Rotational behaviour after unilateral intranigral injection of muscimol in rats

Oberlander, Claude; Dumont, C; Boissier, Jacques R.

doi:10.1016/0014-2999(77)90047-4

Cited by 99 publications

(10 citation statements)

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“…In contrast to the behavior obtained with muscimol in STN, muscimol (200 or 45 pmol) injected into the center of SNpr resulted in a high rate of contralaterally directed circling in both the presence and absence of tail lift stimulation (Table 1 ; Fig. 3); this effect confirms well established findings (Oberlander et al, 1977;Olpe et al, 1977;Scheel-Kruger et al, 1977;Olianas et al, 1978;Waddington, 1978a;Kozlowski and Marshall, 1980;Childs and Gale, 1984). Similarly, in agreement with previous studies that have shown contralaterally directed circling with the injection of glutamate antagonists into SNpr (Dawbarn and Pycock, 1981;St-Pierre and Bedard, 1994;Murer et al, 1996), kynurenate injected into the center of the SNpr induced a high rate of contralaterally directed circling both in the presence and absence of tail lift stimulation (Table 1).…”

Section: Postural Effectssupporting

confidence: 56%

“…Unilateral intranigral microinjection of GABA A agonists (Oberlander et al, 1977;Olpe et al, 1977;Scheel-Kruger et al, 1977;Olianas et al, 1978;Waddington, 1978a,b; Kozlowski and Marshall, 1980;; Childs and Gale, 1984) or glutamate antagonists (Dawbarn and Pycock, 1981;St-Pierre and Bedard, 1994;Murer et al, 1996) results in locomotor activation, contralaterally directed circling, and postural asymmetry. Bilateral intranigral application of GABA A agonists induces stereotyped hyperactivity (sniffing and gnawing; Scheel-Kruger et al, 1977;Childs and Gale, 1983;Baumeister and Frye, 1984).…”

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confidence: 99%

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Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

2000

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The subthalamic nucleus (STN) plays a crucial role as a regulator of basal ganglia outflow by providing excitatory glutamatergic input into the two output nuclei of the basal ganglia, substantia nigra pars reticulata (SNpr), and entopeduncular nucleus. This study examined the effects of suppressing activity in the STN of the awake, behaving rat. Specifically, we evaluated the effects of unilateral and bilateral focal inhibition of STN on posture, locomotion, and susceptibility to limbic motor seizures.Unilateral microinjection of a GABA A receptor agonist (muscimol, 200 pmol) into STN produced a site-dependent contralaterally directed postural asymmetry without locomotor activation. This effect differed from responses produced by the same dose of muscimol placed into SNpr, which included locomotor activation in addition to contralaterally directed postural asymmetry. Locomotor activation and postural asymmetry were obtained also after blockade of glutamate transmission in SNpr by the unilateral application of kynurenate (100 nmol). Our observation that STN inhibition did not induce the locomotor activation characteristic of SNpr inhibition suggests that there are glutamatergic inputs to SNpr, other than those from STN, that are responsible for controlling locomotion.Bilateral, but not unilateral, injection of muscimol (200 pmol) into STN protected against limbic motor seizures evoked either by intravenous bicuculline or by focal application of bicuculline into anterior piriform cortex (area tempestas). These results demonstrate that focal inhibition of STN reproduces the postural asymmetry and anticonvulsant actions that are obtained with the inhibition of SNpr. This provides behavioral support for the concept that STN contributes a crucial tonic excitatory (glutamatergic) drive to the rat SNpr.

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Section: Postural Effectssupporting

confidence: 56%

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confidence: 99%

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

2000

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“…Several investigators have found that unilateral injection of GABA mimetics into the substantia nigra of control rats produces contralateral rotation similar to that observed in animals with unilateral nigrostriatal dopamine depletion given apomorphine {4, 6,7,[17][18][19][20]241. We explored the possibility that activation of striatal GABA receptors by GABA-mimetic treatment was also involved in augmenting apomorphine-induced turning.…”

Section: Discussionmentioning

confidence: 80%

“…When injected into dopamine-denervated striata (data not shown), muscimol produced the same type of rapid-onset ipsiiateral circling behavior, which, however, was not followed by contralateral circling after 30 minutes as was the case with control rats. 7,[17][18][19][20]241 studies support the concept that GABA-utilizing efferent pathways from striatum to substantia nigra reticulata and from nigra reticulata to caudal brainstem centers mediate the postural asymmetry and rotational behavior induced by agonist stimulation of denervated "supersensitive" striatal DA receptors. Disruption of the nigrostriatal pathway in experimental animals consistently results in a 20 to 74% increase in GABA synthetic capacity (glutamate decarboxylase activity [GAD}) in basal ganglia nuclei [I, 6, 16, 251, whereas postmortem studies of human PD basal ganglia demonstrate variable GAD reductions 112, 14, 15,221.…”

Section: Resultsmentioning

confidence: 85%

GABA‐mimetic drugs enhance apomorphine‐induced contralateral turning in rats with unilateral nigrostriatal dopamine denervation: Implications for the therapy of Parkinson's disease

Bennett

Ferrari

Cruz

1987

Annals of Neurology

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The underlying mechanisms responsible for advanced Parkinson's disease's becoming refractory to dopamimetic therapies are unclear. Postmortem brain studies indicate that patients with Parkinson's disease have decreased basal ganglia gamma-aminobutyric acid (GABA) function in addition to profound striatal dopamine (DA) deficiencies. In experimental animals, GABA-utilizing striatal and nigral projection neurons appear to mediate motor behaviors arising from the stimulation of striatal DA receptors by agonists. We have examined the ability of directly and indirectly acting GABA-mimetic drugs to alter turning behavior elicited by administering apomorphine, a DA agonist, to rats with unilateral lesions of dopaminergic nigrostriatal neurons. Low doses of directly acting postsynaptic GABA agonists (progabide, 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin--3-01) or a neuronal GABA transport inhibitor (SKF 100330-A) potentiate apomorphine-induced turning. Higher doses of these agents or acute inhibition of GABA catabolism inhibits turning. Our results suggest that low doses of certain GABA mimetics will improve the responses of patients with Parkinson's disease to concurrent DA receptor agonist therapy.

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“…Circling is a common feature in animals with an imbalance between the basal ganglia outputs in the two hemispheres (Oberlander et al, 1977;Olpe et al, 1977, Scheel-Kruger et al, 1977Hikosaka and Wurtz, 1983a-c;Sirinathsinghji, 1985;Bankiewicz et al, 1986). For instance, localized inactivation of the medial SNr induces contraversive turning, which has been attributed to abnormalities of the nigro-collicular projection (Hikosaka and Fig.…”

Section: Circling and Other Behavioral Disturbancesmentioning

confidence: 99%

Effects of Transient Focal Inactivation of the Basal Ganglia in Parkinsonian Primates

Baron

Wichmann²,

Ma³

et al. 2002

J. Neurosci.

122

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Ablative and chronic stimulation procedures targeting the internal pallidum (GPi) and the subthalamic nucleus (STN) have led to major advancements in the treatment of Parkinson's disease and other movement disorders. Although these procedures have evolved to primarily target the posterior ventrolateral sensorimotor portion of GPi and to less selectively target STN, centrally, the ideal targets within these structures remain to be fully established. In this study, we sought to identify the optimal targeting sites in GPi and STN for reversal of parkinsonian signs through a series of reversible injections of the GABA A agonist muscimol in these nuclei in parkinsonian primates.Akinesia and bradykinesia were strongly ameliorated by discrete inactivation within the centromedial extent of the sensorimotor territory in GPi and the lateral portion of the sensorimotor territory in STN. This suggests that akinesia and bradykinesia might, in fact, originate from abnormalities in the same, or at least overlapping, motor circuits in the parkinsonian state. Inactivation of areas outside of the motor territories did not improve parkinsonism but induced circling and behavioral abnormalities. The segregation of basal ganglia-thalamocortical circuits appears to be therefore maintained, at least to a large extent, in the parkinsonian state.These results underscore that inactivation of discrete regions in the central territory of GPi and the lateral portion of STN are sufficient to ameliorate parkinsonian motor signs and that extension of lesions into nonmotor territories may be deleterious. Surgical outcomes might therefore be optimized by placing more discrete lesions and by restricting the extent of chronic stimulation.

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Rotational behaviour after unilateral intranigral injection of muscimol in rats

Cited by 99 publications

References 3 publications

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

GABA‐mimetic drugs enhance apomorphine‐induced contralateral turning in rats with unilateral nigrostriatal dopamine denervation: Implications for the therapy of Parkinson's disease

Effects of Transient Focal Inactivation of the Basal Ganglia in Parkinsonian Primates

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