma-aminobutyric acid or GABA (Kerr, 1995). GABA has been found to be formed using the synthesizing enzyme, L-glutamic acid carboxylase, or GAD (Lloyd, 1983). Additionally, GABA has found to be synthesized via the excitatory neurotransmitter glutamate. GABA receptors regulate synaptic transmission via the opening of ion channels, causing membrane hyperpolarization and the inhibition of further signal transmission.
StructureStructure
FunctionFunction
It has been found that GABAB receptors provide an inhibitory function through the coupling to G-proteins and the recruitment of second messengers (Bettler, 2004). Presynaptic GABAB receptors effectively repress the influx of calcium ions (Ca2+) via the inhibition of voltage gated Ca2+ channels through the activation of Gβγ subunits (Bettler, 2004). Postsynaptic GABAB receptors then activate the opening of potassium ion (K+) channels, again through the activation of Gβγ subunits (Bettler, 2004). The efflux of potassium ions results in the hyperpolarization of the neuronal membrane due to the greatly negative Nernst value of potassium in cerebrospinal fluid. This hyperpolarization of the neuronal membrane causes the neuron’s membrane potential to move away from threshold, thus inhibiting the gaba neuronal function (Bettler, 2004). This functions in opposition of the GABAA receptor to control and slow the inhibitory postsynaptic potentials (Cryan, 2005). Aside from the interaction with ion channels, GABAB receptors also inhibit adenylyl cyclase through the Giα/Goα subunits and activate adenylyl cyclase through Gβγ subunits (Bettler, 2004). It has been found that the Giα/Goα subunits inhibit adenylyl cyclase types I, III, V, and VI (Bettler, 2004). Additionally, the Gβγ subunits stimulates adenylyl cyclase types II, IV, and VII (Bettler, 2004). This control of adenylyl cyclase is expected to control neuronal function for a longer period of time compared to the control via ion channels (Geng, 2013). The GABAB1 sushi domains are axonal trafficking signals that help to localize the receptors to glutmatergic terminals (Cryan 2005).
DiseaseDisease
RelevanceRelevance
Structural highlightsStructural highlights
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