Integrating neurotransmission in striatal medium spiny neurons.
Identifieur interne : 001118 ( Main/Curation ); précédent : 001117; suivant : 001119Integrating neurotransmission in striatal medium spiny neurons.
Auteurs : Jean-Antoine Girault [France]Source :
- Advances in experimental medicine and biology [ 0065-2598 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Cell Nucleus (genetics), Cell Nucleus (metabolism), Cerebral Cortex (physiology), Corpus Striatum (physiology), Dopamine (metabolism), Dopamine and cAMP-Regulated Phosphoprotein 32 (genetics), Dopamine and cAMP-Regulated Phosphoprotein 32 (metabolism), Epigenesis, Genetic (physiology), Extracellular Signal-Regulated MAP Kinases (genetics), Extracellular Signal-Regulated MAP Kinases (metabolism), Gene Expression (physiology), Glutamic Acid (metabolism), Humans, Motivation (physiology), Neuronal Plasticity (physiology), Neurons (physiology), Parkinson Disease (genetics), Parkinson Disease (metabolism), Receptors, Dopamine D2 (genetics), Receptors, Dopamine D2 (metabolism), Receptors, Glutamate (genetics), Receptors, Glutamate (metabolism), Synapses (genetics), Synapses (metabolism), Synaptic Transmission (physiology), Thalamus (physiology).
- MESH :
- chemical , genetics : Dopamine and cAMP-Regulated Phosphoprotein 32, Extracellular Signal-Regulated MAP Kinases, Receptors, Dopamine D2, Receptors, Glutamate.
- chemical , metabolism : Dopamine, Dopamine and cAMP-Regulated Phosphoprotein 32, Extracellular Signal-Regulated MAP Kinases, Glutamic Acid, Receptors, Dopamine D2, Receptors, Glutamate.
- genetics : Cell Nucleus, Parkinson Disease, Synapses.
- metabolism : Cell Nucleus, Parkinson Disease, Synapses.
- physiology : Cerebral Cortex, Corpus Striatum, Epigenesis, Genetic, Gene Expression, Motivation, Neuronal Plasticity, Neurons, Synaptic Transmission, Thalamus.
- Animals, Humans.
Abstract
The striatum is a major entry structure of the basal ganglia. Its role in information processing in close interaction with the cerebral cortex and thalamus has various behavioral consequences depending on the regions concerned, including control of body movements and motivation. A general feature of striatal information processing is the control by reward-related dopamine signals of glutamatergic striatal inputs and of their plasticity. This relies on specific sets of receptors and signaling proteins in medium-sized spiny neurons which belong to two groups, striatonigral and striatopallidal neurons. Some signaling pathways are activated only by dopamine or glutamate, but many provide multiple levels of interactions. For example, the cAMP pathway is mostly regulated by dopamine D1 receptors in striatonigral neurons, whereas the ERK pathway detects a combination of glutamate and dopamine signals and is essential for long-lasting modifications. These adaptations require changes in gene expression, and the signaling pathways linking synaptic activity to nuclear function and epigenetic changes are beginning to be deciphered. Their alteration underlies many aspects of striatal dysfunction in pathological conditions which include a decrease or an increase in dopamine transmission, as encountered in Parkinson's disease or exposure to addictive drugs, respectively.
DOI: 10.1007/978-3-7091-0932-8_18
PubMed: 22351066
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pubmed:22351066Le document en format XML
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(genetics)</term><term>Receptors, Glutamate (metabolism)</term><term>Synapses (genetics)</term><term>Synapses (metabolism)</term><term>Synaptic Transmission (physiology)</term><term>Thalamus (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dopamine and cAMP-Regulated Phosphoprotein 32</term><term>Extracellular Signal-Regulated MAP Kinases</term><term>Receptors, Dopamine D2</term><term>Receptors, Glutamate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Dopamine and cAMP-Regulated Phosphoprotein 32</term><term>Extracellular Signal-Regulated MAP Kinases</term><term>Glutamic Acid</term><term>Receptors, Dopamine D2</term><term>Receptors, Glutamate</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Nucleus</term><term>Parkinson Disease</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Nucleus</term><term>Parkinson Disease</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cerebral Cortex</term><term>Corpus Striatum</term><term>Epigenesis, Genetic</term><term>Gene Expression</term><term>Motivation</term><term>Neuronal Plasticity</term><term>Neurons</term><term>Synaptic Transmission</term><term>Thalamus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The striatum is a major entry structure of the basal ganglia. Its role in information processing in close interaction with the cerebral cortex and thalamus has various behavioral consequences depending on the regions concerned, including control of body movements and motivation. A general feature of striatal information processing is the control by reward-related dopamine signals of glutamatergic striatal inputs and of their plasticity. This relies on specific sets of receptors and signaling proteins in medium-sized spiny neurons which belong to two groups, striatonigral and striatopallidal neurons. Some signaling pathways are activated only by dopamine or glutamate, but many provide multiple levels of interactions. For example, the cAMP pathway is mostly regulated by dopamine D1 receptors in striatonigral neurons, whereas the ERK pathway detects a combination of glutamate and dopamine signals and is essential for long-lasting modifications. These adaptations require changes in gene expression, and the signaling pathways linking synaptic activity to nuclear function and epigenetic changes are beginning to be deciphered. Their alteration underlies many aspects of striatal dysfunction in pathological conditions which include a decrease or an increase in dopamine transmission, as encountered in Parkinson's disease or exposure to addictive drugs, respectively.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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