Our previous studies have shown that an environment of constant light (CL) can lead to development of high degree of hyperopia in newborn chicks by inducing severe corneal flattening, and compensatory growth of the vitreous chamber. We wish to know whether the abnormal eye growth and progressive hyperopia under CL conditions is accomplished by a mechanism that uses the visual processing pathways of the central nervous system (CNS) or by a mechanism located in the eye. Thirty white leghorn chicks (Cornell K-strain) were raised under 12 h light/12 h dark (12L/12D) for either optic nerve section (ONS) or ciliary ganglion section (CGS). Another 30 chicks were raised under CL for ONS or CGS. Refractive states and corneal curvatures were measured by infrared (IR) photoretinoscopy and IR keratometry, respectively. The axial lengths of the ocular components were measured by A-scan ultrasonography. Both ONS and CGS surgery produced dilated pupils and accommodative paralysis. Four weeks after surgery, CGS eyes exhibited a hyperopic defocus, flatter cornea, and shorter vitreous chamber depth under both CL and normal conditions, whereas ONS eyes showed a smaller radius of corneal curvature and shallow vitreous chamber only in the normal light cycle group. CGS eyes of CL chicks showed significantly deeper vitreous chambers than did fellow control eyes. Our results indicate that optic nerve section does not seem to influence CL effects. Thus, local mechanisms may play a major role in the ocular development of chicks. The ciliary nerve is necessary for the normal corneal and anterior chamber growth, and prevents CL effects. The progressively increasing vitreous chamber depth under CL may be influenced by both local and central mechanisms.