The development of axon number in the anterior commissure (AC) was analyzed in 39 normal and 37 hypothyroid rats using conventional electron microscopy. Hypothyroid rats underwent antithyroid treatment with methimazole from embryonic day (E) 14 onwards, followed in a fraction of the animals by thyroidectomy at postnatal day (P) 6. In normal rats, the midsagittal cross-sectional anterior commissure area (ACA) increased throughout their life; in hypothyroid rats, ACA was stationary from P4 onwards and at P174-180 it was reduced by 39% relative to normal rats. In normal rats, the number of AC axons increased rapidly from 168,500 at E18 to, on average, 1,049,000 from P4 onwards. Similarly, in hypothyroid rats, the number of axons increased from 135,000 at E18 to, on average, 1,052,000 from P4 onwards. At all ages, the number of axons was similar in normal and hypothyroid rats. During development of the AC, the evolution of axon number observed in normal and hypothyroid rats is different from what was reported for other telencephalic commissures, including the AC of the monkey, where an important fraction of the axons are eliminated postnatally. Antithyroid treatment dissociated ACA from total number of AC axons.