2019Neuropsychopharmacology ReportsOpen access

Induced neuronal activity does not attenuate amyloid beta‐induced synaptic loss in vitro

Rena Kono, Gyu Li Kim, Hidetaka Nagata, Yuji Ikegaya, Ryuta Koyama

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Abstract

AIM: The accumulation of amyloid beta (Aβ) is one of the characteristics of Alzheimer's disease. The excessive accumulation of Aβ has been suggested to result in a decrease in the number of synapses. Although the number of synapses is generally modulated by neuronal activity, whether neuronal activity affects Aβ-induced synapse loss remains unknown. Therefore, we addressed this question using a primary culture of hippocampal neurons. METHOD: The neuronal activity of cultured hippocampal neurons from mouse pups was increased using the chemogenetic technique designer receptors exclusively activated by designer drugs (DREADD). The cultured neurons were treated with Aβ, and synapse density was assessed by immunocytochemistry. RESULTS: Aβ decreased the synapse density probably by decreasing postsynapse. On the other hand, enhanced neuronal activity did not affect the synapse density significantly. However, there was a trend that enhanced neuronal activity increased especially presynapse density. CONCLUSION: We found that enhanced neuronal activity did not affect Aβ-induced synapse loss in vitro.

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AIM: The accumulation of amyloid beta (Aβ) is one of the characteristics of Alzheimer's disease. The excessive accumulation of Aβ has been suggested to result in a decrease in the number of synapses. Although the number of synapses is generally modulated by neuronal activity, whether neuronal activity affects Aβ-induced synapse loss remains unknown. Therefore, we addressed this question using a primary culture of hippocampal neurons. METHOD: The neuronal activity of cultured hippocampal neurons from mouse pups was increased using the chemogenetic technique designer receptors exclusively activated by designer drugs (DREADD). The cultured neurons were treated with Aβ, and synapse density was assessed by immunocytochemistry. RESULTS: Aβ decreased the synapse density probably by decreasing postsynapse. On the other hand, enhanced neuronal activity did not affect the synapse density significantly. However, there was a trend that enhanced neuronal activity increased especially presynapse density. CONCLUSION: We found that enhanced neuronal activity did not affect Aβ-induced synapse loss in vitro.

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Available abstract

AIM: The accumulation of amyloid beta (Aβ) is one of the characteristics of Alzheimer's disease. The excessive accumulation of Aβ has been suggested to result in a decrease in the number of synapses. Although the number of synapses is generally modulated by neuronal activity, whether neuronal activity affects Aβ-induced synapse loss remains unknown. Therefore, we addressed this question using a primary culture of hippocampal neurons. METHOD: The neuronal activity of cultured hippocampal neurons from mouse pups was increased using the chemogenetic technique designer receptors exclusively activated by designer drugs (DREADD). The cultured neurons were treated with Aβ, and synapse density was assessed by immunocytochemistry. RESULTS: Aβ decreased the synapse density probably by decreasing postsynapse. On the other hand, enhanced neuronal activity did not affect the synapse density significantly. However, there was a trend that enhanced neuronal activity increased especially presynapse density. CONCLUSION: We found that enhanced neuronal activity did not affect Aβ-induced synapse loss in vitro.

Key concepts: Synapse, Hippocampal formation, Premovement neuronal activity, Neuroscience, Immunocytochemistry, In vitro, Biology, BETA (programming language)

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