ParkinsonFranceV1, PascalFrancis, Curation, bibRecord, 000425

Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors

Identifieur interne : 000425 ( PascalFrancis/Curation ); précédent : 000424; suivant : 000426

Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors

Auteurs : Diego Centonze [Italie] ; Alessandro Usiello [France] ; Paolo Gubellini [Italie] ; Antonio Pisani [Italie] ; Emiliana Borrelli [France] ; Giorgio Bernardi [Italie] ; Paolo Calabresi [Italie]

Source :

Neuropsychopharmacology : (New York, NY) [ 0893-133X ] ; 2002.

RBID : Pascal:03-0073367

Descripteurs français

Pascal (Inist)
- Récepteur dopaminergique D2, Autorécepteur, Locus niger, Forme moléculaire, Aire tegmentaire ventrale, Encéphale, Système nerveux central, Récepteur dopaminergique D2S, Mécanisme action, Electrophysiologie, Parkinson maladie, Souris, Animal.

English descriptors

KwdEn :
- Animal, Autoreceptor, Brain (vertebrata), Central nervous system, D2 Dopamine receptor, D2S dopamine receptor, Electrophysiology, Locus niger, Mechanism of action, Molecular form, Mouse, Parkinson disease, Ventral tegmental area.

Abstract

Two isoforms of the dopamine (DA) D2 receptor are generated from the same gene by alternative splicing, D2L and D2S. To identify which isoform is involved in the autoregulation of midbrain DA neuron activity, intracellular electrophysiological recordings were performed from substantia nigra and ventral tegmental area neurons of mice lacking either D2L(D2L -/-) or both D2L and D2S receptors (D2-/-). In midbrain DA neurons from wild-type mice, DA and quinpirole, a DA D2-like receptor agonist, produced a significant somatic membrane hyperpolarization, which led to a reversible inhibition of firing activity. Interestingly, this effect was fully abolished in D2 -/- neurons but still present in D2L -/- DA neurons. These data clearly show that D2S receptors are the main somatodendritic autoreceptors of central DA neurons. Thus, pharmacological compounds able to interfere selectively with presynaptic D2S receptors might constitute effective therapeutic strategies in neuropsychiatric disorders, by causing negligible side-effects.

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C01	`01`		`ENG`	@0 Two isoforms of the dopamine (DA) D2 receptor are generated from the same gene by alternative splicing, D2L and D2S. To identify which isoform is involved in the autoregulation of midbrain DA neuron activity, intracellular electrophysiological recordings were performed from substantia nigra and ventral tegmental area neurons of mice lacking either D2L(D2L -/-) or both D2L and D2S receptors (D2-/-). In midbrain DA neurons from wild-type mice, DA and quinpirole, a DA D2-like receptor agonist, produced a significant somatic membrane hyperpolarization, which led to a reversible inhibition of firing activity. Interestingly, this effect was fully abolished in D2 -/- neurons but still present in D2L -/- DA neurons. These data clearly show that D2S receptors are the main somatodendritic autoreceptors of central DA neurons. Thus, pharmacological compounds able to interfere selectively with presynaptic D2S receptors might constitute effective therapeutic strategies in neuropsychiatric disorders, by causing negligible side-effects.
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C07	`08`	`X`	`FRE`	`@0 Maladie dégénérative @5 73`
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N21				`@1 041`
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Pascal:03-0073367

Le document en format XML

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<term>D2S dopamine receptor</term>
<term>Electrophysiology</term>
<term>Locus niger</term>
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<front><div type="abstract" xml:lang="en">Two isoforms of the dopamine (DA) D2 receptor are generated from the same gene by alternative splicing, D2L and D2S. To identify which isoform is involved in the autoregulation of midbrain DA neuron activity, intracellular electrophysiological recordings were performed from substantia nigra and ventral tegmental area neurons of mice lacking either D2L(D2L -/-) or both D2L and D2S receptors (D2-/-). In midbrain DA neurons from wild-type mice, DA and quinpirole, a DA D2-like receptor agonist, produced a significant somatic membrane hyperpolarization, which led to a reversible inhibition of firing activity. Interestingly, this effect was fully abolished in D2 -/- neurons but still present in D2L -/- DA neurons. These data clearly show that D2S receptors are the main somatodendritic autoreceptors of central DA neurons. Thus, pharmacological compounds able to interfere selectively with presynaptic D2S receptors might constitute effective therapeutic strategies in neuropsychiatric disorders, by causing negligible side-effects.</div>
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<fA11 i1="07" i2="1"><s1>CALABRESI (Paolo)</s1>
</fA11>
<fA14 i1="01"><s1>Clinica Neurologica, Dipartimento di Neuroscienze, Università "Tor Vergata" and Fondazione Santa Lucia, IRCCS</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS-INSERM-ULP, CU de Strasbourg</s1>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</fA14>
<fA20><s1>723-726</s1>
</fA20>
<fA21><s1>2002</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>21601</s2>
<s5>354000102151020040</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2003 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>17 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>03-0073367</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Neuropsychopharmacology : (New York, NY)</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Two isoforms of the dopamine (DA) D2 receptor are generated from the same gene by alternative splicing, D2L and D2S. To identify which isoform is involved in the autoregulation of midbrain DA neuron activity, intracellular electrophysiological recordings were performed from substantia nigra and ventral tegmental area neurons of mice lacking either D2L(D2L -/-) or both D2L and D2S receptors (D2-/-). In midbrain DA neurons from wild-type mice, DA and quinpirole, a DA D2-like receptor agonist, produced a significant somatic membrane hyperpolarization, which led to a reversible inhibition of firing activity. Interestingly, this effect was fully abolished in D2 -/- neurons but still present in D2L -/- DA neurons. These data clearly show that D2S receptors are the main somatodendritic autoreceptors of central DA neurons. Thus, pharmacological compounds able to interfere selectively with presynaptic D2S receptors might constitute effective therapeutic strategies in neuropsychiatric disorders, by causing negligible side-effects.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A04F03B</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Récepteur dopaminergique D2</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>D2 Dopamine receptor</s0>
<s5>01</s5>
<s6>«D2» Dopamine receptor</s6>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Receptor dopaminérgico D2</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Autorécepteur</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Autoreceptor</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Autoreceptor</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Locus niger</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Locus niger</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Locus níger</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Forme moléculaire</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Molecular form</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Forma molecular</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Aire tegmentaire ventrale</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Ventral tegmental area</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Area tegmental ventral</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Brain (vertebrata)</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Récepteur dopaminergique D2S</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>D2S dopamine receptor</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Receptor dopaminérgico D2S</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Mécanisme action</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Mechanism of action</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Mecanismo acción</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Electrophysiologie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Electrophysiology</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Electrofisiología</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Souris</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Mouse</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Ratón</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Animal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Animal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Animal</s0>
<s5>15</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>69</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>69</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>69</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>70</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>70</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>70</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>71</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>71</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>71</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>72</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>72</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>72</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>73</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>73</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>73</s5>
</fC07>
<fN21><s1>041</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors

Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors

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