Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors
Identifieur interne : 001009 ( PascalFrancis/Corpus ); précédent : 001008; suivant : 001010Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors
Auteurs : Diego Centonze ; Alessandro Usiello ; Paolo Gubellini ; Antonio Pisani ; Emiliana Borrelli ; Giorgio Bernardi ; Paolo CalabresiSource :
- Neuropsychopharmacology : (New York, NY) [ 0893-133X ] ; 2002.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 03-0073367 INIST |
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ET : | Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors |
AU : | CENTONZE (Diego); USIELLO (Alessandro); GUBELLINI (Paolo); PISANI (Antonio); BORRELLI (Emiliana); BERNARDI (Giorgio); CALABRESI (Paolo) |
AF : | Clinica Neurologica, Dipartimento di Neuroscienze, Università "Tor Vergata" and Fondazione Santa Lucia, IRCCS/Rome/Italie (1 aut., 3 aut., 4 aut., 6 aut., 7 aut.); Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS-INSERM-ULP, CU de Strasbourg/France (2 aut., 5 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neuropsychopharmacology : (New York, NY); ISSN 0893-133X; Coden NEROEW; Etats-Unis; Da. 2002; Vol. 27; No. 5; Pp. 723-726; Bibl. 17 ref. |
LA : | Anglais |
EA : | 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. |
CC : | 002A04F03B |
FD : | 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 |
FG : | Rodentia; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative |
ED : | D2 Dopamine receptor; Autoreceptor; Locus niger; Molecular form; Ventral tegmental area; Brain (vertebrata); Central nervous system; D2S dopamine receptor; Mechanism of action; Electrophysiology; Parkinson disease; Mouse; Animal |
EG : | Rodentia; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease |
SD : | Receptor dopaminérgico D2; Autoreceptor; Locus níger; Forma molecular; Area tegmental ventral; Encéfalo; Sistema nervioso central; Receptor dopaminérgico D2S; Mecanismo acción; Electrofisiología; Parkinson enfermedad; Ratón; Animal |
LO : | INIST-21601.354000102151020040 |
ID : | 03-0073367 |
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Pascal:03-0073367Le document en format XML
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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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<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>
<server><NO>PASCAL 03-0073367 INIST</NO>
<ET>Dopamine D2 receptor-mediated inhibition of dopaminergic neurons in mice lacking D2L receptors</ET>
<AU>CENTONZE (Diego); USIELLO (Alessandro); GUBELLINI (Paolo); PISANI (Antonio); BORRELLI (Emiliana); BERNARDI (Giorgio); CALABRESI (Paolo)</AU>
<AF>Clinica Neurologica, Dipartimento di Neuroscienze, Università "Tor Vergata" and Fondazione Santa Lucia, IRCCS/Rome/Italie (1 aut., 3 aut., 4 aut., 6 aut., 7 aut.); Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS-INSERM-ULP, CU de Strasbourg/France (2 aut., 5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuropsychopharmacology : (New York, NY); ISSN 0893-133X; Coden NEROEW; Etats-Unis; Da. 2002; Vol. 27; No. 5; Pp. 723-726; Bibl. 17 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A04F03B</CC>
<FD>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</FD>
<FG>Rodentia; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>D2 Dopamine receptor; Autoreceptor; Locus niger; Molecular form; Ventral tegmental area; Brain (vertebrata); Central nervous system; D2S dopamine receptor; Mechanism of action; Electrophysiology; Parkinson disease; Mouse; Animal</ED>
<EG>Rodentia; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Receptor dopaminérgico D2; Autoreceptor; Locus níger; Forma molecular; Area tegmental ventral; Encéfalo; Sistema nervioso central; Receptor dopaminérgico D2S; Mecanismo acción; Electrofisiología; Parkinson enfermedad; Ratón; Animal</SD>
<LO>INIST-21601.354000102151020040</LO>
<ID>03-0073367</ID>
</server>
</inist>
</record>
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