Unilateral lesion of the nigroestriatal pathway with 6-OHDA induced allodynia and hyperalgesia reverted by pramipexol in rats

Romero-Sánchez, Héctor Alonso; Mendieta, Liliana; Austrich-Olivares, Amaya; Garza-Mouriño, Gabriela; Mirón, Marcela Benitez-Diaz; Coen, Arrigo; Godínez‐Chaparro, Beatriz

doi:10.1016/j.ejphar.2019.172814

Cited by 11 publications

(10 citation statements)

References 35 publications

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“…Romero-Sánchez et al (2020) administered 6, 10, and 16 µg of 6-OHDA in 2 µL (at 0.1 µL/min) unilaterally into left substantia nigra to induce the lesion and revealed that the impaired nigrostriatal dopaminergic pathway in male Wistar rat models. The 6-OHDA (16 µg dose) unilateral lesion affected the animal as a neurotoxic model of PD; i.e., the painful sensation, for instance, caused the allodynia and hyperalgesia [ 98 ]. Besides, a regular pramipexole (3.0 mg/kg, intraperitoneally) treatment prevented the allodynia and hyperalgesia-induced by 6-OHDA in PD model rats [ 98 ].…”

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

“…The 6-OHDA (16 µg dose) unilateral lesion affected the animal as a neurotoxic model of PD; i.e., the painful sensation, for instance, caused the allodynia and hyperalgesia [ 98 ]. Besides, a regular pramipexole (3.0 mg/kg, intraperitoneally) treatment prevented the allodynia and hyperalgesia-induced by 6-OHDA in PD model rats [ 98 ]. Huang et al (2019) administered 8 µg of 6-OHDA dose in 4 µL (saline and ascorbic acid) and applied unilateral injection to induce PD symptoms in male Sprague Dawley rat models.…”

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

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Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Prasad

Hung

2020

Antioxidants

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Currently, neurodegenerative diseases are a major cause of disability around the world. Parkinson’s disease (PD) is the second-leading cause of neurodegenerative disorder after Alzheimer’s disease. In PD, continuous loss of dopaminergic neurons in the substantia nigra causes dopamine depletion in the striatum, promotes the primary motor symptoms of resting tremor, bradykinesia, muscle rigidity, and postural instability. The risk factors of PD comprise environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular injury, aging, and hereditary defects. The pathologic features of PD include impaired protein homeostasis, mitochondrial dysfunction, nitric oxide, and neuroinflammation, but the interaction of these factors contributing to PD is not fully understood. In neurotoxin-induced PD models, neurotoxins, for instance, 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-Methyl-4-phenylpyridinium (MPP+), paraquat, rotenone, and permethrin mainly impair the mitochondrial respiratory chain, activate microglia, and generate reactive oxygen species to induce autooxidation and dopaminergic neuronal apoptosis. Since no current treatment can cure PD, using a suitable PD animal model to evaluate PD motor symptoms’ treatment efficacy and identify therapeutic targets and drugs are still needed. Hence, the present review focuses on the latest scientific developments in different neurotoxin-induced PD animal models with their mechanisms of pathogenesis and evaluation methods of PD motor symptoms.

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Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

Section: Neurotoxins Used To Induce Pd In Vivo Modelsmentioning

confidence: 99%

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Prasad

Hung

2020

Antioxidants

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“…As the frequency of spontaneous blinking increased, the perception of pain decreased. In this regard, abnormal pain perception has been observed both in animal models 24,54,55 and human pathological conditions characterized by a reduction in central dopaminergic tone 16,17,56,57 , such as depression and PD. Moreover, recent pharmacological studies strongly support the role of dopamine in antinociception.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, recent pharmacological studies strongly support the role of dopamine in antinociception. Dopamine agonists, like pramipexole, have been shown to induce antiallodynic and antihyperalgesic effects in rats with nigrostriatal lesions 55 . The selective activation of D2 receptors led to decreased nociception, increasing the pain threshold in a transitory or lasting manner according to the experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

Painful stimulation increases spontaneous blink rate in healthy subjects

Paparella

Stefano

Fasolino

et al. 2020

Sci Rep

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Spontaneous blink rate is considered a biomarker of central dopaminergic activity. Recent evidence suggests that the central dopaminergic system plays a role in nociception. In the present study, we aimed to investigate whether pain modulates spontaneous blink rate in healthy subjects. We enrolled 15 participants. Spontaneous blink rate was quantified with an optoelectronic system before and after: (1) a painful laser stimulation, and (2) an acoustic startling stimulation. In control experiments, we investigated whether laser stimulation effects depended on stimulation intensity and whether laser stimulation induced any changes in the blink reflex recovery cycle. Finally, we investigated any relationship between spontaneous blink rate modification and pain modulation effect during the cold pressor test. Laser, but not acoustic, stimulation increased spontaneous blink rate. This effect was independent of stimulation intensity and negatively correlated with pain perception. No changes in trigeminal-facial reflex circuit excitability were elicited by laser stimulation. The cold pressor test also induced an increased spontaneous blink rate. Our study provides evidence on the role of dopamine in nociception and suggests that dopaminergic activity may be involved in pain modulation. These findings lay the groundwork for further investigations in patients with pathological conditions characterized by dopaminergic deficit and pain.

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“…Some nociceptive pain associated with PD is a secondary consequence of the motor impairment (abnormal muscular tone, spasms, rigidity, reduced active mobility, osteoarticular problems, and local inflammation), however, as many as 43% of Parkinson patients exhibits characteristics typical of neuropathic dysfunction (burning, tingling, formicating, decreased nocifensive flexion reflex, and lowered cold threshold) (Reichling and Levine, 2011;Skogar and Lokk, 2016;de Tommaso et al, 2017). Neuropathic pain has been recently studied in a model of nigro-estriatal pathway lesion, which induces allodynia and hyperalgesia in rats (Romero-Sánchez et al, 2019).…”

Section: Trps Involvement In Pain Alzheimer's and Parkinson's Diseasesmentioning

confidence: 99%

TRP Channels Role in Pain Associated With Neurodegenerative Diseases

et al. 2020

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Transient receptor potential (TRP) are cation channels expressed in both non-excitable and excitable cells from diverse tissues, including heart, lung, and brain. The TRP channel family includes 28 isoforms activated by physical and chemical stimuli, such as temperature, pH, osmotic pressure, and noxious stimuli. Recently, it has been shown that TRP channels are also directly or indirectly activated by reactive oxygen species. Oxidative stress plays an essential role in neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases, and TRP channels are involved in the progression of those diseases by mechanisms involving changes in the crosstalk between Ca 2+ regulation, oxidative stress, and production of inflammatory mediators. TRP channels involved in nociception include members of the TRPV, TRPM, TRPA, and TRPC subfamilies that transduce physical and chemical noxious stimuli. It has also been reported that pain is a complex issue in patients with Alzheimer's and Parkinson's diseases, and adequate management of pain in those conditions is still in discussion. TRPV1 has a role in neuroinflammation, a critical mechanism involved in neurodegeneration. Therefore, some studies have considered TRPV1 as a target for both pain treatment and neurodegenerative disorders. Thus, this review aimed to describe the TRP-dependent mechanism that can mediate pain sensation in neurodegenerative diseases and the therapeutic approach available to palliate pain and neurodegenerative symptoms throughout the regulation of these channels.

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Unilateral lesion of the nigroestriatal pathway with 6-OHDA induced allodynia and hyperalgesia reverted by pramipexol in rats

Cited by 11 publications

References 35 publications

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Painful stimulation increases spontaneous blink rate in healthy subjects

TRP Channels Role in Pain Associated With Neurodegenerative Diseases

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