Increased burst firing in substantia nigra pars reticulata neurons and enhanced response to selective D2 agonist in hemiparkinsonian rats after repeated administration of apomorphine.

Intermittent administrations of dopaminergic agents in hemiparkinsonian rat enhances the behavioral response to subsequent administration of the drugs. This phenomenon is known as "priming" and thought as comparable to drug-induced dyskinesia in patients with Parkinson's disease. We investigated the behavioral and electrophysiological changes in 6-hydroxydopamine (6-OHDA)-lesioned hemiparkinsonian rats after repeated administrations of apomorphine. Administration of apomorphine (0.32 mg/kg, intraperitoneal, i.p.) twice daily for 6 days enhanced the rotation induced by apomorphine from 341 turns/hour at the beginning to 755 turns/hr at the end. At the same time, the response to selective D2 agonist quinpirole (0.26 mg/kg, i.p.) was also enhanced from 203 to 555 turns/hr. Extracellular single unit recording revealed no significant difference in the basal firing rates of substantia nigra pars reticulata (SNr) neurons between the ipsilateral and contralateral side of the 6-OHDA lesion regardless of the repeated administrations of apomorphine. In SNr of the lesion side, the units with burst firing pattern were found more frequently after repeated administrations of apomorphine and the suppressive effect of quinpirole on the firing rate was enhanced. These findings suggest that the increased percentage of the burst units is the important electrophysiological change in the development of enhanced response to selective D2 agonist.

• Publication year

  2001

• Venue

  Journal of Korean medical science

• Publication date

  2001-10-01

• Fields of study

  Medicine

• Identifiers
  DOI 10.3346/JKMS.2001.16.5.636PMID 11641536PMCID 3057592
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Acute monoaminergic depletion in the rat potentiates the excitatory effect of the subthalamic nucleus in the substantia nigra pars reticulata but not in the pallidal complex

  2005cited by this paper
• Reduction of apomorphine-induced rotational behaviour by subthalamic lesion in 6-OHDA lesioned rats is associated with a normalization of firing rate and discharge pattern of pars reticulata neurons

  2004cited by this paper
• Substantia nigra pars reticulata units in 6‐hydroxydopamine‐lesioned rats: responses to striatal D2 dopamine receptor stimulation and subthalamic lesions

  2000cited by this paper
• Chronological Changes in the Rotational Behavior in Response to Apomorphine Administration in 6-Hydroxydopamine Parkinsonian Rat.

  1999cited by this paper
• Comparison of MPTP-induced changes in spontaneous neuronal discharge in the internal pallidal segment and in the substantia nigra pars reticulata in primates

  1999cited by this paper
• Characterization of enhanced behavioral responses to L-DOPA following repeated administration in the 6-hydroxydopamine-lesioned rat model of Parkinson's disease.

  1998cited by this paper
• De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset

  1998cited by this paper
• Identification and characterization of neurons with tremor-frequency activity in human globus pallidus

  1997cited by this paper
• Apomorphine priming alters the response of striatal outflow pathways to D2 agonist stimulation in 6-hydroxydopamine-lesioned rats.

  1997cited by this paper
• Substantia nigra pars reticulata single unit activity in normal and 60HDA‐lesioned rats: Effects of intrastriatal apomorphine and subthalamic lesions

  1997influential reference
• Enhancement of the behavioral response to apomorphine administration following repeated treatment in the 6-hydroxydopamine-lesioned rat is temporally correlated with a rise in striatal preproenkephalin-B, but not preproenkephalin-A, gene expression.

  1997cited by this paper
• Hemispheric asymmetries in spontaneous firing characteristics of substantia nigra pars reticulata neurons following a unilateral 6-hydroxydopamine lesion of the rat nigrostriatal pathway.

  1997cited by this paper
• DOPA-induced "peak dose" dyskinesia: clues implicating D2 receptor-mediated mechanisms using dopaminergic agonists in MPTP monkeys.

  1995cited by this paper
• The primate subthalamic nucleus. II. Neuronal activity in the MPTP model of parkinsonism.

  1994cited by this paper
• Evidence that the parafascicular projection to the subthalamic nucleus is glutamatergic.

  1993cited by this paper
• Levodopa-Induced Dyskinesia: Facts and Fancy. What Does the MPTP Monkey Model Tell Us?

  1992cited by this paper
• Abnormal spontaneous activity of globus pallidus neurons in monkeys with MPTP-induced parkinsonism.

  1991cited by this paper
• Naloxone reverses L-dopa induced overstimulation effects in a Parkinson's disease animal model analogue.

  1991cited by this paper
• D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons.

  1990cited by this paper
• Motor complications associated with chronic levodopa therapy in Parkinson's disease.

  1989cited by this paper
• Parkinsonian Symptomatology An Anatomical and Physiological Analysisa a

  1988cited by this paper
• Parkinsonian symptomatology. An anatomical and physiological analysis.

  1988cited by this paper
• Somatosensory inputs to the subthalamic nucleus: a combined retrograde and anterograde horseradish peroxidase study in the rat.

  1988cited by this paper
• Effects of D1 and D2 dopamine receptor stimulation on the activity of substantia nigra pars reticulata neurons in 6-hydroxydopamine lesioned rats: D1/D2 coactivation induces potentiated responses.

  1987cited by this paper
• Chronic treatment with L-DOPA, but not bromocriptine induces dyskinesia in MPTP-parkinsonian monkeys. Correlation with [3H]spiperone binding.

  1986cited by this paper
• Bursts and recurrences of bursts in the spike trains of spontaneously active striate cortex neurons.

  1985cited by this paper
• Repeated apomorphine treatment causes behavioural supersensitivity and dopamine D2 receptor hyposensitivity.

  1983cited by this paper
• Sustained bromocriptine therapy in previously untreated patients with Parkinson's disease.

  1981cited by this paper
• Effects of interruption of the nigrostriatal pathway and of dopaminergic agents on the spontaneous activity of globus pallidus neurons in the awake monkey.

  1979cited by this paper
• Success and problems of long-term levodopa therapy in Parkinson's disease.

  1977cited by this paper
• Bromocriptine in Parkinsonism

  1974cited by this paper
• Postsynaptic supersensitivity after 6-hydroxy-dopamine induced degeneration of the nigro-striatal dopamine system.

  1971cited by this paper
• Quantitative recording of rotational behavior in rats after 6-hydroxy-dopamine lesions of the nigrostriatal dopamine system.

  1970cited by this paper

• Targeting parvalbumin-expressing neurons in the substantia nigra pars reticulata restores motor function in parkinsonian mice.

  2023cites this paper
• Comparison between Tail Suspension Swing Test and Standard Rotation Test in Revealing Early Motor Behavioral Changes and Neurodegeneration in 6-OHDA Hemiparkinsonian Rats

  2020cites this paper
• Proliferation of Inhibitory Input to the Substantia Nigra in Experimental Parkinsonism

  2019cites this paper
• Neuronal firing activity in the basal ganglia after striatal transplantation of dopamine neurons in hemiparkinsonian rats.

  2017cites this paper
• Alterations in neuronal activity in basal ganglia-thalamocortical circuits in the parkinsonian state

  2015cites this paper
• Short- and long-term unilateral 6-hydroxydopamine lesions in rats show different changes in characteristics of spontaneous firing of substantia nigra pars reticulata neurons

  2012cites this paper
• Basal ganglia activity patterns in parkinsonism and computational modeling of their downstream effects

  2012cites this paper
• The Antiparkinsonian and Antidyskinetic Mechanisms of Mucuna pruriens in the MPTP-Treated Nonhuman Primate

  2012cites this paper
• Application of Complementary and Alternative Medicine on Neurodegenerative Disorders: Current Status and Future Prospects

  2012cites this paper
• Gamma-aminobutyric acidB receptor activation suppresses stimulus-evoked burst firing in rat substantia nigra reticulata neurons

  2012cites this paper
• The Functional Significance of Oscillatory Activities in the Basal Ganglia and Pedunculopontine Nucleus Region in Parkinson’s Disease and Dystonia

  2012cites this paper
• THE ROLE OF INTERHEMISPHERIC PATHWAYSIN PARKINSON’S DISEASE AND DRUG-INDUCED DYSKINESIAS

  2011cites this paper
• Pathological basal ganglia activity in movement disorders.

  2011cites this paper
• Beta frequency synchronization in basal ganglia output during rest and walk in a hemiparkinsonian rat.

  2010cites this paper
• Noradrenergic lesion of the locus coeruleus increases apomorphine-induced circling behavior and the firing activity of substantia nigra pars reticulata neurons in a rat model of Parkinson's disease.

  2010cites this paper
• Substantia nigra pars reticulata neuronal activity during bradykinesia and levodopa -induced movements in a rodent model of Parkinson's disease

  2009cites this paper
• Mean-field analysis of basal ganglia and thalamocortical dynamics.

  2009cites this paper
• Mean-field modeling of the basal ganglia-thalamocortical system. II Dynamics of parkinsonian oscillations.

  2009cites this paper
• Bilateral changes in neuronal activity of the basal ganglia in the unilateral 6‐hydroxydopamine rat model

  2008cites this paper
• Invited review Pathophysiology of Parkinsonism

  2008cites this paper
• Pathophysiology of parkinsonism.

  2008cites this paper
• Neuronal firing before and after burst discharges in the monkey basal ganglia is predictably patterned in the normal state and altered in parkinsonism.

  2006cites this paper
• beta-Phenylethylamines and the isoquinoline alkaloids.

  2004cites this paper