Early increase in dopamine release in the ipsilateral striatum after unilateral intranigral administration of lactacystin produces spontaneous contralateral rotations in rats
Abstract
Since the discovery of the role of the ubiquitin-proteasome system (UPS) in the pathogenesis of Parkinson's disease, UPS inhibitors, such as lactacystin have been used to investigate the relationship between UPS impairment and degeneration of dopamine (DA) neurons. However, mostly long-term neurotoxic effects of lactacystin have been studied in animal models. Therefore, the aim of our study was to investigate behavioral and biochemical changes related to the DA system during the first week following unilateral intranigral injection of lactacystin to rats. We found that lactacystin produced early spontaneous contralateral rotations which were inhibited by combined administration of DA D1 and D2 receptor antagonists. Simultaneously, an increase in the extracellular level of DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanilic acid (HVA) was found in the ipsilateral striatum. In contrast, one week after lesion, when turning behavior was no longer visible, a decrease in the extracellular level of DA, DOPAC and HVA was demonstrated. It was accompanied by a substantial reduction in the tissue levels of DA and its metabolites in the lesioned substantia nigra and striatum. We concluded that unilateral intranigral administration of lactacystin produces an early increase in DA neurotransmission which precedes a decrease in the striatal and nigral tissue DA content. It is manifested by the appearance of spontaneous contralateral rotations and an elevation of the…
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Unilateral damage to the SNc can cause contralateral rotations in mice via postsynaptic and/or presynaptic mechanisms.
“unilateral damage to the SNc can cause contralateral rotations in mice via postsynaptic and/or presynaptic mechanisms.”
From Mitochondrial DNA Damage in Substantia Nigra Pars Compacta Astrocytes Exacerbates Dopaminergic Neuron Loss in a 6-Hydroxydopamine Mouse Model of Parkinsonism (2026) · cites this paper as Konieczny et al. 2016
A presynaptic mechanism could depend on excessive dopamine release by axonal terminals of SNc neurons in the DLS on the side with SNc damage, which can result in increased contralateral rotational behavior.
“a presynaptic mechanism could depend on excessive dopamine release by axonal terminals of SNc neurons in the DLS on the side with SNc damage, which can also similarly result in increased contralateral rotational behavior (Konieczny et al. 2016).”
From Mitochondrial DNA Damage in Substantia Nigra Pars Compacta Astrocytes Exacerbates Dopaminergic Neuron Loss in a 6-Hydroxydopamine Mouse Model of Parkinsonism (2026) · cites this paper as Konieczny et al. 2016
An increase in contralateral rotations could be caused by either abnormal presynaptic axonal dopamine release by SNc DA neurons or hypersensitive postsynaptic D1/D2 dopamine receptors.
“An increase in contralateral rotations could be caused by either abnormal presynaptic axonal dopamine release by SNc DA neurons (Konieczny et al. 2016) and/or hypersensitive postsynaptic D1/D2 dopamine receptors (Creese et al. 1977; Groppetti et al. 1986; Rouillard et al. 1987).”
From Mitochondrial DNA Damage in Substantia Nigra Pars Compacta Astrocytes Exacerbates Dopaminergic Neuron Loss in a 6-Hydroxydopamine Mouse Model of Parkinsonism (2026) · cites this paper as Konieczny et al. 2016
Cites
Sulzer, D., Chen, T., Lau, Y., Kristensen, H., Rayport, S., & Ewing, A. (1995) · The Journal of Neuroscience · doi:10.1523/jneurosci.15-05-04102.1995 · Cited by 688 · see citing works
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Ayala, D. A., Hall, G. M., Das, D., Tijerina, E., Villagran, L. L., Khan, Z., Paliwal, D., Anand, A., Rimer, M., & Srinivasan, R. (2026) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-026-01713-x · Cited by 1 · see citing works
- Authors
- Konieczny, J., Lenda, T., & Czarnecka, A.
- Affiliations
- Maj Institute of Pharmacology (PL)
- Corresponding author
- Konieczny, J.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 324
- Pages
- 92-106
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2294448461
- Cited by
- 12
- References
- 1
- Citations by year
- 2026: 1 · 2020: 1 · 2019: 4 · 2018: 3 · 2017: 1 · 2016: 2
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Polish Ministry of Science and Higher Education (NN401 647340)
- Institute of Pharmacology
- Polish Academy of Sciences
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- lactacystin, dopamine release, dopamine D1 receptor, dopamine D2 receptor, ubiquitin-proteasome system, Parkinson's disease, substantia nigra, striatum, DOPAC, homovanillic acid, dopamine signaling, neurotoxicity, rotenone, MPP+, 6-hydroxydopamine
- MeSH terms
- Acetylcysteine, Amphetamine, Animals, Benzazepines, Central Nervous System Agents, Corpus Striatum, Dopamine, Haloperidol, Homovanillic Acid, Functional Laterality, Male, Movement, Receptors, Dopamine, Rotation, Substantia Nigra, 3,4-Dihydroxyphenylacetic Acid, Rats, Wistar, Dopamine Antagonists, Glutamic Acid, Parkinsonian Disorders
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