Chronic and acute acrylamide exposure on cell-type-specific neurotoxicity in bumblebee brain

Acrylamide (AA) is a common carcinogen that affects the development and function of the central nervous system (CNS). At present, the toxic injuries of common AA are mainly divided into acute and chronic attacks, and the damage caused to the CNS is different. To investigate whether different doses of AA have different effects on brain cells, we performed single-nucleus RNA sequencing of the brain. The findings indicated that short-term high-dose (acute) AA directly disrupted protein synthesis and protein structure stability on the endoplasmic reticulum. Additionally, acute AA was observed to downregulate genes that inhibit apoptosis and autophagy, promote apoptosis, accelerate cell aging, and affect cell function in glial cells (Glia). Long-term low-dose (chronic) AA exposure elevated Ca²⁺ concentration, increased protein autophosphorylation, and induced mitochondrial dysfunction, resulting in impaired axonal transport and disrupted metabolism of Kenyon cells (KCs). These findings highlight the cell type-specific effects of AA, where acute exposure disrupts Glia protein homeostasis, and chronic exposure impairs calcium signaling and axonal transport in KCs. Such results deepen our understanding of AA-induced neurotoxicity and lay the groundwork for developing targeted therapeutic strategies to mitigate its effects on the CNS.