The unfolded protein response (UPR) is a homeostatic signaling pathway activated by the accumulation of misfolded or unfolded proteins in the endoplasmic reticulum (ER). In addition to its protective function, in recent years the UPR has been described playing essential roles during normal development, particularly in response to increased demands for protein folding. Several UPR effectors exhibit dynamic temporal and spatial expression patterns that correlate with milestones of the central nervous system (CNS) development. Notably, UPR activity has been shown to be specifically induced during dendrite development. Mammalian cells have three ER stress sensors, ATF6, IRE1alpha, and PERK, all of which are present in the ER of dendrites in primary mouse neurons. Although ATF6 deletion impacts embryonic brain development, its role in axonal growth and dendrite morphogenesis remains incompletely understood. Here, we investigated the requirement for basal ATF6 activity in the regulation of axonal growth, dendrite morphology, and spine density in primary hippocampal neurons treated or not with the neurotrophin BDNF.