Asset Details
Do you wish to reserve the book?
Hericium erinaceus potentially rescues behavioural motor deficits through ERK-CREB-PSD95 neuroprotective mechanisms in rat model of 3-acetylpyridine-induced cerebellar ataxia
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Hericium erinaceus potentially rescues behavioural motor deficits through ERK-CREB-PSD95 neuroprotective mechanisms in rat model of 3-acetylpyridine-induced cerebellar ataxia
Do you wish to request the book?
Hericium erinaceus potentially rescues behavioural motor deficits through ERK-CREB-PSD95 neuroprotective mechanisms in rat model of 3-acetylpyridine-induced cerebellar ataxia
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Hericium erinaceus potentially rescues behavioural motor deficits through ERK-CREB-PSD95 neuroprotective mechanisms in rat model of 3-acetylpyridine-induced cerebellar ataxia
2020
Overview
Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although several studies have demonstrated the neuroprotective effects of
Hericium erinaceus
(H.E.), its mechanisms in cerebellar ataxia remain largely unknown. Here, we investigated the neuroprotective effects of H.E. treatment in an animal model of 3-acetylpyridine (3-AP)-induced cerebellar ataxia. Animals administered 3-AP injection exhibited remarkable impairments in motor coordination and balance. There were no significant effects of 25 mg/kg H.E. on the 3-AP treatment group compared to the 3-AP saline group. Interestingly, there was also no significant difference in the 3-AP treatment group compared to the non-3-AP control, indicating a potential rescue of motor deficits. Our results revealed that 25 mg/kg H.E. normalised the neuroplasticity-related gene expression to the level of non-3-AP control. These findings were further supported by increased protein expressions of pERK1/2-pCREB-PSD95 as well as neuroprotective effects on cerebellar Purkinje cells in the 3-AP treatment group compared to the 3-AP saline group. In conclusion, our findings suggest that H.E. potentially rescued behavioural motor deficits through the neuroprotective mechanisms of ERK-CREB-PSD95 in an animal model of 3-AP-induced cerebellar ataxia.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Behavior, Animal - drug effects
/ Cerebellar Ataxia - chemically induced
/ Cerebellar Ataxia - drug therapy
/ Cerebellar Ataxia - psychology
/ Cyclic AMP Response Element-Binding Protein - genetics
/ Cyclic AMP Response Element-Binding Protein - metabolism
/ Disks Large Homolog 4 Protein - genetics
/ Disks Large Homolog 4 Protein - metabolism
/ Extracellular Signal-Regulated MAP Kinases - genetics
/ Extracellular Signal-Regulated MAP Kinases - metabolism
/ Hericium - growth & development
/ Humanities and Social Sciences
/ Male
/ Motor Disorders - metabolism
/ Motor Disorders - prevention & control
/ Neuroprotective Agents - pharmacology
/ Platinum
/ Purkinje Cells - drug effects
/ Rats
/ Science
/ Tumors
