Alzheimer’s disease (AD) is characterized by the accumulation of amyloid plaques, neuronal decline, and memory deficits. The Taconic 1349-RD1 mouse model expresses the human APP695 gene with the Swedish mutation (K670N, M671L), which leads to elevated levels of β-amyloid, promoting the formation of significant amyloid plaques in the brain and resulting in neurotoxicity and cognitive impairments. This model is highly relevant for studying APP expression, amyloid plaque formation, neuronal decline, and memory loss associated with AD.
Using multi-electrode array (MEA) technology, we investigated synaptic properties in Taconic 1349-RD1 mice in comparison with wild-type littermates using electrophysiological assays such as Input/Output (IO) curves, paired-pulse facilitation (PPF), and long-term potentiation (LTP).
By comparing Taconic 1349-RD1 mice with wild-type littermates, we observed reduced synaptic activity across all these readouts, with more significant impairments in IO curves and LTP. These results have been reproduced and validate the Taconic 1349-RD1 mouse as a reliable model for synaptic dysfunction, providing high translational value for studying neurodegenerative diseases such as AD.
This model has been developed after overnight incubation, enabling the preincubation of test compounds to assess their effects on synaptic plasticity. It represents a powerful tool for drug discovery and therapeutic testing, for the evaluation of novel treatments aimed at restoring synaptic function and plasticity.
Synaptic activity is assessed by recording field excitatory post-synaptic potentials (fEPSPs) elicited in the CA1 region through electrical stimulation of the Schaffer collateral pathway. Stimulation is applied at the CA3/CA1 border of the Schaffer collaterals, with an intensity set to 40% of the maximum input intensity (Imax), as determined from the input-output (I-O) curve
Input/Output (IO) curves, paired-pulse facilitation (PPF), and long-term potentiation (LTP) are key electrophysiological assays for assessing synaptic function and plasticity. IO curves provide a measure of baseline synaptic transmission, revealing potential deficits in synaptic strength. Paired-pulse facilitation is used to evaluate presynaptic function and short-term plasticity measuring changes in neurotransmitter release, which can indicate alterations in synaptic connectivity or vesicle dynamics. LTP reflects the brain’s ability to strengthen synaptic connections over time, a fundamental process underlying learning and memory.
By comparing Taconic 1349-RD1 mice with wild-type littermates, we observed reduced synaptic activity across all these readouts, with more significant impairments in IO curves and LTP. These results have been reproduced and validate the Taconic 1349-RD1 mouse as a reliable model for synaptic dysfunction, providing high translational value for studying neurodegenerative diseases such as AD.
This model has been developed after overnight incubation, enabling the preincubation of test compounds to assess their effects on synaptic plasticity. It represents a powerful tool for drug discovery and therapeutic testing, for the evaluation of novel treatments aimed at restoring synaptic function and plasticity
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Bruno Buisson, PhD Romain Teyssie
Co-Founder, President & CSO MEA Engineer
Bruno BUISSON is a neurophysiologist and With a Degree in Biological Sciences
neuropharmacologist with over 30 years of and a Master’s Degree in Biotechnology,
experience in research projects both in Romain has 14 years of experience leading
academic laboratories and pharma/ customer and R&D projects for the MEA
biotech companies laboratory in France
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