Neuroendocrine response to pheromones and its plasticity

Neuroendocrine response to pheromones and its plasticity

s41 NEUROENDOCRINE MS07-3 RESPONSE TO PHEROMONES AND ITS PLASTICITY HIDETO KABA Department of Physiology, Kochi Medical School, Nankoku, Koch...

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s41

NEUROENDOCRINE

MS07-3

RESPONSE

TO PHEROMONES

AND ITS PLASTICITY

HIDETO KABA

Department of Physiology,

Kochi Medical School, Nankoku,

Kochi 783-8505 and CREST, JST

Olfactory cues (pheromones) exert their effects on behaviour (signaIling effect) and reproductive physiology (primer effect) of a number of mammalian species including man. In the context of primer effects, it is in rodents and particularly in mice that the most dramatic effects are elicited. These include the acceleration of puberty, induction of oestrus in grouped anoestrous female and the blocking of pregnancy in newly mated females following exposure to male urinary pheromones. Of particular note is the fact that male primer pheromones bring the female to a common endocrine effect, oestrus. All three primer effects ate mediated by the accessory olfactory system. We have elucidated the functional pathway of the centrally projecting accessory olfactory system. Although a common neural and neuroendocrine mechanism can account for the three primer effects in mice, the olfactory block to pregnancy (known as the Bruce effect) is different from the other two effects in that only pheromones of a ‘strange’ male are effective. Pheromones of the stud male have the capacity to block pregnancy but do not block his own pregnancy. Hence, a mechanism exists to bring about the recognition and subsequent gating of the pheromonal signal from the stud male. Our studies have localized the memory trace responsible for the prevention of pregnancy block to the reciprocal

dendrodendritic synapses between mitral cells and granule cells in the accessory olfactory bulb, the first relay in the accessory olfactory pathway. Our studies have also pointed to several molecules responsible for the formation of this olfactory memory,

MSO7_4

THE EFFECT ON BIOLOGICAL

CLOCK FOR HUMAN REPRODUCTION

KOU SUEOKA

Dept. of Obstetrics Gynecology, The reproductive reproductive

Keio University

School of Medicine, 35 Shinanomachi,

functions have been analysed mostly for infertility treatment in previous decades.

technologies(ARTs)

endocrinological

circumstances

represended

However,

MSO7_5

of assisted

have elucidated

Human oocyte has two peaks of fertilization timing after ovu-

stress, dopaminergic

administration

to synchronize

functions exist in human in contrast to few positive

hormonal malfunction (hyper prolactinemia),

of ARTS can afford to administrate reproductive

these exogenous

more precisely programmed

Japan

This human biological clock is also slightly affected by seasonal changes and

Especially many negative effects toward reproductive

effects as far as fatigue, psychological etc. The development

The development

by in vitro fertilization (IVF) and its implicated technologies

lation which are within 5 hours and 20-25 hours. life circumstances.

Tokyo #160-0016,

and their biological clocks. Ovulation-inducing LH surge used to begin among 7 to 9 a.m. and

ovulation occur among 36-40 hours following this LH surge.

clock.

Shinjuku-ku,

functions without implication of endogenous

is not always tit to infertility patients.

endogenous

side effects of drugs,

The administration

biological

of ARTS should be

biological clock for improving results of infertility treatment,

EFFECTS OF SEX STEROID HORMONES ON THE CIRCADIAN

CLOCK

SHINOHARA, K., FUNARASHI. T. & KIMURA, F., Department of physiology, 236-0004, Japan.

Yokohama

City University

School of Medicine,

3-9 Fukuura,

Kanazawa-ku,

Yokohama

To determine the effects of sex steroid hormone on the circadian clock, first we examined the effect of 17Bestradiol (E2) on the expression of connexin-32 (a neuronal gap junction (GJ) protein) and connexin-43 (a glial GJ protein) mRNAs in the rat suprachiasmatic nucleus (SCN) the site of the circadian clock. E2 treatment increased the expression of connexin-32 mRNA in the SCN but not in the cerebral cortex (CX), while the treatment increased connexin-43 in the CX but not in the SCN. This indicated that estrogen increased GJ communications between SCN neurons. Second, we continuously recorded wrist activity and rectal temperature rhythms throughout the menstrual cycle in a woman with normal menstrual cycles. Plasma melatonin was measured over a 32 hr period in the follicular phase (FP) and LP. She showed progressive phase delays of sleep, temperature and melatonin rhythms only in the luteal phase (LP), which suggested that her circadian clock was phase-delayed by progesterone.