اﻟﻘﺎي ﻣﺪل ﺑﯿﻤﺎري آﻟﺰاﯾﻤﺮ ﺑﺎ ﺑﺘﺎ آﻣﯿﻠﻮﺋﯿﺪ در ﻣﻮش ﻫﺎي ﺻﺤﺮاﯾﯽ ﻧﺮ ﺷﮑﻞ ﭘﺬﯾﺮي ﺳﯿﻨﺎﭘﺴﯽ ﮐﻮﺗﺎه ﻣﺪت در ﻧﺎﺣﯿﻪ CA1 ﻫﯿﭙﻮﮐﻤﭗ را ﺗﻐﯿﯿﺮ ﻧﺪاد

Induction of a rat model of Alzheimer’s disease by amyloid-β did not change short term synaptic plasticity in CA1 area of hippocampus

ﺳﺎﺑﻘﻪ و ﻫﺪف: ﺑﯿﻤﺎري آﻟﺰاﯾﻤﺮ ﺑﻪ ﻋﻨﻮان ﻧﻮﻋﯽ از اﺧﺘﻼل ﺷﮑﻞ ﭘﺬﯾﺮي ﻋﺼﺒﯽ ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﺳﺖ. ﻋـﻼوه ﺑـﺮ وﻗـﻮع ﺗﻐﯿﯿﺮات دراز ﻣﺪت ﻧﺎﻣﻨﺎﺳﺐ در ﮐﺎرﮐﺮد ﺳﯿﻨﺎﭘﺴﯽ ﮐﻪ ﺑﻪ دﻧﺒﺎل آﻟﺰاﯾﻤﺮ در ﻣﻐﺰ اﯾﺠﺎد ﻣﯽ ﺷﻮد، ﺷـﮑﻞ ﭘـﺬﯾﺮي ﺳﯿﻨﺎﭘﺴـﯽ ﮐﻮﺗﺎه ﻣﺪت ﮐﻪ در ﭘﺮدازش اﻃﻼﻋﺎت ﻧﻘﺶ اﯾﻔﺎ ﻣﯽﮐﻨﺪ ﻧﯿﺰ ﻣﯽﺗﻮاﻧﺪ ﺗﻐﯿﯿﺮ ﻧﻤﺎﯾﺪ ﮐﻪ در اﯾﻦ ﻣﻄﺎﻟﻌﻪ ﺑﺮرﺳﯽ ﮔﺮدﯾﺪ. ﻣﻮاد و روش ﻫﺎ: ﭘﺘﺎﻧﺴﯿﻞ ﭘﺲ ﺳﯿﻨﺎﭘﺴﯽ ﺗﺤﺮﯾﮑﯽ ﻣﯿﺪاﻧﯽ (fEPSP) از ﻧﺎﺣﯿﻪ اﺳـﺘﺮاﺗﻮم رادﯾـﺎﺗﻮم CA1 ﺑـﻪ دﻧﺒـﺎل ﺗﺤﺮﯾﮏ ﺷﺎﺧﻪ ﻫﺎي ﺟﺎﻧﺒﯽ ﺷﺎﻓﺮ در ﻣﻮش ﻫﺎي ﻣﺪل آﻟﺰاﯾﻤﺮي ﺷﺪه ﺛﺒﺖ ﮔﺮدﯾﺪ. ﺟﻬﺖ اﻟﻘﺎي آﻟﺰاﯾﻤﺮ µl 1 از ﻣﺤﻠﻮل ﭘﭙﺘﯿﺪ µg/µl) Aβ 5) و µl 1 ﻣﺤﻠﻮل اﯾﺒﻮﺗﻨﯿﮏ اﺳﯿﺪ(µg/µl 5) ﺑﻪ ﺻﻮرت دوﻃﺮﻓﻪ داﺧﻞ ﻫﯿﭙﻮﮐﻤﭗ ﭘﺸﺘﯽ ﺗﺰرﯾـﻖ ﮔﺮدﯾـﺪ. ﺑـﻪ ﻣﻨﻈﻮر ﺑﺮرﺳﯽ ﺷﮑﻞ پذﯾﺮي ﺳﯿﻨﺎﭘﺴﯽ ﮐﻮﺗﺎه ﻣﺪت از ﺗﺤﺮﯾﮑﺎت زوج ﭘﺎﻟﺲ ﺑﺎ ﻓﻮاﺻﻞ ﺑﯿﻦ دو ﺗﺤﺮﯾـﮏ ) IPI( 80 ،20 و 200 ﻣﯿﻠﯽ ﺛﺎﻧﯿﻪ اﺳﺘﻔﺎده ﺷﺪ و ﺳﭙﺲ ﺷﺎﺧﺺ زوج ﭘﺎﻟﺲ ﻣﺤﺎﺳﺒﻪ ﮔﺮدﯾﺪ. ﯾﺎﻓﺘﻪ ﻫﺎ: اﮔﺮ ﭼﻪ اﻟﻘﺎي آﻟﺰاﯾﻤﺮ ﺳﺒﺐ ﮐﺎﻫﺶ ﭘﺎﺳﺦ ﺳﯿﻨﺎﭘﺴﯽ ﭘﺎﯾﻪ ﺑﻪ ﺧﺼﻮص در ﺷﺪت ﻫﺎي ﺗﺤﺮﯾﮏ ﺑﺎﻻ ﺷﺪ، اﻣﺎ اﯾـﻦ ﮐﺎﻫﺶ ﻣﻌﻨﯽ دار ﻧﺒﻮد (ANOVA, P>0/05). ﻫﻢ ﭼﻨﯿﻦ ﺷﺎﺧﺺ زوج ﭘﺎﻟﺲ در ﺣﯿﻮاﻧﺎت ﻣﺪل آﻟﺰاﯾﻤﺮ ﻧﯿﺰ در ﻫﯿﭻ ﮐـﺪام از IPI ﻫﺎ ﺷﺎﻣﻞ 20 ﻣﯿﻠﯽ ﺛﺎﻧﯿﻪ (4/68±40/4% و 5=n(، 80 ﻣﯿﻠﯽ ﺛﺎﻧﯿﻪ (129/8±4/1% و 5=n) و 200 ﻣﯿﻠﯽ ﺛﺎﻧﯿﻪ (129±6/89% و 5=n) ﺗﻔﺎوت ﻣﻌﻨﯽ داري ﺑﺎ ﮔﺮوه ﮐﻨﺘـﺮل (ﺑـﻪ ﺗﺮﺗﯿـﺐ 75/2±5/08%، 7/56±138%، 2/09±4/108% و 5=n) ﻧﺪاﺷـﺖ (P>0/05 ,unpaired t-test). ﻧﺘﯿﺠﻪ ﮔﯿﺮي: اﯾﻦ ﻧﺘﺎﯾﺞ ﻧﺸﺎن ﻣﯽدﻫﺪ ﮐﻪ اﻟﻘﺎي آﻟﺰاﯾﻤﺮ ﺑﻪ وﺳﯿﻠﻪ ﺗﺰرﯾﻖ آﻣﯿﻠﻮﺋﯿﺪ ﺑﺘﺎ در ﻫﯿﭙﻮﮐﻤﭗ ﻣﻨﺠﺮ ﺑـﻪ اﺧـﺘﻼل اﻧﺘﻘﺎل ﺳﯿﻨﺎﭘﺴﯽ ﭘﺎﯾﻪ و ﺷﮑﻞ ﭘﺬﯾﺮي ﺳﯿﻨﺎﭘﺴﯽ ﮐﻮﺗﺎه ﻣﺪت ﻧﻤﯽﺷﻮد.

Introduction: Alzheimer’s disease (AD) has been suggested to be a form of neuroplasticity failure. In addition to long term maladaptive changes in synaptic function, short term synaptic plasticity that has a role in information processing can be affected in AD that was investigated in this study. Materials and Methods: Field excitatory post synaptic potential (fEPSP) from Stratum radiatum of CA1 neurons were recorded following Schaffer collateral stimulation in a rat model of Alzheimer’s disease (AD). 1 µl of Aβ 1-42 (5µg/µl) and 1 µl of ibotenic acid (5µg/µl) were injected in dorsal hippocampus of male rats for AD induction. For examining the short-term synaptic plasticity, paired pulse stimulations with inter pulse interval (IPI) of 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated. Results: Results showed that although AD induction decreased basal synaptic responses especially at high stimulus intensity, this change was not significant (ANOVA; P>0.05). Also there were no significant changes in PPI of AD rats at different IPIs including 20 ms (%40.4±4.68, n=5), 80 ms (%129.8±4.1, n=5), and 200 ms (%129±6.8, n=5) in comparison with control ones (%75.2±5.08, %138±7.56, %108.4±2.09 respectively, n=5, P>0.05, unpaired t-test). Conclusion: Such results indicate that hippocampal Aβ treatment does not lead to impairment of basal synaptic response and short term synaptic plasticity.