<p>The injury to neurons and connection structures in the nervous system is a key factor leading to neurodegenerative diseases. Self-repair function refers to the innate capacity of the neuron–astrocyte network to partially restore or maintain its function following injury, without external intervention. When the brain’s nervous system is injured, how self-repair mechanisms work under various injury conditions and how to improve self-repair function remain unresolved. Through computational simulations of three distinct neurological injury scenarios, we investigated the self-repair function of spiking neuron–astrocyte networks in working memory tasks. Despite varying degrees of disruption of the network, all experiments (Self-Repair activated by synaptic connection injury, astrocytes injury, and internal noise interference) reveal that astrocytes can promote self-repair of the network during working memory tasks. Experiments on synaptic connection injury demonstrated that the network can maintain effective repair functionality under high injury conditions, which is associated with elevated calcium ion concentrations induced by increased glutamate release from presynaptic neurons. The modulation of astrocyte contributes to self-repair, and self-repair function decreases with increasing astrocyte injury. In addition, compared to the health network, internal noise interference has a small enhancement in the self-repair function of the network. Our findings elucidate the critical role of astrocyte-mediated signaling in maintaining network under different synaptic injury. This provides novel mechanistic insights into the threshold dynamics governing neuron network stability and early pathological transition in response to diverse neural injuries.</p>