The influence of gonadal steroids on insulin-like growth factor I (IGF-I)-like immunoreactivity was assessed in the rat arcuate nucleus, an area of the hypothalamus that regulates pituitary secretion. IGF-I-like immunoreactivity was observed in hypothalamic cells with the morphological aspects of tanycytes and astrocytes. The surface density of IGF-I-like immunoreactive glia increased with puberty in the arcuate nucleus of male and female rats, while decreasing with age in other brain areas. Gender differences in the surface density of IGF-I-like immunoreactive glia were detected in adult animals, with males and androgenized females having significantly higher values than normal females. In the latter, the surface density of IGF-I-like immunoreactive glia was increased in the afternoon of proestrus and in the morning of estrus compared to the morning of proestrus, diestrus and metestrus. In addition, IGF-I-like immunoreactivity showed a dose-dependent increase in ovariectomized rats injected with 17β-estradiol, but not in those receiving 17α-estradiol. The effect of 17β-estradiol was blocked by simultaneous administration of progesterone, while this hormone alone had no effect. These results indicate that IGF-I-like immunoreactivity in arcuate glial cells is affected by the hormonal environment and suggest that IGF-I-like immunoreactive glia may be involved in neuroendocrine events within the hypothalamus.

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Among the numerous endocrine signals that affect the central nervous system, sex steroids play an important +role. It has been recently postulated that part of the effects of these hormones on the brain may be mediated by trophic factors, such as insulin-like growth factor I (IGF-I). Both estradiol and IGF-I increase the survival and differentiation of developing fetal rat hypothalamic neurons in culture. The effect of estradiol is blocked by the pure estrogen receptor antagonist ICI 182,780, by an antisense oligonucleotide to the estrogen receptor, and by an antisense oligonucleotide to IGF-I. In turn, the effect of IGF-I is blocked by ICI 182,780 and by the antisense oligonucleotide to the estrogen receptor. These findings indicate that estrogen-induced activation of the estrogen receptor in developing hypothalamic neurons requires the presence of IGF-I and that both estradiol and IGF-I use the estrogen receptor to mediate their trophic effects on hypothalamic cells. In vivo, sex steroids affect IGF-I levels in the endocrine hypothalamus. IGF-I levels in tanycytes, a specific subtype of glial cells present in the arcuate nucleus and median eminence, are sexually dimorphic in the rat, increase with the onset of puberty, and are regulated by perinatal and adult levels of sex steroids. These changes may be due to hormonal modifications of IGF-I uptake by tanycytes from blood or cerebrospinal fluid. Therefore, this type of glial cell appears to play a central role in the interaction of sex steroids and IGF-I in the hypothalamus.

1. Recent evidence indicates that astroglia participate in the metabolism of gonadal hormones, in the synthesis of neurosteroids, and in the plastic responses of neurons to gonadal steroids. The role of astroglia on plastic responses of neural tissue to gonadal hormones and neurosteroids is examined in this review. 2. Gonadal steroids and neurosteroids promote astroglia plasticity in several areas of the central nervous system, including the hypothalamus, the striatum, and the hippocampus. 3. Gonadal steroids and neurosteroids modulate astroglia proliferation and the formation of reactive astroglia after brain injury. 4. Astroglia is a source of trophic factors that may mediate effects of gonadal steroids on neural tissue. 5. Astroglia is involved in the promotion of synaptic plastic changes by gonadal hormones. 6. The effect of gonadal hormones on astroglial plasticity is dependent on specific membrane interactions with neurons and on the expression of the embryonic highly polysialylated isoform of the neural cell adhesion molecule on neuronal membranes. 7. In conclusion, coordinated responses of neurons and astroglia appear to be involved in the modulation of neural function and response to injury by gonadal hormones and neurosteroids.

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