ArticlebioRxiv : the preprint server for biology2025
PKC-dependent enhancement of glutamate input to VTA dopamine neurons in 3xTg-AD mice.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
A growing body of work has recently linked ventral tegmental area (VTA) dopamine neuron dysfunction to Alzheimer's disease (AD). Work in AD mouse models suggests that VTA dopamine neurons are intrinsically hyperexcitable, yet release less dopamine and exhibit disrupted downstream signaling. Significant focus has been placed on describing dopamine release in projection regions; however, dopamine neurons somatodendritically integrate vast synaptic input, altering action potential output and ultimately determining neurotransmiter release. Synaptic transmission is broadly disrupted in AD, but it is not known to what extent excitatory and inhibitory inputs to the VTA are altered. Here we describe enhanced synaptic excitation in dopamine neurons in the amyloid + tau-driven 3xTg-AD mouse model. Patch-clamp electrophysiology experiments revealed enhanced AMPAR-mediated excitatory input in a subset of perisomatic connections. In contrast, GABA
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Registered trials
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