Interaction of adenosine receptors with other receptors from therapeutic perspective in Parkinson's disease.
Identifieur interne : 000807 ( PubMed/Corpus ); précédent : 000806; suivant : 000808Interaction of adenosine receptors with other receptors from therapeutic perspective in Parkinson's disease.
Auteurs : Nicolas Morin ; Thérèse Di PaoloSource :
- International review of neurobiology [ 0074-7742 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (therapeutic use), Basal Ganglia (pathology), Dyskinesia, Drug-Induced (pathology), GABAergic Neurons (drug effects), GABAergic Neurons (metabolism), Humans, Levodopa (adverse effects), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (therapy), Receptors, Dopamine (metabolism), Receptors, Metabotropic Glutamate (metabolism), Receptors, Purinergic P1 (metabolism).
- MESH :
- chemical , adverse effects : Levodopa.
- chemical , metabolism : Receptors, Dopamine, Receptors, Metabotropic Glutamate, Receptors, Purinergic P1.
- chemical , therapeutic use : Antiparkinson Agents.
- drug effects : GABAergic Neurons.
- metabolism : GABAergic Neurons, Parkinson Disease.
- pathology : Basal Ganglia, Dyskinesia, Drug-Induced, Parkinson Disease.
- therapy : Parkinson Disease.
- Animals, Humans.
Abstract
Altered dopaminergic neurotransmission in the basal ganglia is observed in Parkinson's disease (PD) and L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesias (LID). An attractive alternative for treating LID is to use adjunct drugs to modulate nondopaminergic neurotransmitter systems in the basal ganglia. For example, adenosine receptors have received attention over the past years for the treatment of PD and LID. Adenosine interacts closely with dopamine and plays an important role in the function of striatal GABAergic efferent neurons. Excitatory glutamatergic neurotransmission is also modulated by adenosine in the striatum. Hence, based on the unique cellular and regional distribution of this system, adenosine neurotransmission could have an important implication for the development of new therapeutic strategies targeting the basal ganglia disorders. Indeed, A2A adenosine receptor antagonists were shown to improve motor deficits in PD and to reduce the severity of LID. A2A receptor subtypes are selectively found on striatopallidal neurons and can couple with receptors of interest in PD, such as D2 dopamine and metabotropic glutamate receptor type 5 (mGlu5) receptors, and form functional heteromeric complexes. This chapter will review relevant studies investigating the role and contribution of adenosine receptor subtypes in pathophysiology of PD and LID. The interactions of adenosine receptors, especially A1 and A2A receptor subtypes, with other receptors implicated in the pathophysiology of PD and LID such as dopaminergic and glutamatergic receptors will be reviewed. The implication of these interactions in the development and expression of PD symptoms and LID needs further investigation to find novel drug targets.
DOI: 10.1016/B978-0-12-801022-8.00007-6
PubMed: 25175965
Links to Exploration step
pubmed:25175965Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interaction of adenosine receptors with other receptors from therapeutic perspective in Parkinson's disease.</title><author><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name><affiliation><nlm:affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec, Quebec, Canada; Faculty of Pharmacy, Laval University, Quebec, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><affiliation><nlm:affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec, Quebec, Canada; Faculty of Pharmacy, Laval University, Quebec, Quebec, Canada. Electronic address: therese.dipaolo@crchul.ulaval.ca.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25175965</idno><idno type="pmid">25175965</idno><idno type="doi">10.1016/B978-0-12-801022-8.00007-6</idno><idno type="wicri:Area/PubMed/Corpus">000807</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000807</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Interaction of adenosine receptors with other receptors from therapeutic perspective in Parkinson's disease.</title><author><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name><affiliation><nlm:affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec, Quebec, Canada; Faculty of Pharmacy, Laval University, Quebec, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><affiliation><nlm:affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec, Quebec, Canada; Faculty of Pharmacy, Laval University, Quebec, Quebec, Canada. Electronic address: therese.dipaolo@crchul.ulaval.ca.</nlm:affiliation></affiliation></author></analytic><series><title level="j">International review of neurobiology</title><idno type="ISSN">0074-7742</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (therapeutic use)</term><term>Basal Ganglia (pathology)</term><term>Dyskinesia, Drug-Induced (pathology)</term><term>GABAergic Neurons (drug effects)</term><term>GABAergic Neurons (metabolism)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (therapy)</term><term>Receptors, Dopamine (metabolism)</term><term>Receptors, Metabotropic Glutamate (metabolism)</term><term>Receptors, Purinergic P1 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Dopamine</term><term>Receptors, Metabotropic Glutamate</term><term>Receptors, Purinergic P1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>GABAergic Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>GABAergic Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</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">Altered dopaminergic neurotransmission in the basal ganglia is observed in Parkinson's disease (PD) and L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesias (LID). An attractive alternative for treating LID is to use adjunct drugs to modulate nondopaminergic neurotransmitter systems in the basal ganglia. For example, adenosine receptors have received attention over the past years for the treatment of PD and LID. Adenosine interacts closely with dopamine and plays an important role in the function of striatal GABAergic efferent neurons. Excitatory glutamatergic neurotransmission is also modulated by adenosine in the striatum. Hence, based on the unique cellular and regional distribution of this system, adenosine neurotransmission could have an important implication for the development of new therapeutic strategies targeting the basal ganglia disorders. Indeed, A2A adenosine receptor antagonists were shown to improve motor deficits in PD and to reduce the severity of LID. A2A receptor subtypes are selectively found on striatopallidal neurons and can couple with receptors of interest in PD, such as D2 dopamine and metabotropic glutamate receptor type 5 (mGlu5) receptors, and form functional heteromeric complexes. This chapter will review relevant studies investigating the role and contribution of adenosine receptor subtypes in pathophysiology of PD and LID. The interactions of adenosine receptors, especially A1 and A2A receptor subtypes, with other receptors implicated in the pathophysiology of PD and LID such as dopaminergic and glutamatergic receptors will be reviewed. The implication of these interactions in the development and expression of PD symptoms and LID needs further investigation to find novel drug targets.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25175965</PMID><DateCreated><Year>2014</Year><Month>09</Month><Day>01</Day></DateCreated><DateCompleted><Year>2015</Year><Month>05</Month><Day>12</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0074-7742</ISSN><JournalIssue CitedMedium="Internet"><Volume>119</Volume><PubDate><Year>2014</Year></PubDate></JournalIssue><Title>International review of neurobiology</Title><ISOAbbreviation>Int. Rev. Neurobiol.</ISOAbbreviation></Journal><ArticleTitle>Interaction of adenosine receptors with other receptors from therapeutic perspective in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>151-67</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/B978-0-12-801022-8.00007-6</ELocationID><ELocationID EIdType="pii" ValidYN="Y">B978-0-12-801022-8.00007-6</ELocationID><Abstract><AbstractText>Altered dopaminergic neurotransmission in the basal ganglia is observed in Parkinson's disease (PD) and L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesias (LID). An attractive alternative for treating LID is to use adjunct drugs to modulate nondopaminergic neurotransmitter systems in the basal ganglia. For example, adenosine receptors have received attention over the past years for the treatment of PD and LID. Adenosine interacts closely with dopamine and plays an important role in the function of striatal GABAergic efferent neurons. Excitatory glutamatergic neurotransmission is also modulated by adenosine in the striatum. Hence, based on the unique cellular and regional distribution of this system, adenosine neurotransmission could have an important implication for the development of new therapeutic strategies targeting the basal ganglia disorders. Indeed, A2A adenosine receptor antagonists were shown to improve motor deficits in PD and to reduce the severity of LID. A2A receptor subtypes are selectively found on striatopallidal neurons and can couple with receptors of interest in PD, such as D2 dopamine and metabotropic glutamate receptor type 5 (mGlu5) receptors, and form functional heteromeric complexes. This chapter will review relevant studies investigating the role and contribution of adenosine receptor subtypes in pathophysiology of PD and LID. The interactions of adenosine receptors, especially A1 and A2A receptor subtypes, with other receptors implicated in the pathophysiology of PD and LID such as dopaminergic and glutamatergic receptors will be reviewed. The implication of these interactions in the development and expression of PD symptoms and LID needs further investigation to find novel drug targets.</AbstractText><CopyrightInformation>© 2014 Elsevier Inc. 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