Ameliorative effect of gastrodin on 3,3′-iminodipropionitrile-induced memory impairment in rats

Wang, Xiaona; Yuan, Tao; Zhang, Feng

doi:10.1016/j.neulet.2015.03.049

Cited by 15 publications

(5 citation statements)

References 33 publications

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“…Therefore, this model may be useful to identify the cellular and molecular basis of vestibular dysfunction and recovery associated with chronic ototoxicity and washout. Although the literature contains a noticeable number of references on the CNS toxicity of IDPN ( Wang et al, 2015 ), their value is dubious as they ignore the firmly established fact that the effects of IDPN on spontaneous motor behavior are a syndrome of vestibular dysfunction ( Llorens et al, 1993 ; Llorens and Rodríguez-Farré, 1997 ; Boadas-Vaello et al, 2005 ; Soler-Martín et al, 2007 ; Saldaña-Ruíz et al, 2012a , b ). The test battery used in the present study to assess vestibular dysfunction is highly specific and not affected by the alleged CNS effects of IDPN ( Llorens and Rodríguez-Farré, 1997 ; Seoane et al, 1999 ; Boadas-Vaello et al, 2005 ).…”

Section: Discussionmentioning

confidence: 99%

Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.

Sedó-Cabezón

Jedynak

Boadas-Vaello

et al. 2015

Disease Models &Amp; Mechanisms

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Ototoxicity is known to cause permanent loss of vestibule function through degeneration of sensory hair cells (HCs). However, functional recovery has been reported during washout after chronic ototoxicity, although the mechanisms underlying this reversible dysfunction are unknown. Here, we study this question in rats chronically exposed to the ototoxic compound 3,3′-iminodipropionitrile (IDPN). Pronounced alterations in vestibular function appeared before significant loss of HCs or stereociliary coalescence became evident by ultrastructural analyses. This early dysfunction was fully reversible if the exposure was terminated promptly. In cristae and utricles, the distinct junctions formed between type I HCs (HCI) and calyx endings were completely dismantled at these early stages of reversible dysfunction, and completely rebuilt during washout. Immunohistochemical observations revealed loss and recovery of the junction proteins CASPR1 and tenascin-C and RT-PCR indicated that their loss was not due to decreased gene expression. KCNQ4 was mislocalized during intoxication and recovered control-like localization after washout. At early stages of the intoxication, the calyces could be classified as showing intact or lost junctions, indicating that calyceal junction dismantlement is triggered on a calyx-by-calyx basis. Chronic toxicity also altered the presence of ribeye, PSD-95 and GluA2 puncta in the calyces. These synaptic alterations varied between the two types of calyx endings (formed by calyx-only or dimorphic afferents) and some persisted at the end of the washout period. The present data reveal new forms of plasticity of the calyx endings in adult mammals, including a robust capacity for rebuilding the calyceal junction. These findings contribute to a better understanding of the phenomena involved in progressive vestibular dysfunction and its potential recovery during and after ototoxic exposure.

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Section: Discussionmentioning

confidence: 99%

Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.

Sedó-Cabezón

Jedynak

Boadas-Vaello

et al. 2015

Disease Models &Amp; Mechanisms

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“…The antiamnestic effect has been explored as well [ 58 , 59 ]. By normalizing the serotoninergic system [ 60 ] and the dopaminergic system [ 61 ], GAS ameliorates memory deficits in 3,3′-iminodipropionitrile-induced rats. Our present study demonstrates the memory protective effect of BBB opening via FUS combined with GAS treatment in A β 1-42 -induced AD-like mouse, possibly via the BDNF-stimulating and neuroplasticity-promoting effect.…”

Section: Discussionmentioning

confidence: 99%

Treatment Combining Focused Ultrasound with Gastrodin Alleviates Memory Deficit and Neuropathology in an Alzheimer’s Disease-Like Experimental Mouse Model

et al. 2022

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Alzheimer’s disease (AD) is the most common type of dementia but lacks effective treatment at present. Gastrodin (GAS) is a phenolic glycoside extracted from the traditional Chinese herb—Gastrodia elata—and has been reported as a potential therapeutic agent for AD. However, its efficiency is reduced for AD patients due to its limited BBB permeability. Studies have demonstrated the feasibility of opening the blood-brain barrier (BBB) via focused ultrasound (FUS) to overcome the obstacles preventing medicines from blood flow into the brain tissue. We explored the therapeutic potential of FUS-mediated BBB opening combined with GAS in an AD-like mouse model induced by unilateral intracerebroventricular (ICV) injection of Aβ1-42. Mice were divided into 5 groups: control, untreated, GAS, FUS and FUS+GAS. Combined treatment (FUS+GAS) rather than single intervention (GAS or FUS) alleviated memory deficit and neuropathology of AD-like mice. The time that mice spent in the novel arm was prolonged in the Y-maze test after 15-day intervention, and the waste-cleaning effect was remarkably increased. Contents of Aβ, tau, and P-tau in the observed (also the targeted) hippocampus were reduced. BDNF, synaptophysin (SYN), and PSD-95 were upregulated in the combined group. Overall, our results demonstrate that FUS-mediated BBB opening combined with GAS injection exerts the potential to alleviate memory deficit and neuropathology in the AD-like experimental mouse model, which may be a novel strategy for AD treatment.

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“…Although the underlying mechanisms have not been well understood, evidence suggests it could lead to alterations in the 5-HT, DA, and ACh neuronal systems and cause damage to hippocampus. Wang X. et al ( 2014 ) established a rat model of cognitive impairment by IDPN exposure, and discovered that gastrodin could significantly mitigate the IDPN-induced cognitive deficits in the Y-maze test, passive avoidance task and Morris water maze (Wang X. et al, 2014 ; Wang et al, 2015 , 2016 ). In addition, gastrodin could prevent IDPN-induced decrease of DA, 5-HT, and GABA levels and elevation of DA turnover and 5-HT turnover ratios.…”

Section: Effects Of Gastrodin On Cns Diseasesmentioning

confidence: 99%

A Review on Central Nervous System Effects of Gastrodin

et al. 2018

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Rhizoma Gastrodiae (also known as Tian ma), the dried rhizome of Gastrodia elata Blume, is a famous Chinese herb that has been traditionally used for the treatment of headache, dizziness, spasm, epilepsy, stoke, amnesia and other disorders for centuries. Gastrodin, a phenolic glycoside, is the main bioactive constituent of Rhizoma Gastrodiae. Since identified in 1978, gastrodin has been extensively investigated on its pharmacological properties. In this article, we reviewed the central nervous system (CNS) effects of gastrodin in preclinical models of CNS disorders including epilepsy, Alzheimer's disease, Parkinson's disease, affective disorders, cerebral ischemia/reperfusion, cognitive impairment as well as the underlying mechanisms involved and, where possible, clinical data that support the pharmacological activities. The sources and pharmacokinetics of gastrodin were also reviewed here. As a result, gastrodin possesses a broad range of beneficial effects on the above-mentioned CNS diseases, and the mechanisms of actions include modulating neurotransmitters, antioxidative, anti-inflammatory, suppressing microglial activation, regulating mitochondrial cascades, up-regulating neurotrophins, etc. However, more detailed clinical trials are still in need for positioning it in the treatment of neurological disorders.

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Ameliorative effect of gastrodin on 3,3′-iminodipropionitrile-induced memory impairment in rats

Cited by 15 publications

References 33 publications

Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.

Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.

Treatment Combining Focused Ultrasound with Gastrodin Alleviates Memory Deficit and Neuropathology in an Alzheimer’s Disease-Like Experimental Mouse Model

A Review on Central Nervous System Effects of Gastrodin

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