Hi,
I am a Mechatronics Engineering student with no formal training in neuroscience. While exploring biologically inspired homeostatic mechanisms, I developed a hypothesis concerning inhibitory autapses.
Full hypothesis manuscript (PDF)
My central hypothesis is:
In neuron classes capable of inhibitory self-innervation, sustained elevated activity may, when self-apposition geometry and the biological context are permissive, increase the probability that a new self-contact forms or stabilizes and subsequently matures into a functional inhibitory autapse. The resulting autapse could then contribute negative feedback to neuronal excitability.
I found evidence supporting several individual parts of this idea: inhibitory autapses can suppress repetitive firing, neuronal activity can influence inhibitory synaptic plasticity and structural remodeling, and autaptic synaptogenesis can depend on biological context.
However, I have not found direct experimental evidence showing the complete causal step:
sustained elevated activity → formation or stabilization of a new inhibitory autapse.
My questions are:
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Is this hypothesis biologically plausible?
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Is there existing literature that directly tests this activity-to-autapse formation relationship?
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What would be the most appropriate experiment to test it?
I have attached a short hypothesis manuscript with the relevant references and proposed experimental test.
As my background is in mechatronics rather than neuroscience, I may have overlooked important mechanisms or literature, so critical feedback would be very valuable.
Thank you.