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  • dopamine  (2)
  • 6-hydroxydopamine  (1)
Materialart
Erscheinungszeitraum
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Experimental brain research 58 (1985), S. 45-55 
    ISSN: 1432-1106
    Schlagwort(e): Apomorphine ; Muscimol ; Electrolesion ; Circling ; Holeboard ; 6-hydroxydopamine ; γ-vinyl GABA ; Angular complex ; Stereotypy
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The role of the midbrain angular complex (AC) in the execution of motor behaviours was investigated in the rat. In an automated holeboard apparatus bilateral AC electrolesions attenuated exploration and increased locomotor performance of drug-free rats on the first and second test occasions respectively; the latter result may signify a retarding of between-session habituation. Apomorphine also decreased locomotion and almost abolished head dipping and rearing in the holeboard; bilateral AC lesions reinstated locomotion to a normal level without modifying the other behavioural parameters. An electrolesion of one AC did not affect the animal's posture or spontaneous locomotion in the open field, but gave rise to pronounced ipsiversive circling when coupled with systemic administration of apomorphine. In unilaterally 6-hydroxydopamine (6-OHDA) treated rats subcutaneous injection of apomorphine evoked robust contraversive circling. A concomitant lesion of the ipsilateral AC introduced an additional ipsilateral bias to these animals' movements; contraversive circling was initially curtailed and posture reduced (or reversed), while stereotyped activities (particularly grooming) were suppressed. Contralateral orientation and circling were restored by subsequently lesioning the contralateral AC as well; bilateral AC lesions significantly potentiated circling to systemic apomorphine. Contralateral locomotor asymmetry was also produced by depositing apomorphine stereotaxically into the supersensitive caudate, or by microinjecting one substantia nigra zona reticulata with muscimol (in naive rats). Both rotational responses were facilitated by injury to the ipsilateral AC. The effects of electrocoagulating the AC were generally duplicated by discrete microinjection of muscimol or γ-vinyl GABA into this area, suggesting GABA-mediated synapses are normally operative in this part of the brain. These results do not support the claim that the AC is specifically engaged in mediating postural asymmetry in the unilaterally 6-OHDA denervated rat. Instead, we believe that impairment of neurotransmission through one AC imposes an independent and reciprocal tendency to move towards that side of the brain, as well as attenuating stereotypy and facilitating locomotion. The resultant behavioural response to systemic apomorphine shown by animals bearing these two types of lesion embodies these separate actions.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1435-1463
    Schlagwort(e): Motor behaviour ; dopamine ; MK 801 ; reserpine
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The akinesia induced by reserpine in mice was effectively reversed by the dopamine D1 receptor agonists SKF 38393 (5–30 mg/kg IP) and CY 208-243 (1–5 mg/kg IP), and by the mixed D1/D2 agonist pergolide (5 mg/kg SC), but less well by the D2 agonists lisuride, PHNO, LY 171555 and RU 24213 (each at 5 mg/kg SC) and not at all by the NMDA receptor antagonist MK 801 (0.1–10 mg/kg IP). MK 801 potentiated D1-dependent locomotion, but always suppressed rearing and grooming. D2-dependent locomotion was inhibited by MK 801. The D2 agonist RU 24213 was antagonised by as little as 6.25 μg/kg MK 801, while PHNO and LY 171555 were antagonised by 0.1 mg/kg MK 801. Lisuride was not inhibited by up to 1.6 mg/kg MK 801. Importantly, all animals showed signs of incapacitation with MK 801 in certain elements of their behaviour, most notably ataxia and hind limb abduction. Thus whilst NMDA receptor blockade can facilitate the restoration of movement by dopamine D1 (though not D2) agonists in monoamine-depleted mice, the fluency of the motor response is adversely affected.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Journal of neural transmission 5 (1993), S. 89-100 
    ISSN: 1435-1463
    Schlagwort(e): Pilocarpine ; seizure ; striatum ; dialysis ; dopamine ; homovanillic acid
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary In this study rats were fitted with a concentric dialysis probe in one striatum and extracellular concentrations of dopamine and HVA measured by reverse phase high performance liquid chromatography. Injections of saline or the D1 agonist SKF 38393 (30 mg/kg) did not affect the releases of these compounds. On the other hand, the D2 agonist LY 171555 (0.5 mg/kg) inhibited the release of both dopamine and HVA, whilst amphetamine (1 mg/kg) increased the output of dopamine but not HVA. Treatment with 200 mg/kg pilocarpine caused minimal signs of epileptic activity and did not affect striatal dopamine neurotransmission. Concomitant administration of SKF 38393 (30 mg/kg) to this dose of pilocarpine greatly facilitated the incidence and severity of motor seizures, which were accompanied by an irregular pattern of dopamine release and a significant rise in HVA overflow. Similar results were obtained with rats made to convulse with 400 mg/mg pilocarpine, and to a lesser extent if these animals were first pretreated with a protective dose of LY 171555 (0.5 mg/kg). It is concluded that dopamine neurotransmission in the striatum is disrupted in rats undergoing a pilocarpine-induced motor seizure, and that the extent of this disruption increases as the seizure becomes more severe. An irregular release of dopamine could signify a loss of sensorimotor control by the striatum, which might conceivably contribute to the intractability of the seizure. An increase in the dialysate concentrations of metabolite and not dopamine, is consistent with a heightened glutamate-stimulated release of dopamine from a discrete striatal pool, caused by the seizure spreading through the cortex and activating the cortico-striatal system.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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