Content area
Abstract
It is known that gonadal steroids induce synaptic plasticity in several areas of the developing and adult nervous system. Most of the data concerning synaptic remodeling have been obtained from the hypothalamic arcuate nucleus. The nucleus integrates different hormonal and neural signals to control neuroendocrine events, feeding, energy balance and reproduction. Previous studies have shown that in adult female rats the arcuate nucleus undergoes a 17β-estradiol-triggered phasic synaptic remodeling as a function of changing hormone levels, resulting in a decrease in the number of inhibitory synaptic inputs, an increase in the number of excitatory synapses and an enhancement of the frequency of neuronal firing (Perez et al., 1993; Parducz et al., 2002; Kis et al., 1999).
Our findings indicate that there is a significant decrease in the number of GABAergic axo-somatic synapses on proestrus afternoon and estrus day compared to other phases of the estrus cycle. This decrease in GABAergic synapses is accompanied by an increase in the number of dendritic spine synapses. The synaptic density appears to cycle back to proestrus morning values on metestrus day. In contrast, the number of synapses on dendritic shafts does not change during the cycle. These results indicate that a rapid and selective synaptic turnover of arcuate synapses occurs in physiological circumstances.
Recent experimental data indicate that neurosteroids are also important in synaptic remodeling (Hajszan et al., 2004; Leranth et al., 2004; MacLusky et al., 2004). We have observed that in females similarly to estrogen, DHEA treatment also induces a significant decrease in the numerical density of GABAergic axo-somatic synapses in the arcuate nucleus, while the non-GABAergic synapses remain unaffected. Because DHEA and its metabolites have multiple effects in the CNS, more detailed studies are needed to determine the exact mechanism of their actions.
The specificity of the hormonal effect is not confined to the presynaptic element, it is observable at the level of postsynaptic cells, as well (Parducz et al., 2003). We selected the tyrosine hydroxylase immunoreactive neurons in the arcuate and studied the changes in their synaptic connectivity. Our study shows that the effect of 17β-estradiol is sex and cell specific in the sense that not all arcuate neurons are affected by the structural synaptic remodeling. In ovariectomized females hormonal treatment results in a significant decrease in the numerical density of GABAergic axosomatic contacts synapsing on TH-IR neurons, while in orchidectomized and 17βestradiol-treated males the non-labeled neurons receive higher number of inhibitory terminals. Our data indicate that the hormonally induced plastic changes in synaptic connectivity of TH-IR neurons may serve as the morphological basis for the cyclic regulation of the anterior pituitary.
