The development of axon number in the anterior commissure (AC) was ana
lyzed in 39 normal and 37 hypothyroid rats using conventional electron
microscopy. Hypothyroid rats underwent antithyroid treatment with met
himazole from embryonic day (E) 14 onwards, followed in a fraction of
the animals by thyroidectomy at postnatal day (P) 6. In normal rats, t
he midsagittal cross-sectional anterior commissure area (ACA) increase
d throughout their life; in hypothyroid rats, ACA was stationary from
P4 onwards and at P174-180 it was reduced by 39% relative to normal ra
ts. 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 hy
pothyroid 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 axon
s was similar in normal and hypothyroid rats. During development of th
e AC, the evolution of axon number observed in normal and hypothyroid
rats is different from what was reported for other telencephalic commi
ssures, including the AC of the monkey, where an important fraction of
the axons are eliminated postnatally. Antithyroid treatment dissociat
ed ACA from total number of AC axons.