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20. Multiple Adenosine-Dopamine (A2A-D2 Like) Heteroreceptor Complexes in the Brain and Their Role in Schizophrenia

Author

Borroto-Escuela, Dasiel O., Ferraro, Luca, Narvaez, Manuel, Tanganelli, Sergio, Beggiato, Sarah, Liu, Fang, Rivera, Alicia, Fuxe, Kjell, [Borroto-Escuela,DO, Fuxe,K] Department of Neuroscience, Karolinska Institutet, Stockholm , Sweden. [Borroto-Escuela,DO] Observatorio Cubano de Neurociencias, Grupo Bohío-Estudio, Yaguajay, Cuba. [Ferraro,L, Beggiato,S] Department of Life sciences and Biotechnology, University of Ferrara, Ferrara, Italy. [Narvaez,M] Facultad de Medicina, Instituto de Investigacion de Málaga, Universidad de Malaga, Malaga, Spain. [Tanganelli,S] Department of Medical Sciences, University of Ferrara, Ferrara, Italy. [Liu,F] Campbell Research, Centre for Addiction and Mental Health Institute, University of Toronto, Toronto, Canada. [Rivera,A] Department of Cell Biology, University of Malaga, Instituto de Investigación Biomédica (IBIMA), Malaga, Spain., This work was supported by grants from Swedish Medical Research Council (Vetenskapsrådet, and 04X-715), from Parkinson Fonden to KF and from Hjärnfonden (2018-286 and 2019-296) to DOBE.

Subjects
A2A-D2 heteroreceptor complexes, Anatomy::Nervous System::Central Nervous System [Medical Subject Headings], Proteínas del núcleo viral, Farmacología, Brain, Receptor de adenosina A2A, Esquizofrenia, Anatomy::Nervous System::Central Nervous System::Brain [Medical Subject Headings], Chemicals and Drugs::Organic Chemicals::Amines::Biogenic Amines::Biogenic Monoamines::Catecholamines::Dopamine [Medical Subject Headings], Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings], Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Receptors, Cell Surface::Receptors, Purinergic::Receptors, Purinergic P1::Receptors, Adenosine A2::Receptor, Adenosine A2A [Medical Subject Headings], Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Receptors, Cell Surface::Receptors, G-Protein-Coupled::Receptors, Catecholamine::Receptors, Dopamine::Receptors, Dopamine D2 [Medical Subject Headings], Encéfalo, Novel pharmacology, Schizophrenia, Psychiatry and Psychology::Mental Disorders::Schizophrenia and Disorders with Psychotic Features::Schizophrenia [Medical Subject Headings], Heterobivalent drugs, Sigma 1 receptor, Adenosine receptors, Anatomy::Nervous System::Neurons [Medical Subject Headings]
Abstract

In the 1980s and 1990s, the concept was introduced that molecular integration in the Central Nervous System could develop through allosteric receptor-receptor interactions in heteroreceptor complexes presents in neurons. A number of adenosine-dopamine heteroreceptor complexes were identified that lead to the A2A-D2 heteromer hypothesis of schizophrenia. The hypothesis is based on strong antagonistic A2A-D2 receptor-receptor interactions and their presence in the ventral striato-pallidal GABA anti-reward neurons leading to reduction of positive symptoms. Other types of adenosine A2A heteroreceptor complexes are also discussed in relation to this disease, such as A2A-D3 and A2A-D4 heteroreceptor complexes as well as higher order A2A-D2-mGluR5 and A2A-D2-Sigma1R heteroreceptor complexes. The A2A receptor protomer can likely modulate the function of the D4 receptors of relevance for understanding cognitive dysfunction in schizophrenia. A2A-D2-mGluR5 complex is of interest since upon A2A/mGluR5 coactivation they appear to synergize in producing strong inhibition of the D2 receptor protomer. For understanding the future of the schizophrenia treatment, the vulnerability of the current A2A-D2like receptor complexes will be tested in animal models of schizophrenia. A2A-D2-Simag1R complexes hold the highest promise through Sigma1R enhancement of inhibition of D2R function. In line with this work, Lara proposed a highly relevant role of adenosine for neurobiology of schizophrenia. Yes

Published
2020

21. Multiple Adenosine-Dopamine (A2A-D2 Like) Heteroreceptor Complexes in the Brain and Their Role in Schizophrenia

Author

Borroto-Escuela, Dasiel O, Ferraro, Luca, Narvaez, Manuel, Tanganelli, Sergio, Beggiato, Sarah, Liu, Fang, Rivera, Alicia, and Fuxe, Kjell

Subjects
A2A-D2 heteroreceptor complexes, Central Nervous System, Neurons, heterobivalent drugs, Adenosine, Receptor, Adenosine A2A, Receptors, Dopamine D2, brain, Dopamine, Review, adenosine receptors, NO, schizophrenia, novel pharmacology, lcsh:Biology (General), mental disorders, Humans, sigma 1 receptor, lcsh:QH301-705.5
Abstract

In the 1980s and 1990s, the concept was introduced that molecular integration in the Central Nervous System could develop through allosteric receptor–receptor interactions in heteroreceptor complexes presents in neurons. A number of adenosine–dopamine heteroreceptor complexes were identified that lead to the A2A-D2 heteromer hypothesis of schizophrenia. The hypothesis is based on strong antagonistic A2A-D2 receptor–receptor interactions and their presence in the ventral striato-pallidal GABA anti-reward neurons leading to reduction of positive symptoms. Other types of adenosine A2A heteroreceptor complexes are also discussed in relation to this disease, such as A2A-D3 and A2A-D4 heteroreceptor complexes as well as higher order A2A-D2-mGluR5 and A2A-D2-Sigma1R heteroreceptor complexes. The A2A receptor protomer can likely modulate the function of the D4 receptors of relevance for understanding cognitive dysfunction in schizophrenia. A2A-D2-mGluR5 complex is of interest since upon A2A/mGluR5 coactivation they appear to synergize in producing strong inhibition of the D2 receptor protomer. For understanding the future of the schizophrenia treatment, the vulnerability of the current A2A-D2like receptor complexes will be tested in animal models of schizophrenia. A2A-D2-Simag1R complexes hold the highest promise through Sigma1R enhancement of inhibition of D2R function. In line with this work, Lara proposed a highly relevant role of adenosine for neurobiology of schizophrenia.

Published
2020

35. Understanding the Functional Plasticity in Neural Networks of the Basal Ganglia in Cocaine Use Disorder: A Role for Allosteric Receptor-Receptor Interactions in A2A-D2 Heteroreceptor Complexes

Author

Borroto-Escuela, Dasiel O., Wydra, Karolina, Pintsuk, Julia, Narvaez, Manuel, Corrales, Fidel, Zaniewska, Magdalena, Agnati, Luigi F., Franco, Rafael, Tanganelli, Sergio, Ferraro, Luca, Filip, Malgorzata, Fuxe, Kjell, [Borroto-Escuela, Dasiel O.] Karolinska Inst, Dept Neurosci, Retzius Vag 8, S-17177 Stockholm, Sweden, [Pintsuk, Julia] Karolinska Inst, Dept Neurosci, Retzius Vag 8, S-17177 Stockholm, Sweden, [Agnati, Luigi F.] Karolinska Inst, Dept Neurosci, Retzius Vag 8, S-17177 Stockholm, Sweden, [Fuxe, Kjell] Karolinska Inst, Dept Neurosci, Retzius Vag 8, S-17177 Stockholm, Sweden, [Borroto-Escuela, Dasiel O.] Univ Urbino, Physiol Sect, Dept Biomol Sci, Campus Sci Enrico Mattei,Via Cale Suore 2, I-61029 Urbino, Italy, [Borroto-Escuela, Dasiel O.] Observ Cubanos Neurociencias, Grp Bohio Estudio, Yaguajay, Cuba, [Corrales, Fidel] Observ Cubanos Neurociencias, Grp Bohio Estudio, Yaguajay, Cuba, [Wydra, Karolina] Polish Acad Sci, Inst Pharmacol, Lab Drug Addict Pharmacol, 12 Smetna St, PL-31343 Krakow, Poland, [Zaniewska, Magdalena] Polish Acad Sci, Inst Pharmacol, Lab Drug Addict Pharmacol, 12 Smetna St, PL-31343 Krakow, Poland, [Filip, Malgorzata] Polish Acad Sci, Inst Pharmacol, Lab Drug Addict Pharmacol, 12 Smetna St, PL-31343 Krakow, Poland, [Pintsuk, Julia] Univ Tartu, Inst Biomed & Translat Med, Dept Physiol, 19 Ravila St, EE-50411 Tartu, Estonia, [Narvaez, Manuel] Univ Malaga, Inst Invest Biomed Malaga, Fac Med, Malaga, Spain, [Corrales, Fidel] Univ Malaga, Inst Invest Biomed Malaga, Fac Med, Malaga, Spain, [Corrales, Fidel] Ctr Nacl Neurociencias, Havana, Cuba, [Franco, Rafael] Univ Barcelona, Fac Biol, Dept Bioquim & Biomed Mol, Barcelona, Spain, [Franco, Rafael] Ctr Invest Red Enfermedades Neurodegenerat CIBERN, Madrid, Spain, [Tanganelli, Sergio] Univ Ferrara, Dept Life Sci & Biotechnol, Ferrara, Italy, [Ferraro, Luca] Univ Ferrara, Dept Life Sci & Biotechnol, Ferrara, Italy, [Tanganelli, Sergio] Univ Ferrara, Dept Med Sci, Ferrara, Italy, Swedish Medical Research Council, AFA Forsakring, Hjarnfonden, and Institute of Pharmacology Polish Academy of Sciences (Krakow, Poland)

Subjects
D2 receptors, Modulation, Article Subject, Synaptic-transmission, Adenosine a(2a) receptors, Dopamine, Communication, Integrative mechanism, Glutamate, Proximity ligation assay, Higher-order oligomers
Abstract

Our hypothesis is that allosteric receptor-receptor interactions in homo- and heteroreceptor complexes may form the molecular basis of learning and memory. This principle is illustrated by showing how cocaine abuse can alter the adenosine A2AR-dopamine D2R heterocomplexes and their receptor-receptor interactions and hereby induce neural plasticity in the basal ganglia. Studies with A2AR ligands using cocaine self-administration procedures indicate that antagonistic allosteric A2AR-D2R heterocomplexes of the ventral striatopallidal GABA antireward pathway play a significant role in reducing cocaine induced reward, motivation, and cocaine seeking. Anticocaine actions of A2AR agonists can also be produced at A2AR homocomplexes in these antireward neurons, actions in which are independent of D2R signaling. At the A2AR-D2R heterocomplex, they are dependent on the strength of the antagonistic allosteric A2AR-D2R interaction and the number of A2AR-D2R and A2AR-D2R-sigma1R heterocomplexes present in the ventral striatopallidal GABA neurons. It involves a differential cocaine-induced increase in sigma1Rs in the ventral versus the dorsal striatum. In contrast, the allosteric brake on the D2R protomer signaling in the A2AR-D2R heterocomplex of the dorsal striatopallidal GABA neurons is lost upon cocaine self-administration. This is potentially due to differences in composition and allosteric plasticity of these complexes versus those in the ventral striatopallidal neurons.

Published
2016

38. Acute Cocaine Enhances Dopamine D2R Recognition and Signaling and Counteracts D2R Internalization in Sigma1R-D2R Heteroreceptor Complexes.

Author

Borroto-Escuela, Dasiel O., Narváez, Manuel, Romero-Fernández, Wilber, Pinton, Luca, Wydra, Karolina, Filip, Malgorzata, Beggiato, Sarah, Tanganelli, Sergio, Ferraro, Luca, and Fuxe, Kjell

Abstract

The current study was performed to establish the actions of nanomolar concentrations of cocaine, not blocking the dopamine transporter, on dopamine D2 receptor (D2R)-sigma 1 receptor (δ1R) heteroreceptor complexes and the D2R protomer recognition, signaling and internalization in cellular models. We report the existence of D2R-δ1R heteroreceptor complexes in subcortical limbic areas as well as the dorsal striatum, with different distribution patterns using the in situ proximity ligation assay. Also, through BRET, these heteromers were demonstrated in HEK293 cells. Furthermore, saturation binding assay demonstrated that in membrane preparations of HEK293 cells coexpressing D2R and δ1R, cocaine (1 nM) significantly increased the D2R Bmax values over cells singly expressing D2R. CREB reporter luc-gene assay indicated that coexpressed δ1R significantly reduced the potency of the D2R-like agonist quinpirole to inhibit via D2R activation the forskolin induced increase of the CREB signal. In contrast, the addition of 100 nM cocaine was found to markedly increase the quinpirole potency to inhibit the forskolin-induced increase of the CREB signal in the D2R-δ1R cells. These events were associated with a marked reduction of cocaine-induced internalization of D2R protomers in D2R-δ1R heteromer-containing cells vs D2R singly expressing cells as studied by means of confocal analysis of D2R-δ1R trafficking and internalization. Overall, the formation of D2R-δ1R heteromers enhanced the ability of cocaine to increase the D2R protomer function associated with a marked reduction of its internalization. The existence of D2R-δ1R heteromers opens up a new understanding of the acute actions of cocaine. [ABSTRACT FROM AUTHOR]

Published
2019
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42. Brain Dopamine Transmission in Health and Parkinson's Disease: Modulation of Synaptic Transmission and Plasticity Through Volume Transmission and Dopamine Heteroreceptors.

Author

Borroto-Escuela, Dasiel O., Perez De La Mora, Miguel, Manger, Paul, Narváez, Manuel, Beggiato, Sarah, Crespo-Ramírez, Minerva, Navarro, Gemma, Wydra, Karolina, Díaz-Cabiale, Zaida, Rivera, Alicia, Ferraro, Luca, Tanganelli, Sergio, Filip, Małgorzata, Franco, Rafael, and Fuxe, Kjell

Published
2018
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48. Palmitoylethanolamide Blunts Amyloid-β42-Induced Astrocyte Activation and Improves Neuronal Survival in Primary Mouse Cortical Astrocyte-Neuron Co-Cultures.

Author

Beggiato, Sarah, Borelli, Andrea Celeste, Ferraro, Luca, Tanganelli, Sergio, Antonelli, Tiziana, and Tomasini, Maria Cristina

Subjects
AMYLOID, GLYCOPROTEINS, ASTROCYTES, ALZHEIMER'S disease, NEURONS, NEURAL physiology, ANALYSIS of variance, ANIMAL populations, ANIMALS, CELL culture, CELL physiology, CELLS, CEREBRAL cortex, ETHANOLAMINES, FATTY acids, RESEARCH methodology, MICE, NERVE tissue proteins, NONSTEROIDAL anti-inflammatory agents, PEPTIDES, TIME, TISSUE culture, PHARMACODYNAMICS
Abstract

Background: Based on the pivotal role of astrocytes in brain homeostasis and the strong metabolic cooperation existing between neurons and astrocytes, it has been suggested that astrocytic dysfunctions might cause and/or contribute to neuroinflammation and neurodegenerative processes. Therapeutic approaches aimed at both neuroprotection and neuroinflammation reduction may prove particularly effective in slowing the progression of these diseases. The endogenous lipid mediator palmitoylethanolamide (PEA) displayed neuroprotective and anti(neuro)inflammatory properties, and demonstrated interesting potential as a novel treatment for Alzheimer's disease.Objective and Methods: We firstly evaluated whether astrocytes could participate in regulating the Aβ42-induced neuronal damage, by using primary mouse astrocytes cell cultures and mixed astrocytes-neurons cultures. Furthermore, the possible protective effects of PEA against Aβ42-induced neuronal toxicity have also been investigated by evaluating neuronal viability, apoptosis, and morphometric parameters.Results: The presence of astrocytes pre-exposed to Aβ42 (0.5μM; 24 h) induced a reduction of neuronal viability in primary mouse astrocytes-neurons co-cultures. Furthermore, under these experimental conditions, an increase in the number of neuronal apoptotic nuclei and a decrease in the number of MAP-2 positive neurons were observed. Finally, astrocytic Aβ42 pre-exposure induced an increase in the number of neurite aggregations/100μm as compared to control (i.e., untreated) astrocytes-neurons co-cultures. These effects were not observed in neurons cultured in the presence of astrocytes pre-exposed to PEA (0.1μM), applied 1 h before and maintained during Aβ42 treatment.Conclusion: Astrocytes contribute to Aβ42-induced neurotoxicity and PEA, by blunting Aβ42-induced astrocyte activation, improved neuronal survival in mouse astrocyte-neuron co-cultures. [ABSTRACT FROM AUTHOR]

Published
2018
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