Appearance of EMG activity and motor asymmetry after unilateral lesions of the dopaminergic innervation to the subthalamic nucleus in the rat

Flores, Gonzalo; Valencia, Jaime; Rosales, Manuel G.; Sierra, Arturo; Aceves, Jorge

doi:10.1016/0304-3940(93)90583-7

Cited by 28 publications

(17 citation statements)

References 13 publications

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“…It is well accepted that dopamine is released from the dendrites of dopaminergic neurones in the substantia nigra (Cheramy et al 1981) and can interact with both D2 autoreceptors and with D1 receptors located on the terminals of striato-nigral GABA neurons. It has been reported that when these D1 receptors are stimulated they increase the release of GABA (Flores et al 1993), so that their blockade by SCH23390 will result in a reduction in GABA release. As a consequence the tonically active nigro-thalamic GABAergic neurons are less inhibited, leading to greater inhibition of the thalamus resulting in inhibition of thalamo-cortical glutamatergic neurones culminating in increased muscle tone and akinesia (DeLong 1990;Crocker 1997).…”

Section: Discussionmentioning

confidence: 99%

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Hemsley

Crocker

2001

Neuropsychopharmacology

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Muscle rigidity associated with antipsychotic drug treatment is believed to result from reduced striatal dopamine neurotransmission. In the current study the regulatory roles of dopamine D1 and D2 receptor subfamilies in the dorsal (DSTR) and ventral striatum (VSTR) and substantia nigra (SN) were investigated on muscle tone, assessed as increases in tonic electromyographic (EMG) activity. Rats were injected with the irreversible The use of antipsychotic drugs to treat the symptoms of schizophrenia can be associated with extrapyramidal side effects, which resemble the symptoms of Parkinson's disease and include increased muscle rigidity in up to 40% of patients (Baldessarini and Tarsy 1980). Further, it has been estimated that up to 30% of patients stop taking their medication because of these motor side effects (Hoge et al. 1990). It is not fully understood why antipsychotic drugs, all antagonists at the dopamine D2 receptor (Creese et al. 1976;Seeman et al. 1976; Peroutka and Snyder 1980) produce motor side effects, although there is some early experimental evidence supporting the view that antagonism of D2 receptors in the striatum is important (Chiodo and Bunney 1983;Creese 1983). Findings from studies in humans using positron emission tomography (PET) have led to the concept that a "threshold" of D2 antagonism by antipsychotic drugs of approximately 70%, exists in the striatum, above which patients experience motor side effects (Farde et al. 1992;Nordstrom et al. 1995). Additional support for the striatal D2 threshold hypothesis has N EUROPSYCHOPHARMACOLOGY 2001 -VOL . 25 , NO . 4 Dopamine D1 & D2 Receptors Regulate Muscle Tone 515 been provided by studies using experimental animals Ogren et al. 1994;Alcock and Crocker 1999;Hemsley and Crocker 1999a) and other imaging techniques in humans (Scherer et al. 1994). Further, it has been reported that clozapine, which does not produce motor side effects in humans or animals (Claghorn et al. 1987;Casey 1989), occupies sub-threshold levels of D2 receptors in the striatum (Farde et al. 1992;Hemsley and Crocker 1999a) and substantia nigra (Hemsley and Crocker 1999a). The role of dopamine D1 receptors in the production of motor side effects is unclear, and no relationship to D1 receptor occupancy was shown in PET studies (Farde et al. 1992). However, there is evidence that antagonism of D1 receptors may result in motor side effects Sedvall et al. 1995) and elicit such motor behaviors as catalepsy in rats (Ogren and Fuxe 1988). As many commonly used antipsychotic drugs, such as chlorpromazine, fluphenazine, and clozapine, are also potent dopamine D1 antagonists (Hacksell et al. 1995), it would be useful to understand the contribution that antagonism of the D1 receptor subfamily makes to the production of muscle rigidity.Experimental research investigating the mechanisms underlying the motor side effects associated with the use of antipsychotic drugs has been handicapped by the lack of a relevant, objective, and quantifiable endpoint of extrapyramidal side effects ...

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Section: Discussionmentioning

confidence: 99%

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Hemsley

Crocker

2001

Neuropsychopharmacology

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“…In addition, unilateral 6-OHDA lesions of the rat STN may result in contralateral muscle rigidity (Flores et al, 1993). …”

Section: Extrastriatal Dopamine Loss In Parkinsonismmentioning

confidence: 99%

Extrastriatal dopaminergic circuits of the basal ganglia

2010

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The basal ganglia are comprised of the striatum, the external and internal segment of the globus pallidus (GPe and GPi, respectively), the subthalamic nucleus (STN), and the substantia nigra pars compacta and reticulata (SNc and SNr, respectively). Dopamine has long been identified as an important modulator of basal ganglia function in the striatum, and disturbances of striatal dopaminergic transmission have been implicated in diseases such as Parkinson's disease (PD), addiction and attention deficit hyperactivity disorder. However, recent evidence suggests that dopamine may also modulate basal ganglia function at sites outside of the striatum, and that changes in dopaminergic transmission at these sites may contribute to the symptoms of PD and other neuropsychiatric disorders. This review summarizes the current knowledge of the anatomy, functional effects and behavioral consequences of the dopaminergic innervation to the GPe, GPi, STN, and SNr. Further insights into the dopaminergic modulation of basal ganglia function at extrastriatal sites may provide us with opportunities to develop new and more specific strategies for treating disorders of basal ganglia dysfunction.

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“…After localizing the precise site of the ventral hippocampus lesion by taking coronal serial slices (thickness 100 M) at the level of the ventral hippocampus and stained with 0.5% cresyl violet, they were examined under a light microscope. The medial part of the prefrontal cortex, nucleus accumbens, caudate-putamen, hippocampus and olfactory tubercle were microdissected, and homogenized in 0.05 M perchloric acid (Flores et al, 1993). Homogenates were then centrifuged at 30 psi for 1 min and the supernatant removed and filtered.…”

Section: Assay Of Dopamine and Dopacmentioning

confidence: 99%

“…Homogenates were then centrifuged at 30 psi for 1 min and the supernatant removed and filtered. Dopamine and DOPAC were determined in the supernatant using a C18 column (4.6mm × 250 mm i.d., 5 m, Metachem) as we previously reported (Flores et al, 1993). The mobil phase contained 0.09 M sodium acetate, 0.035 M citric acid, 130 M ethylenediamine tetraacetic acid (EDTA), 230 M 1-octanesulfonic acid (sodium salt, SOS), at pH 4.35 adjusted with 6 M sodium hydroxide and methanol 10.5% (v/v).…”

Section: Assay Of Dopamine and Dopacmentioning

confidence: 99%

Neonatal ventral hippocampus lesion alters the dopamine content in the limbic regions in postpubertal rats

Alquicer

Silva-Gómez

Peralta³

et al. 2004

Intl J of Devlp Neuroscience

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The neonatal ventral Hippocampus (nVH) lesion in rats has been used as a model to test the hypothesis that early neurodevelopmental abnormalities lead to behavioral changes putatively linked to schizophrenia. The schizophrenic patients tend to social isolation. In addition, considerable evidence from behavioral and neurochemistry studies strongly implicate the dopamine (DA) system and the medial part of the prefrontal cortex (mPFC) in the pathophysiology of the social isolation syndrome. In order to assess effects of the postweaning social isolation (pwSI) on the DA system of the nVH lesions, we investigated the DA content and its metabolite, DOPAC in different limbic subregions in rats postpubertally at postnatal day (P) 78 following nVH lesions at P7 with and without pwSI for 8 weeks. The DA and DOPAC were measured by HPLC with electrochemical detection. The nVH lesion induces increase in the DA content in the hippocampus with no effect in the mPFC, nucleus accumbens and caudate-putamen, while the pwSI induces major increase in the DA content in limbic subregions such as the mPFC, nucleus accumbens and hipocampus with opposite effect in the caudate-putamen. These results suggest that while pwSI has an effect in the postpubertal content of DA in both sham and nVH lesions in rats, the nVH-lesioned rats appear to be affected to a greater extent than the sham animals underscoring the influence of pwSI differences in the development of behaviors in the nVH-lesioned animals.

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Appearance of EMG activity and motor asymmetry after unilateral lesions of the dopaminergic innervation to the subthalamic nucleus in the rat

Cited by 28 publications

References 13 publications

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Extrastriatal dopaminergic circuits of the basal ganglia

Neonatal ventral hippocampus lesion alters the dopamine content in the limbic regions in postpubertal rats

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