Head-down tilt (HDT) causes a fluid shift towards the upper body, which increases intracranial pressure (ICP). In the present study, the time course of ICP changes during prolonged exposure to HDT was investigated in conscious rabbits through a catheter chronically implanted into the subarachnoid space. The production of cerebrospinal fluid (CSF) after exposure to 7-days HDT was also examined by a ventriculo-cisternal perfusion method. The ICP increased from 4.3+/-0.4 (mean+/-S.E.M.) mmHg to 8.0+/-0.8 mmHg immediately after the onset of 45 degrees HDT, reached a peak value of 15.8+/-1.9 mmHg at 11 h, and then decreased to 10.4+/-1.1 mmHg at 24 h. During 7-days HDT, it also increased from 4.8+/-0.9 mmHg to 9.2+/-1.6 mmHg immediately after the onset of 45 degrees HDT, reached a peak value of 12.8+/-2.5 mmHg at 12 h of HDT, and then decreased gradually towards the pre-HDT baseline value for 7 days. The rate of CSF production was 10.1+/-0.6 microl/min in rabbits exposed to 7-days HDT, and 9.7+/-0.5 microl/min in control rabbits. These results suggest that the rabbits begin to adapt to HDT within a few days and that the production of CSF is preserved after exposure to 7-days HDT. The time course of ICP changes during HDT in conscious rabbits seems to be considerably different from that in anesthetized rabbits.

No abstract

This study investigated the nature of synaptic inputs from the Forel's field H (FFH) in the medial mesodiencephalic junction to inferior oblique (IO) motoneurons in the oculomotor nucleus and superior oblique (SO) motoneurons in the trochlear nucleus in anesthetized cats, using intracellular recording techniques. Stimulation of the FFH induced monosynaptic EPSPs in IO motoneurons on both sides. Paired stimulation of the ipsilateral FFH and contralateral vestibular nerve substantiated that the FFH-induced EPSPs were caused mainly by direct excitatory fibers from the FFH to IO motoneurons and partly by axon collaterals of excitatory neurons in the vestibular nuclei. Among parts of the FFH, the medial part was most effective for producing the EPSPs. Systematic tracking with the stimulating electrode in and around the FFH revealed that effective sites of stimulation inducing negative field potentials in the IO subdivision of the oculomotor nucleus, identified as extracellular counterparts of the EPSPs in IO motoneurons, were also located in the interstitial nucleus of Cajal, nearby reticular formation and posterior commissure, besides within and near the medial part of the FFH. Areas far rostral, dorsal and ventral to the FFH were ineffective. EPSP-IPSPs or EPSPs were mainly induced in SO motoneurons on both sides by FFH stimulation. Latencies of these EPSPs and IPSPs were close to those of the EPSPs in IO motoneurons, indicating their monosynaptic nature. Effective stimulation sites for inducing these synaptic potentials overlapped those for the EPSPs in IO motoneurons. Based on these results, it was suggested that excitatory and inhibitory premotor neurons directly controlling IO and SO motoneurons were located within and near the medial part of the FFH.

Ischemia-reperfusion has been extensively investigated in the brain, heart, and many other organs, including the eye. Several studies have demonstrated histological [1,2], electrophysiological [3,4], and hemodynamic changes [5,6] in the eye tissues exposed to ischemia-reperfusion. Since an ischemic disease occurs more often in old patients than in young, it is important to know the difference in the ischemia-induced changes between young and aged animals. We recently showed that there were age-dependent differences of hemodynamic and histological changes in rat eyes during reperfusion after exposure to ischemia induced by increasing intraocular pressure (IOP) [7]. To our knowledge, however, the electrophysiological changes in the retinal function of aged animals during and after ischemia have not been reported in literature.The purpose of the present study is to compare the effects of ischemia-reperfusion on flash-elicited electroretinogram (ERG) between young and aged rats. The main components of ERG are a-wave, b-wave, and oscillatory potentials (OPs) that are known to be generated in the photoreceptor cells, bipolar or Müller cells, and amacrine cells, respectively [8][9][10]. Exposure to ischemia reduces the amplitude of these ERG waves in rabbits [3,4,11], cats [12,13], and rats [14][15][16]. Mild ischemia reduces the amplitude of OPs, but not b-wave [4]. During ischemia, b-wave is extinguished earlier than a-wave [3]. These findings suggest some heterogeneity among the three components of ERGs in terms of susceptibility to ischemia-reperfusion. Therefore in the present study we studied the Key words: aging, choroidal blood flow, electroretinogram, ischemia, reperfusion. Abstract:The effects of aging on the electroretinogram (ERG) during ischemia-reperfusion were investigated in rats. Flash-elicited ERG (awave, b-wave, and oscillatory potentials (OPs)) was recorded in young (4 months old) and aged rats (over 18 months old) before, during, and after exposure to 30-or 120-min ischemia induced by increasing intraocular pressure to 80 mmHg. The choroidal blood flow, measured by means of laser Doppler flowmetry, decreased to 40 to 60% of the baseline value during ischemia. Young rats showed no significant difference in the amplitude of each ERG component during ischemia between 30-and 120-min ischemia groups; 78.0Ϯ4.9 vs. 76.1Ϯ3.6% for awave, 63.4Ϯ3.1 vs. 60.6Ϯ3.0% for b-wave, and 59.6Ϯ5.9 vs. 57.5Ϯ6.7% for ⌺OP. In aged rats, however, 120-min ischemia caused a greater decrease, to 56.7Ϯ3.1% of the baseline value, in the a-wave amplitude than 30-min ischemia did, to 70.8Ϯ3.2%. The reduction of each ERG component in both 30-and 120-min ischemia experiments was greater in aged rats than in young rats. The recovery time for the amplitude of each ERG component during reperfusion was longer in aged rats than in young rats. The latency of bwave and the second component of OPs prolonged during ischemia, and recovery time for the latency was longer in aged rats than in young rats. These results suggest that the electroph...

Excitatory inputs to neurons in the Forel's field H (FFH) related to visually induced vertical saccades from the ipsilateral superior colliculus (SC) were investigated in chronically prepared alert cats. By stimulation of the deep or intermediate layer of the SC, upward augmenting neurons (ANs) and one long-lead downward burst neuron (BN) were found to be activated monosynaptically, while medium-lead BNs were activated disynaptically. The monosynaptically activated neurons were not antidromically activated from the oculomotor nucleus, whereas disynaptically activated neurons were also activated antidromically from the inferior rectus subdivision of the nucleus. These results suggest that an excitatory input to the FFH from the SC for inducing vertical saccades of visual origin first reaches upward ANs and/or long-lead downward BNs in the FFH, which in turn drive medium-lead BNs in the same area synapsing with motoneurons related to vertical eye movements.