Sex Steroids and the Brain

Vasomotor instability Hot flushes are a classical menopausal symptom and are considered to result from a temporary derangement of the hypothalamic set-point for thermoregulation. Many studies suggest that modification of some hypothalamic and suprahypothalamic neurotransmitters and neuropeptides is involved in the development of vasomotor instability which could explain hot flushes and the stimulation of GnRHluteinising hormone (LH) pulses. Oestrogen lack increases the activity of the noradrenergic system and reduces dopaminergic activity. Both systems modulate GnRH and LH pulsatile release, and thermoregulation. These data are supported by the efficacy of clonidine, an 0.-2 agonist at presynaptic receptors, and veralipide, a dopamine antagonist in the reduction of vasomotor symptoms. However, alteration in noradrenergic and dopaminergic activity may only partially explain hot flushes. Several studies demonstrate a role of opioid peptides in the regulation of GnRH synthesis and pulsatile release. Naloxone, an opioid receptor antagonist, increases the frequency and amplitude of GnRH-LH release in postmenopausal neuroendocrine impairment at the hypothalamus. Mood changes, anxiety, depression, insomnia, headaches and alterations in cognitive function are related to postmenopausal changes in the limbic system. Furthermore ageing women are more susceptible to chronic degenerative diseases such as Alzheimer's disease and Parkinson's disease than men. I ,2