Search

We examined the effects of silymarin, which was extracted from Silybum marianum, on delayed neuronal cell death in the rat hippocampus. Rats were divided into four groups: sham-operated rats (sham group), rats which underwent ischemic surgery (control group), rats which were treated with silymarin before and after ischemic surgery (pre group), and rats which were treated with silymarin after ischemic surgery only (post group). We performed the ischemic surgery by occluding the bilateral carotid arteries for 20min and sacrificed the rats one week after the surgery. Silymarin was administered orally at 200mg/kg body weight. Smaller numbers of delayed cell deaths were noted in the rat CA1 region of the pre- and post-groups, and no significant difference was observed between these groups. There were few apoptotic cell deaths in all groups. Compared to the control group, significantly fewer cell deaths by autophagy were found in the pre- and post-group. We concluded that silymarin exerts a preservation effect on delayed neuronal cell death in the rat hippocampus and this effect has nothing to do with the timing of administering of silymarin., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Although psychological stress affects skin condition, the neurophysiological mechanism involved is unclear. In this study, we evaluated the relationship between skin condition and left/right asymmetry in prefrontal cortex (PFC) activity during mental stress tasks since recent studies have suggested that the right PFC dominates the regulation of the stress response system, including the hypothalamic-pituitary-adrenal (HPA) axis. Using near-infrared spectroscopy, we measured hemoglobin concentration changes in the bilateral PFC during a mental arithmetic task in normal adults and evaluated the laterality scores (i.e., [(right-left)/(right+left)]) of oxyhemoglobin concentration changes. Elicitation of stress was verified by the State-Trait Anxiety Inventory (STAI) and heart rate. The sebum levels and Propionibacterium acnes populations in the facial skin were measured before the task. The task significantly increased the STAI-II scores (p=0.00079) and heart rate (p=0.0000049). The oxyhemoglobin concentration increased in the bilateral PFC during the task, associated with a decrease in deoxyhemoglobin concentration. The laterality scores of oxyhemoglobin concentration changes were positively correlated with sebum levels (r=+0.50, p=0.026) and P. acnes populations (r=+0.49, p=0.029) in the facial skin before the task. There was a significant positive correlation between heart rate changes and the laterality scores of oxyhemoglobin concentration changes (r=+0.54, p=0.015). These results demonstrate that the subjects with higher sebum levels and higher P. acnes populations in the facial skin have a right dominant PFC activity during a mental stress task and suggest that such subjects are sensitive to mental stress associated with hyperactivity of the stress response system, including the HPA axis system.

GABAA receptor activation can modulate axonal conduction in the isolated dorsal column of the neonatal rat spinal cord in vitro. However, it is not known whether axonal conduction in the dorsal column can be modulated by endogenous GABA in the developing spinal cord. We consequently compared the effects of GABA, a GABAA agonist, and a GABA uptake inhibitor on axonal conduction in the dorsal column of hemisected neonatal (0- to 9-day-old) rat spinal cords in vitro. Extracellular compound action potentials evoked by supramaximal stimuli were recorded at two points with glass microelectrodes. GABA (10(-4) to 10(-3) M) reversibly decreased the compound action potential amplitude and the population conduction velocity. At 10(-4) M, compound action potential amplitudes fell by 45.0 +/- 6.5% of control while the conduction velocity slowed by 11.8 +/- 4.3% (n = 5). The GABAA receptor agonist, isoguvacine, mimicked the effects of GABA on the dorsal column compound action potential. In contrast, while GABA at 10(-5) M decreased the amplitude by 7.7 +/- 3.1%, it increased conduction velocity by 9.7 +/- 1.3% (n = 5). The GABA uptake inhibitor, nipecotic acid (10(-3) M), consistently decreased the compound action potential amplitude by 17.7 +/- 6.5% (n = 6) but the conduction velocity slowed in four out of six preparations. In two instances, nipecotic acid decreased the amplitude and increased the conduction velocity. The effects of nipecotic acid on the dorsal column compound action potential were blocked in the presence of the GABAA antagonist bicuculline.(ABSTRACT TRUNCATED AT 250 WORDS)

GABA (gamma-aminobutyric acid) depresses axonal conduction in neonatal dorsal columns. GABA released by injured spinal neurons may diffuse to white matter and contribute to secondary axonal damage. We studied the effects of hypoxia and GABAA receptor blockade on dorsal column conduction in vitro. The experiments compared the effects of hypoxia on longitudinally hemisected spinal cords and isolated neonatal dorsal columns. Before hypoxia, electrical stimulation elicited robust conducted compound action potentials in both isolated dorsal columns and hemicords. The tissues were superfused for 120 min with a hypoxic Ringer's solution saturated with 95% N2 and 5% CO2, followed by oxygenated Ringer's solution for 90 min. Isolated dorsal columns were remarkably insensitive to hypoxia. Response amplitudes fell by only 11 +/- 7% (n = 5) during hypoxia. In hemicords, however, hypoxia reduced response amplitudes by 56 +/- 16% (n = 5, mean +/- S.E.M.) and re-oxygenation did not restore response amplitude. We applied bicucullin (10(-5) M) to block GABAA receptors in the hemicords during hypoxia. Response amplitudes in bicucullin-treated hemicords fell by only 3 +/- 9% (n = 5) during hypoxia but declined 31 +/- 5% during re-oxygenation. These results suggest that endogenous GABA released from gray matter contributes to hypoxia-induced dorsal-column conduction failure.

The elevation and clearance of extracellular potassium following a standard contusion injury was studied in the thoracic spinal cord of rats. Animals were anesthetized, paralyzed, laminectomized at T9-T11, then artificially ventilated. A 10-g rod was released 5.0 cm above the cord with the dura intact. After impact, the dura-arachnoid and pial membranes were incised to allow penetration of K(+)-selective microelectrodes. Electrodes utilized a valinomycin ionophore and were double-barreled, with tip diameters of 3-5 microns. Extracellular potassium activity ([K+]o) increased with the depth of penetration. The maximum values of [K+]o occurred at depths greater than 500 microns, and remained so with time after injury. These data indicate that a dorsal-ventral gradient of [K+]o develops in spinal cords contused from the dorsal surface, with the greatest elevation of [K+]o in the gray matter. In 8 preparations, the maximum [K+]o was 65 +/- 8 mM (mean +/- S.E.M.) at 5 +/- 1 min after injury. The [K+]o peak values decayed with a half-time of 11.0 +/- 3.4 min. Compared with data available for the injured cat spinal cord, the peak [K+]o recovered relatively rapidly. Although a simple diffusion model could account for the rapid clearance of [K+]o, the persistence of dorsal-ventral [K+]o gradients could not be explained by such a model. It is postulated that secondary injury processes contributed to the persistent [K+]o gradients.

gamma-Aminobutyric acid (GABA) can influence conduction in a number of axonal preparations from the peripheral and central nervous system. In the spinal cord, the excitability of primary afferent terminals has long been known to be affected by GABA. Whether conduction in the long fiber tracts of the spinal cord can be similarly modulated is unknown. Since GABA causes a pronounced depression of excitability in preparations of unmyelinated axons, and myelination is incomplete in the neonatal rat, we tested whether GABA can modulate conduction in the dorsal columns of 10-17-day-old rats. Experiments were performed in vitro, on isolated dorsal column segments (n = 18). The extracellular compound action potential evoked by submaximal stimuli was recorded with a glass micropipette positioned 0.5-2.0 mm from a stimulating electrode. At concentrations of 10(-4) - 10(-3) M, GABA decreased excitability, reversibly depressing the compound action potential amplitude, and increasing the latency by 47 +/- 11% and 22 +/- 9% (mean +/- S.E.M., n = 5, 10(-3) M), respectively. These effects were blocked by picrotoxin and mimicked by isoguvacine (10(-4) M), which decreased the compound action potential amplitude by 44 +/- 10% and increased the latency by 9 +/- 4% (n = 5). Lower concentrations of these agents caused a modest increase in excitability. At 10(-5) M, GABA increased the compound action potential amplitude by 14 +/- 2% and decreased the latency by 3 +/- 2% (n = 5). Our results demonstrate that functional GABAA receptors are present in neonatal dorsal columns.(ABSTRACT TRUNCATED AT 250 WORDS)