Excitatory effects of dopamine on subthalamic nucleus neurons: in vitro study of rats pretreated with 6-hydroxydopamine and levodopa

Zhu, Zhang; Bartol, Muriel; Shen, Ke Zhong; Johnson, Steven W.

doi:10.1016/s0006-8993(02)02543-x

Cited by 72 publications

(65 citation statements)

References 43 publications

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“…Haloperidol-treated mice (2.0 mg/kg) showed highly significant decrease (10.94 ± 2.16 ng/ml) in dopamine level as compared to saline-treated mice (p < 0.05). Dopamine exerted a direct excitatory influence on subthalamic nucleus (STN) neurons via activation of D2-like receptors; the excitatory effect of dopamine was reduced by D2 antagonist haloperidol [34]. Small decrease in dopamine content was found in mice co-treated with BRC solution administered either orally or i.n., having concentrations of 14.00 ± 0.37 and 15.71 ± 1.42 ng/ml, respectively, which showed nonsignificant result among each other (p > 0.05) but relatively significant result as compared to saline (p < 0.05).…”

Section: Dopamine Estimationmentioning

confidence: 99%

Optimised nanoformulation of bromocriptine for direct nose-to-brain delivery: biodistribution, pharmacokinetic and dopamine estimation by ultra-HPLC/mass spectrometry method

Shadab

Haque

Fazil

et al. 2014

Expert Opinion on Drug Delivery

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Section: Dopamine Estimationmentioning

confidence: 99%

Optimised nanoformulation of bromocriptine for direct nose-to-brain delivery: biodistribution, pharmacokinetic and dopamine estimation by ultra-HPLC/mass spectrometry method

Shadab

Haque

Fazil

et al. 2014

Expert Opinion on Drug Delivery

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“…For instance, it has been speculated that pattern abnormalities in STN may result from loss of dopamine in the STN (Meibach and Katzman, 1979;Campbell et al, 1985;Besson et al, 1988;Johnson et al, 1994;Kreiss et al, 1997;Francois et al, 2000;Smith and Kieval, 2000;Zhu et al, 2002) or from changes in the synchronization between STN neurons and cortex (Magill et al, 2000a(Magill et al, ,b, 2001Wichmann et al, 2001b). Other explanations would include altered interactions between STN and brainstem areas such as the pedunculopontine nucleus (Orieux et al, 2000) or between STN and the intralaminar nuclei of the thalamus (Bacci et al, 2002).…”

Section: Gpe Activity Changes and The Development Of Parkinsonian Motmentioning

confidence: 99%

Role of External Pallidal Segment in Primate Parkinsonism: Comparison of the Effects of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism and Lesions of the External Pallidal Segment

Soares¹,

Kliem²,

Betarbet³

et al. 2004

J. Neurosci.

179

185

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These experiments re-examined the notion that reduced activity in the external pallidal segment (GPe) results in the abnormalities of neuronal discharge in the subthalamic nucleus (STN) and the internal pallidal segment (GPi) and in the development of parkinsonian motor signs. Extracellular recording in two rhesus monkeys, which had been rendered parkinsonian by treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), revealed that the average neuronal discharge rate decreased in GPe but increased in STN and GPi. After MPTP, neurons in all three nuclei tended to discharge in oscillatory bursts. In addition, GABA release in STN (measured with microdialysis) was reduced, indicative of reduced activity along the GPe-STN pathway. Finally, the concentration of glutamic acid dehydrogenase (GAD; measured with autoimmunoradiography) was increased in GPe and GPi, likely reflecting increased striatal input and increased activity of local axon collaterals, respectively. Surprisingly, GAD protein in STN remained unchanged, indicating that the usual assumption that GAD levels are determined primarily by the overall activity of GABAergic elements may be too simplistic. The results from the MPTP-treated animals were compared with results obtained in a second group of three animals with ibotenic acid lesions of GPe. GPe lesions resulted in increased discharge in STN and GPi, comparable with the changes seen after MPTP but did not induce oscillatory bursting and had no behavioral effects. The results indicate that a mere reduction of GPe activity does not produce parkinsonism. Other changes, such as altered discharge patterns in STN and GPi, may play an important role in the generation of parkinsonism.

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“…However, these mechanisms do not appear sufficient to generate slow oscillatory activity in the STN-GP network in brain slices that preserve connectivity between GP and STN (Loucif et al, 2005). Nevertheless, these observations provide evidence that GP and STN networks have intrinsic mechanisms for supporting oscillatory activity in slow frequency ranges and led Plenz and Kitai (1999) to propose that activity in the indirect pathway supports changes in firing patterns observed after dopamine loss in vivo.In vitro studies have made considerable progress in characterizing the neurophysiological properties of the STN neurons and exploring how different patterns of inhibitory and excitatory input might affect STN activity (Mintz et al, 1986;Nakanishi et al, 1987;Beurrier et al, 1999;Bevan and Wilson, 1999;Bevan et al, 2000Bevan et al, , 2002aWigmore and Lacey, 2000;Zhu et al, 2002;Do and Bean, 2003;Hallworth et al, 2003; Wilson et al, 2004a,b;Baufreton et al, 2005;Surmeier et al, 2005;Kass and Mintz, 2006). With respect to the interplay of excitatory and inhibitory input, GABAergic inhibition can increase the efficiency of STN response to excitatory input by promoting recovery of inactivated voltage-dependent Na+ (Na v ) channels (Baufreton et al, 2005).…”

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confidence: 99%

Phase relationships support a role for coordinated activity in the indirect pathway in organizing slow oscillations in basal ganglia output after loss of dopamine

et al. 2007

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The goal of the present study was to determine the phase relationships of the slow oscillatory activity that emerges in basal ganglia nuclei in anesthetized rats after dopamine cell lesion in order to gain insight into the passage of this oscillatory activity through the basal ganglia network. Spike train recordings from striatum, subthalamic nucleus (STN), globus pallidus (GP), and substantia nigra pars reticulata (SNpr) were paired with simultaneous local field potential (LFP) recordings from SNpr or motor cortex ipsilateral to a unilateral lesion of substantia nigra dopamine neurons in urethane anesthetized rats. Dopamine cell lesion induced a striking increase in incidence of slow oscillations (0.3-2.5 Hz) in firing rate in all nuclei. Phase relationships assessed through paired recordings using SNpr LFP as a temporal reference showed that slow oscillatory activity in GP spike trains is predominantly antiphase with oscillations in striatum, and slow oscillatory activity in STN spike trains is in-phase with oscillatory activity in cortex but predominantly antiphase with GP oscillatory activity. Taken together, these results imply that after dopamine cell lesion in urethane anesthetized rats, increased oscillatory activity in GP spike trains is shaped more by increased phasic inhibitory input from the striatum than by phasic excitatory input from STN. In addition, results show that oscillatory activity in SNpr spike trains is typically antiphase with GP oscillatory activity and in-phase with STN oscillatory activity. While these observations do not rule out additional mechanisms contributing to the emergence of slow oscillations in the basal ganglia after dopamine cell lesion in the anesthetized preparation, they are compatible with 1) increased oscillatory activity in the GP facilitated by an effect of dopamine loss on striatal 'filtering' of slow components of oscillatory cortical input, 2) increased oscillatory activity in STN spike trains supported by convergent antiphase inhibitory and excitatory oscillatory input from GP and cortex, respectively, and 3) increased oscillatory activity in SNpr spike trains organized by convergent antiphase inhibitory and excitatory oscillatory input from GP and STN, respectively. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errorsmaybe discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2012 May 17. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript KeywordsParkinson's disease; subthalamic nucleus; substantia nigra; globus pallidus; striatum; bursting; local field potentials Dopa...

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Excitatory effects of dopamine on subthalamic nucleus neurons: in vitro study of rats pretreated with 6-hydroxydopamine and levodopa

Cited by 72 publications

References 43 publications

Optimised nanoformulation of bromocriptine for direct nose-to-brain delivery: biodistribution, pharmacokinetic and dopamine estimation by ultra-HPLC/mass spectrometry method

Optimised nanoformulation of bromocriptine for direct nose-to-brain delivery: biodistribution, pharmacokinetic and dopamine estimation by ultra-HPLC/mass spectrometry method

Role of External Pallidal Segment in Primate Parkinsonism: Comparison of the Effects of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism and Lesions of the External Pallidal Segment

Phase relationships support a role for coordinated activity in the indirect pathway in organizing slow oscillations in basal ganglia output after loss of dopamine

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