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Movement Disorders (revue)

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Characterisation of striatal NMDA receptors involved in the generation of Parkinsonian symptoms: Intrastriatal microinjection studies in the 6-OHDA-lesioned rat

Identifieur interne : 000602 ( PascalFrancis/Curation ); précédent : 000601; suivant : 000603

Characterisation of striatal NMDA receptors involved in the generation of Parkinsonian symptoms: Intrastriatal microinjection studies in the 6-OHDA-lesioned rat

Auteurs : Joanne E. Nash [Royaume-Uni] ; Jonathan M. Brotchie [Royaume-Uni]

Source :

RBID : Pascal:02-0370370

Descripteurs français

English descriptors

Abstract

Treatments for Parkinson's disease based on replacement of lost dopamine have several problems. Following loss of dopamine, enhanced N-methyl-D-aspartate (NMDA) receptor-mediated transmission in the striatum is thought to be part of the cascade of events leading to the generation of parkinsonian symptoms. We determined the localisation and pharmacological characteristics of NMDA receptors that play a role in generating parkinsonian symptoms within the striatum. Rats were lesioned unilaterally with 6-hydroxydopamine (6-OHDA), and cannulae implanted bilaterally to allow injection of a range of NMDA receptor antagonists at different striatal sites. When injected rostrally into the dopamine-depleted striatum, the glycine site partial agonist, (+)-HA-966 (44-400 nmol) caused a dose-dependent contraversive rotational response consistent with an antiparkinsonian action. (+)-HA-966 (400 nmol) had no effect when infused into more caudal regions of the dopamine-depleted striatum, or following injection into any striatal region on the dopamine-intact side. To determine the pharmacological profile of NMDA receptors involved in inducing parkinsonism in 6-OHDA-lesioned rats, a range of NMDA receptor antagonists was infused directly into the rostral striatum. Ifenprodil (100 nmol) and 7-chlorokynurenate (37 nmol), but not MK-801 (15 nmol) or D-APV (25 nmol) elicited a dramatic rotational response when injected into the dopamine-depleted striatum. This pharmacological profile is not consistent with an effect mediated via blocking NR2B-containing NMDA receptors. The effect of intrastriatal injection of ifenprodil was increased in animals previously treated with levodopa (L-dopa) methyl ester. This was seen as an increase in on-time and in peak rotational response. We propose that stimulation of NR2B-containing NMDA receptors in the rostral striatum underlies the generation of parkinsonian symptoms. These studies are in line with previous findings suggesting that administration of NR2B-selective NMDA receptor antagonists may be therapeutically beneficial for parkinsonian patients, when given de novo and following L-dopa treatment.
pA  
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A08 01  1  ENG  @1 Characterisation of striatal NMDA receptors involved in the generation of Parkinsonian symptoms: Intrastriatal microinjection studies in the 6-OHDA-lesioned rat
A11 01  1    @1 NASH (Joanne E.)
A11 02  1    @1 BROTCHIE (Jonathan M.)
A14 01      @1 Manchester Movement Disorder Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester @2 Manchester @3 GBR @Z 1 aut. @Z 2 aut.
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C01 01    ENG  @0 Treatments for Parkinson's disease based on replacement of lost dopamine have several problems. Following loss of dopamine, enhanced N-methyl-D-aspartate (NMDA) receptor-mediated transmission in the striatum is thought to be part of the cascade of events leading to the generation of parkinsonian symptoms. We determined the localisation and pharmacological characteristics of NMDA receptors that play a role in generating parkinsonian symptoms within the striatum. Rats were lesioned unilaterally with 6-hydroxydopamine (6-OHDA), and cannulae implanted bilaterally to allow injection of a range of NMDA receptor antagonists at different striatal sites. When injected rostrally into the dopamine-depleted striatum, the glycine site partial agonist, (+)-HA-966 (44-400 nmol) caused a dose-dependent contraversive rotational response consistent with an antiparkinsonian action. (+)-HA-966 (400 nmol) had no effect when infused into more caudal regions of the dopamine-depleted striatum, or following injection into any striatal region on the dopamine-intact side. To determine the pharmacological profile of NMDA receptors involved in inducing parkinsonism in 6-OHDA-lesioned rats, a range of NMDA receptor antagonists was infused directly into the rostral striatum. Ifenprodil (100 nmol) and 7-chlorokynurenate (37 nmol), but not MK-801 (15 nmol) or D-APV (25 nmol) elicited a dramatic rotational response when injected into the dopamine-depleted striatum. This pharmacological profile is not consistent with an effect mediated via blocking NR2B-containing NMDA receptors. The effect of intrastriatal injection of ifenprodil was increased in animals previously treated with levodopa (L-dopa) methyl ester. This was seen as an increase in on-time and in peak rotational response. We propose that stimulation of NR2B-containing NMDA receptors in the rostral striatum underlies the generation of parkinsonian symptoms. These studies are in line with previous findings suggesting that administration of NR2B-selective NMDA receptor antagonists may be therapeutically beneficial for parkinsonian patients, when given de novo and following L-dopa treatment.
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C07 06  X  FRE  @0 Encéphale pathologie @5 39
C07 06  X  ENG  @0 Cerebral disorder @5 39
C07 06  X  SPA  @0 Encéfalo patología @5 39
C07 07  X  FRE  @0 Extrapyramidal syndrome @5 40
C07 07  X  ENG  @0 Extrapyramidal syndrome @5 40
C07 07  X  SPA  @0 Extrapiramidal síndrome @5 40
C07 08  X  FRE  @0 Maladie dégénérative @5 41
C07 08  X  ENG  @0 Degenerative disease @5 41
C07 08  X  SPA  @0 Enfermedad degenerativa @5 41
C07 09  X  FRE  @0 Trouble neurologique @5 45
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C07 09  X  SPA  @0 Trastorno neurológico @5 45
N21       @1 203
N82       @1 PSI

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Pascal:02-0370370

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<s0>Ifenprodil</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Ifenprodil</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>13</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Antiparkinsonien</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Antiparkinson agent</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Antiparkinsoniano</s0>
<s5>14</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Pathogénie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG">
<s0>Pathogenesis</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA">
<s0>Patogenia</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE">
<s0>Traitement</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Treatment</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Tratamiento</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Rat</s0>
<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Rat</s0>
<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Rata</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Animal</s0>
<s5>21</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>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Trouble neurologique</s0>
<s5>45</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Neurological disorder</s0>
<s5>45</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Trastorno neurológico</s0>
<s5>45</s5>
</fC07>
<fN21>
<s1>203</s1>
</fN21>
<fN82>
<s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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