The term "autapse" was first coined in 1972 by Van der Loos and Glaser, who observed them in Golgi preparations of the rabbit occipital cortex while originally conducting a quantitative analysis of neocortex circuitry.
[13] Recently, it has been proposed that autapses could possibly form as a result of neuronal signal transmission blockage, such as in cases of axonal injury induced by poisoning or impeding ion channels.
[14] Dendrites from the soma in addition to an auxiliary axon may develop to form an autapse to help remediate the neuron's signal transmission.
This suggests that autapses act by suppressing the second of two closely timed depolarization steps and therefore, they may provide feedback inhibition onto these cells.
[18] Hindmarsh–Rose (HR) model neurons have demonstrated chaotic, regular spiking, quiescent, and periodic patterns of burst firing without autapses.
In HR model neurons without autapses, the pattern of firing altered from quiescent to periodic and then to chaotic as DC current was increased.
In the 1990s, paroxysmal depolarizing shift-type interictal epileptiform discharges has been suggested to be primarily dependent on autaptic activity for solitary excitatory hippocampal rat neurons grown in microculture.
Using a glia-conditioned medium to treat glia-free purified rat retinal ganglion microcultures has been shown to significantly increase the number of autapses per neuron compared to a control.
[27] This suggests that glia-derived soluble, proteinase K-sensitive factors induce autapse formation in rat retinal ganglion cells.