Motoko Yanase-Fujiwara

Warm and cold signals from the preoptic area : which contribute more to the control of shivering in rats?

1. To find out whether the thermosensitive neurones in the preoptic area that control shivering are predominantly warm or cold sensitive, we tested the effects of injecting the excitatory amino acid L‐glutamate at various sites in and adjacent to the preoptic area of anaesthetized rats shivering at ambient temperatures of 15‐21 degrees C. 2. L‐Glutamate injections (0.2 mM in 0.5‐1.0 microliter), as well as preoptic warming and electrical stimulation, suppressed shivering, whereas control saline injections had no effect. Effective sites were restricted to the anterior part of the preoptic area, and a tenfold lower concentration of L‐glutamate did not influence shivering. 3. Injections of procaine (0.2 M) into the sites where L‐glutamate suppressed shivering did not affect strong shivering activity, but facilitated shivering in three out of seven cases when shivering was weak or absent at higher ambient temperatures (25‐30 degrees C). 4. L‐Glutamate injections, as well as preoptic warming and electrical stimulation, also elicited vasodilatation of the paw skin and the tail. Procaine elicited vasoconstriction when it was applied during vasodilatation induced by local preoptic warming. 5. These results indicate that the contribution of the preoptic area to the control of shivering and vasomotion is influenced more by signals from warm‐sensitive neurones than by signals from cold‐sensitive neurones.

Effect of midbrain stimulations on thermoregulatory vasomotor responses in rats.

1 Efferent projections eliciting vasodilatation when the preoptic area is warmed were investigated by monitoring tail vasomotor responses of ketamine‐anaesthetized rats when brain areas were stimulated electrically (0.2 mA, 200 μs, 0 Hz) or with the excitatory amino acid D,L‐homocysteic acid (1 mM, 0.3 μM). 2 Both stimulations elicited vasodilatation when applied within a region extending from the most caudal part of the lateral hypothalamus to the ventrolateral periaqueductal grey matter (PAG) and the reticular formation ventrolateral to the PAG. 3 Vasodilatation elicited by preoptic warming was suppressed when either stimulation was applied within the rostral part of the ventral tegmental area (VTA). 4 Sustained vasodilatation was elicited by knife cuts caudal to the VTA, and vasodilatation elicited by preoptic warming was suppressed by cuts either rostral to the VTA or in the region including the PAG and the reticular formation ventrolateral to it. 5 These results, together with the results of earlier physiological and histological studies, suggest that warm‐sensitive neurones in the preoptic area send excitatory signals to vasodilatative neurones in the caudal part of the lateral hypothalamus, ventrolateral PAG and reticular formation, and send inhibitory signals to vasoconstrictive neurones in the rostral part of the VTA.

Effect of gonadotropin releasing hormone on thermoregulatory vasomotor activity in ovariectomized female rats

To investigate the effect of gonadotropin releasing hormone (GnRH) on thermoregulatory skin vasomotion, we injected GnRH into various brain regions in both anesthetized and unanesthetized ovariectomized female rats. Local warming of preoptic area (PO) elicited skin vasodilation in anesthetized rats. Injection of 2 microg GnRH into the septal area lowered the threshold hypothalamic temperature for skin vasodilation at least for 2 h. Similar injections of 2 microg GnRH into the lateral ventricle (LV) and PO were ineffective. Although this vasodilative effect was also obtained after the injection of 20 ng GnRH into the septal area, injections of 2 ng GnRH were without effect. Not only injections of 20 ng Antide, a potent GnRH antagonist, but also injections of the mixed solution of 20 ng GnRH and 20 ng Antide were also without effect. In unanesthetized and unrestrained rats at an ambient temperature of 17 degrees C, injections of 20 ng GnRH into the septal area elicited tail vasodilation lasting for 30 minutes, whereas vehicle injections were ineffective. Injections of 20 ng GnRH into LV and PO were also ineffective. These results indicate that GnRH can elicit thermoregulatory skin vasomotion by acting on GnRH receptors in the septal area. This thermoregulatory vasodilative effect of GnRH might be possibly related to the etiology of climacteric hot flush.