Significant effects of 4-aminopyridine and tetraethylammonium in the treatment of 6-hydroxydopamine-induced Parkinson's disease

Haghdoost-Yazdi, Hashem; Faraji, Ayda; Fraidouni, Negin; Movahedi, Mohadeseh; Hadibeygi, Elham; Vaezi, Fatemeh

doi:10.1016/j.bbr.2011.04.021

Cited by 18 publications

(6 citation statements)

References 46 publications

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“…Type AK + channels in dopaminergic nerves of SN contributed to pacemaker-controlling tonic activities 81 . Inhibitory action of type-AK + channel depolarized and increased the excitation by changing over from tonic-firing to burst-firing, thereby influencing dopamine-release 123 . MSN integrates various signaling pathways inside the cell thus causing dynamic modulation of membrane excitation.…”

Section: What Is Known About the Role Of Ion-channels In The Spread O...mentioning

confidence: 99%

Altered neural cell junctions and ion-channels leading to disrupted neuron communication in Parkinson’s disease

Choudhury

Bano

Sen

et al. 2022

npj Parkinsons Dis.

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Parkinson’s disease (PD) is a neurological disorder that affects the movement of the human body. It is primarily characterized by reduced dopamine levels in the brain. The causative agent of PD is still unclear but it is generally accepted that α-synuclein has a central role to play. It is also known that gap-junctions and associated connexins are complicated structures that play critical roles in nervous system signaling and associated misfunctioning. Thus, our current article emphasizes how, alongside α-synuclein, ion-channels, gap-junctions, and related connexins, all play vital roles in influencing multiple metabolic activities of the brain during PD. It also highlights that ion-channel and gap-junction disruptions, which are primarily mediated by their structural-functional changes and alterations, have a role in PD. Furthermore, we discussed available drugs and advanced therapeutic interventions that target Parkinson’s pathogenesis. In conclusion, it warrants creating better treatments for PD patients. Although, dopaminergic replenishment therapy is useful in treating neurological problems, such therapies are, however, unable to control the degeneration that underpins the disease, thereby declining their overall efficacy. This creates an additional challenge and an untapped scope for neurologists to adopt treatments for PD by targeting the ion-channels and gap-junctions, which is well-reviewed in the present article.

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Section: What Is Known About the Role Of Ion-channels In The Spread O...mentioning

confidence: 99%

Altered neural cell junctions and ion-channels leading to disrupted neuron communication in Parkinson’s disease

Choudhury

Bano

Sen

et al. 2022

npj Parkinsons Dis.

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“…Inhibition of A-type K ? channels results in depolarization and an increase in excitability converting the neuronal tonic firing mode to burst firing, thus enhancing the release of DA [48,49].…”

Section: Roles Of A-type K 1 Channels In Pdmentioning

confidence: 99%

“…In addition, 4-aminopyridine, another powerful blocker that inhibits A-type K ? channels, also attenuates functional asymmetry in the apomorphine-induced rotational test in 6-OHDAinduced rats [48,56,57]. Furthermore, glial cell-derived neurotrophic factor, which regulates the development and function of the nervous system, rapidly and reversibly inhibits A-type K ?…”

Section: Roles Of A-type K 1 Channels In Pdmentioning

confidence: 99%

Potassium Channels: A Potential Therapeutic Target for Parkinson’s Disease

et al. 2017

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The pathogenesis of the second major neurodegenerative disorder, Parkinson's disease (PD), is closely associated with the dysfunction of potassium (K) channels. Therefore, PD is also considered to be an ion channel disease or neuronal channelopathy. Mounting evidence has shown that K channels play crucial roles in the regulations of neurotransmitter release, neuronal excitability, and cell volume. Inhibition of K channels enhances the spontaneous firing frequency of nigral dopamine (DA) neurons, induces a transition from tonic firing to burst discharge, and promotes the release of DA in the striatum. Recently, three K channels have been identified to protect DA neurons and to improve the motor and non-motor symptoms in PD animal models: small conductance (SK) channels, A-type K channels, and K7/KCNQ channels. In this review, we summarize the physiological and pharmacological effects of the three K channels. We also describe in detail the laboratory investigations regarding K channels as a potential therapeutic target for PD.

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“…4 Previously, we examined effect of 4-AP and TEA in treatment of the behavioural symptoms of 6-OHDA-induced Parkinsonism. 17 We proposed that 4-AP and TEA can attenuate symptoms of 6-OHDA-induced Parkinsonism by increasing the electrical activity of SN dopaminergic neurons remaining alive after 6-OHDA injection. To do this, we first injected 6-OHDA into the brain of rats and measured severity of behavioural symptoms in them and then evaluated effect of TEA and 4-AP on these symptoms.…”

Section: Introductionmentioning

confidence: 99%

Pretreatment with potassium channel blockers of 4-aminopyridine and tetraethylammonium attenuates behavioural symptoms of Parkinsonism induced by intrastriatal injection of 6-hydroxydopamine; the role of lipid peroxidation

Haghdoost-Yazdi

Piri

Faraji

et al. 2016

Neurological Research

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Since severity of behavioural symptoms of 6-OHDA-induced Parkinsonism is correlated to the degree of nigral dopaminergic cell death, we suggest that antiparkinsonism effect of TEA and 4-AP was mediated by their neuroprotective effect. Because, both Parkinsonism in rat and PD in human, the main pathophysiological hallmark, is neurodegeneration of dopaminergic neurons in substantia nigra, we suggest doing clinical trials for evaluation of effectiveness of 4-AP and TEA in slowing down of PD progress.

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Significant effects of 4-aminopyridine and tetraethylammonium in the treatment of 6-hydroxydopamine-induced Parkinson's disease

Cited by 18 publications

References 46 publications

Altered neural cell junctions and ion-channels leading to disrupted neuron communication in Parkinson’s disease

Altered neural cell junctions and ion-channels leading to disrupted neuron communication in Parkinson’s disease

Potassium Channels: A Potential Therapeutic Target for Parkinson’s Disease

Pretreatment with potassium channel blockers of 4-aminopyridine and tetraethylammonium attenuates behavioural symptoms of Parkinsonism induced by intrastriatal injection of 6-hydroxydopamine; the role of lipid peroxidation

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