Taro Miyahara Gotoh

Sequence of forebrain activation induced by intraventricular injection of hypertonic NaCl detected by Mn2+ contrasted T1-weighted MRI

In order to define the sequence of forebrain activation involved in osmoregulation, central activation in response to intracerebroventricular injection of NaCl solution (10 microl of 0.15, 0.5, or 1.5 M) was detected using manganese-contrasted magnetic resonance imaging (MRI) in anesthetized rats. Changes in renal sympathetic nerve activity (RNA) were also measured, and the time courses of forebrain activation and RNA changes compared. NaCl injection resulted in rapid activation of the subfornical organ (SFO), organum vasculosum lamina terminalis (OVLT), and periventricular regions and the lateral hypothalamic area (LHA), then of the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus (SON). The delay in activation in the PVN and SON showed a wide variation from 0 to 5.78 min, and the average delay in the PVN (2.88+/-0.34 min) and SON (2.90+/-0.39 min) was significantly greater than that in the SFO (0.40+/-0.10 min) and OVLT (0.74+/-0.13 min). NaCl (1.5 M) injection elicited a rapid, large increase in RNA, which consisted of two components, an early rapid increase at 99 s after injection (160+/-27%) and a slower increase at 9 min after injection (209+/-34%). These results suggest that the PVN and SON are activated not only by the afferent input from the SFO and OVLT but also by diffusion of the hypertonic stimulus to these regions and probably by their intrinsic osmosensitivity. The PVN might be responsible for the second slower component of the RNA response, but cannot be responsible for the first component.

Vestibulosympathetic reflex mediates the pressor response to hypergravity in conscious rats: contribution of the diencephalon

To investigate the mechanism of arterial pressure (AP) regulation during hypergravity, the AP response to gravitational force was examined in conscious rats and the AP was found to increase, depending on the degree of gravity load induced by centrifugation. At 20 s after application of 2, 3, or 5 G, the AP increased by 9+/-2, 20+/-3, or 24+/-3 mm Hg, respectively. The AP increase during first 60 s was suppressed by vestibular lesion or pretreatment with hexamethonium, suggesting that the vestibular system and sympathetic nerve system be involved, respectively, in the afferent and efferent pathways. To further examine the central pathway of this response, Fos expression in the brain was examined after exposure to 5 G for 90 min. Intense Fos expression was seen in the medial vestibular nucleus, paraventricular hypothalamic nucleus, autonomic nuclei in the brain stem in intact rats, but not in rats with vestibular lesion. To examine the involvement of the diencephalic nuclei in this pressor response, AP was measured under hypergravity in rats with midcollicular transection. In these rats, the AP change was minimal at 2, 3, and 5 G, indicating that nuclei rostral to the transection level were involved in the pressor response. These results indicate that output from the vestibular system project to the diencephalon, and activation of diencephalic nuclei is indispensable to the pressor response via the sympathetic nerve system.

Roles of the vestibular system in controlling arterial pressure in conscious rats during a short period of microgravity

In order to evaluate the roles of the vestibular system in controlling arterial pressure (AP) during exposure to a short period of microgravity (microG), the AP was measured in conscious free-moving rats having intact vestibular systems and those having vestibular lesions (FM-Intact and FM-VL groups, respectively). During free drop-induced microG, the AP increased in the FM-Intact group; it was 38+/-4 mmHg more than the AP observed during 1G. However, the increase in AP was significantly lower in the FM-VL group (20+/-2 mmHg). Further, to examine the sudden effect of a body floating in the midair in response to the AP during exposure to muG a body stabilizer was placed on the back of rats having intact vestibular systems and those having vestibular lesions (STAB-Intact and STAB-VL groups, respectively). The increase in the AP was significantly depressed in the STAB-Intact group; when compared with that in the FM-Intact group, but the increase was still significant (27+/-2 mmHg). On the other hand, the increase in the AP was completely eliminated in the STAB-VL group (7+/-5 mmHg). These results indicate that the AP increases during exposure to muG in conscious rats, and the vestibular system and body stability are significantly involved in this response.

Controlling arterial blood pressure using a computer-brain interface.

There has been recent interest in the concept of connecting a computer to the brain to control brain functions. However, there are challenges that must be overcome in developing such a computer–brain interface, including a selection of nucleus that is stimulated, and an implantable electrode and electrical stimulator. Another important issue is the designing of the controller, that is, determining how to encode as an electrical signal the information to be sent to the brain. We have applied system identification theory, a method for evaluating dynamic characteristics of a system, to the arterial blood pressure control system of the brain. Our results show that (1) the stimulation–arterial blood pressure response relationship can be described as a mathematical model, which gives a good prediction of the arterial blood pressure response, facilitating the designing of a computer–brain interface, and (2) the arterial blood pressure can be actually controlled using a computer–brain interface.