Thyon Chentanez

Exercise during pregnancy increases hippocampal brain-derived neurotrophic factor mRNA expression and spatial learning in neonatal rat pup

Physical activities for a few days can increase brain-derived neurotrophic factor (BDNF) mRNA in rat hippocampus. To investigate the influence of maternal exercise during pregnancy on rat pup hippocampal BDNF mRNA, we studied its expression by a semi-quantitative RT-PCR method after young pregnant rats were exercised on a motor driven treadmill. Pups of exercised mothers had significantly increased hippocampal BDNF mRNA expression compared to the control rat pups at birth (on postnatal day 0) (P<0.001). In contrast, hippocampal BDNF mRNA expression in pups of exercised mothers decreased significantly on postnatal day 28 (P<0.002). Spatial learning of rat pups was examined by multiple T maze training for 7 consecutive days between postnatal days 40 and 47. Pups of exercised mothers showed a significant increase in spatial learning ability as demonstrated by significant decreases in total time from starting to target and total number of errors as compared to age-matched control pups during the first 4 days of 7 consecutive days on multiple T maze training (P<0.05). Thus, physical exercise during gestation in pregnant mothers can increase hippocampal BDNF mRNA expression of postnatal pups and result in an improvement in spatial learning in pups from exercised dams.

Effects of cortisol pretreatment on the acute hepatotoxicity of aflatoxin B1

Effects of cortisol pretreatment on acute hepatotoxicity induced by aflatoxin B1 (AFB1) were investigated in female rats. Pretreatment of cortisol (1.0-10.0 mg/kg body weight) for 7 consecutive days markedly increased mortality rate, activity of plasma glutamic pyruvic transaminase (PGPT), plasma glutamic oxaloacetic transaminase (PGOT) and liver triglycerides induced by AFB1 (3.0 mg/kg body weight). The potentiating action of cortisol on hepatic necrosis of AFB1 showed a dose-dependent pattern. The possible mechanism of its action may be related to an increase in the activity of aniline hydroxylase and formation of AFB1-2,3-epoxide which in turn caused a marked increase in AFB1 binding to hepatic DNA and proteins, and lipid peroxide formation. Therefore, the potentiating action of cortisol on AFB1 hepatotoxicity may possibly increase the damage to DNA and membranes of various organelles.

Correlation between positive chronotropic effect and norepinephrine release induced by acetone in the rat right atrium

The effects of acetone on contraction rate and norepinephrine (NE) release of rat right atrium were investigated. Acetone, in the concentration range 10-210 mM increased the atrial contraction rate (ACR) in a dose-dependent manner, but in concentrations exceeding 210 mM, caused a gradual reduction in the ACR from the peak. The positive chronotropic effect of acetone on ACR can be reduced by adding 0.002 mM of propranolol (a non-selective beta 1- and beta 2-adrenergic receptor blocker), or by pretreating the rat with reserpine (an NE depleter) (5 mg/kg body weight, i.p., 24 h prior to experiment). These findings lead to the hypothesis that the increase in ACR induced by acetone may be partly due to an increase in NE release from sympathetic nerve endings in the atrium by acetone. To test this speculative hypothesis, the effect of acetone on [14C]NE + cold NE release from the right atrium, preinoculated with 0.25 microM of [14C]NE + cold NE for 20 min at 35 degrees C, was carried out using a simple technique developed in our laboratory. The acetone (10-1000 mM)-stimulated peak of NE release (pmol/g atrium/min) and summed NE release (pmol/g atrium/5 min) in excess of the basal spontaneous NE release were analyzed. The dose-response curves of the effect of 10-210 mM of acetone on the ACR and the peak of NE release were parallel. However, acetone concentrations above 210 mM caused a gradual drop of the curve of the ACR from its maximum while still enhancing the curve of the NE release. This continued gradually up to an acetone concentration of 500 mM. The atrial NE release reached a maximum at acetone concentrations between 500 and 1000 mM. This indicates that the increase in ACR caused by acetone in the range 10-210 mM may be partly due to an increase in NE release from the sympathetic nerve terminals in the atrium. However, an acetone concentration above 210 mM may be too toxic to the muscle fibers and/or the pacemaker and/or the conducting system, and so even though the NE release is still increasing, it can not enhance the ACR any further. It is generally speculated that the release of NE from the sympathetic nerve endings in the heart induced by the great number of organic solvents and general anesthetics contributes to the cause of tachycardia, arrhythmia and fibrillation of the heart.(ABSTRACT TRUNCATED AT 400 WORDS)

Reaction time, impulse speed, overall synaptic delay and number of synapses in tactile reaction neuronal circuits of normal subjects and thinner sniffers

In control subjects, warned auditory reaction time (RT) for a given effector organ was less than the warned visual RT for the same organ. The RT of the circuits between eye or ear or sites of tactile stimulation (SOS) and the index fingers were significantly shorter than that between eye or ear or the same SOS and the right or left big toes. The greater the distance between the SOS and the brain the longer the RT of the response by a given effector organ. The overall signal speed (OASS) from the neck to the index finger was less than that from the neck to the big toe. The OASS from the neck to a given effector was less than that from the toe to the same effector. Sensory nerve impulse speed was slightly faster than motor nerve impulse speed. The overall synaptic delay and estimated number of synapses (ENOS) of simple tactile reaction neuronal circuits of normal subjects did not significantly vary with site of tactile stimulation or effector organ. The mean number of synapses of various tactile reaction neuronal circuits of normal subjects was estimated to be between 69 and 77, which is far greater than the number of synapses in the touch-tactile and motor pathways combined. The overall synaptic delay in the tactile reaction neuronal circuits between SOS and the left and right big toes were significantly lower in sniffers than in control subjects. This may be due to a decrease in either the average synaptic delay, the number of synapses, or both in the tactile reaction neuronal circuits between sites of stimulation and big toes (but not index fingers) in sniffers.

Synaptosomal neurotransmitter uptake systems in the retina and brain nuclei of light- and dark-adapted rabbits.

High affinity uptake rate for [14C]aspartate and [3H]dopamine by retinal homogenate (H), Pl (outer plexiform layer, OPL), and P2 (inner plexiform layer, IPL) retinal synaptosomal fractions were not significantly different between light- and dark-adapted rabbits. However, there were significant increases in the dark in [3H]gamma-aminobutyric acid high affinity uptake rate by retinal H and P2 but not that of Pl. There was a significantly higher [3H]choline uptake rate by retinal H, Pl and P2 in the dark-adapted compared to light-adapted rabbits, but there was no significant change in this rate for synaptosomal fractions from the lateral geniculate body, superior colliculus, visual cortex (VA I + II), caudate nucleus (CN) and hippocampus (HP). Data obtained in this study, along with reports of others, indicate that the change in retinal neurotransmission functions may not always be parallel with the change in high affinity uptake rates of neurotransmitters by retinal synaptosomal fractions. Data obtained indicate an increase in retinal cholinergic neuronal activities in the dark and indicate that optic nerves are not cholinergic and cholinergic neurons in brain nuclei, such as VA, CN and HP, are not significantly influenced by optic nerve inputs in light and dark conditions.

Effect of morphine in vivo on uptake of [3H]choline and release of [3H]acetylcholine from rat striatal synaptosomes

Abstract The effect of morphine on the rat striatal cholinergic system was investigated in vitro by measuring the rates of [ 3 H]choline uptake and [ 3 H]acetylcholine release in striatal synaptosomes after in vivo injections of morphine sulfate. Morphine caused a 50 per cent increase in the V max of [ 3 H]choline uptake. Although a concomitant increase was also measured in the amount of [ 3 H] acetylcholine released, it could be explained by the previous increase in uptake. It is suggested that morphine had an overall stimulatory effect on the striatal cholinergic system which may be a transynaptic phenomenon rather than a direct effect on the cholinergic cell.