Stress and Combined Exposure to Low Doses of Pyridostigmine Bromide, DEET, and Permethrin Produce Neurochemical and Neuropathological Alterations in Cerebral Cortex, Hippocampus, and Cerebellum

2004 ◽  
Vol 67 (2) ◽  
pp. 163-192 ◽  
Author(s):  
A. Abdel-Rahman ◽  
Suzanne M. Abou-Donia ◽  
Eman M. El-Masry ◽  
Ashok K. Shetty ◽  
Mohamed B. Abou-Donia
2017 ◽  
Vol 91 (12) ◽  
pp. 3961-3989 ◽  
Author(s):  
Steffen Schneider ◽  
Karma C. Fussell ◽  
Stephanie Melching-Kollmuss ◽  
Roland Buesen ◽  
Sibylle Gröters ◽  
...  

1967 ◽  
Vol 16 (3) ◽  
pp. 275-309 ◽  
Author(s):  
W. Geets

SUMMARYThe first cellular differentiation in the process of segmentation leads to the embryonic period, the major organogenetic period for the nervous system. In man, it appears between the second and the eighth week after conception.During the foetal and perinatal periods, the nervous organization mainly develops at the cerebellum and cerebral cortex levels. The cerebrum functional maturation continues well beyond birth.Neuroblasts are the most widespread mother-cells in the developing nervous system during the embryonic period, but some are still to be found after birth.Animal experiment has demonstrated that ionizing radiations were able to disorganize neurogenesis in any of its maturation stages, even at very low doses. It is possible to establish a chronological table showing the anatomical or functional deformities in relation with the embryonic age at which rays have been given.It appears that in man the most dangerous period is between the beginning of the second and the end of the eighth week after conception. At that moment, pregnancy is often ignored and a dose of 20 to 40 r is sufficient to entail serious damages, such as microcephaly, protrusions of the brain or mental retardation. On drawing near to birth the foetal or neonatal nervous system of rodents or primates is still radiosensitive, especially at the cerebral cortex level and the consequences will be of a neurophysiologic or psychosensorial nature. Certain embryopathies or neurologic alterations would only be apparent in subsequent generations, following mutations induced into the mother-cells of the nervous system. Genetic deformities of the nervous system can also result from moderate irradiations of the gonads.Further to the precise experimental research work on the radiovulnerability of the embryonic or foetal nervous system of the animal, certain clinical observations are presented, which lead to similar conclusions.The atomic bombardments have caused numerous neurological trouble among the children who had been irradiated in utero. And the genetic effects are not yet perfectly known to-date.This set of experimental and clinical data must prompt us to be very careful when using ionizing radiations, even at low doses, in pregnant women and newborn.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Eric W. Fish ◽  
Laura B. Murdaugh ◽  
Chengjin Zhang ◽  
Karen E. Boschen ◽  
Oswald Boa-Amponsem ◽  
...  

Abstract We tested whether cannabinoids (CBs) potentiate alcohol-induced birth defects in mice and zebrafish, and explored the underlying pathogenic mechanisms on Sonic Hedgehog (Shh) signaling. The CBs, Δ9-THC, cannabidiol, HU-210, and CP 55,940 caused alcohol-like effects on craniofacial and brain development, phenocopying Shh mutations. Combined exposure to even low doses of alcohol with THC, HU-210, or CP 55,940 caused a greater incidence of birth defects, particularly of the eyes, than did either treatment alone. Consistent with the hypothesis that these defects are caused by deficient Shh, we found that CBs reduced Shh signaling by inhibiting Smoothened (Smo), while Shh mRNA or a CB1 receptor antagonist attenuated CB-induced birth defects. Proximity ligation experiments identified novel CB1-Smo heteromers, suggesting allosteric CB1-Smo interactions. In addition to raising concerns about the safety of cannabinoid and alcohol exposure during early embryonic development, this study establishes a novel link between two distinct signaling pathways and has widespread implications for development, as well as diseases such as addiction and cancer.


2006 ◽  
Vol 57 (4) ◽  
pp. 433-439 ◽  
Author(s):  
L. Institóris ◽  
Dóra Kovács ◽  
I. Kecskeméti-Kovács ◽  
Anita Lukács ◽  
Andrea Szabó ◽  
...  
Keyword(s):  

1984 ◽  
Vol 221 (1223) ◽  
pp. 235-244 ◽  

Glycine and γ -aminobutyric acid (GABA) receptors from the foetal human brain were ‘transplanted’ into the Xenopus oocyte membrane by injecting the oocytes with poly(A) + -mRNA extracted from the cerebral cortex. Activation of both glycine and GABA receptors induced membrane currents carried largely by chloride ions. However, unlike the GABAactivated current, the glycine current was blocked by strychnine, and was not potentiated by barbiturate. At low doses, the glycine current increased with concentration following a 2.7th power relation, suggesting that binding of three molecules of glycine may be required to open a single membrane channel. The current induced by steady application of glycine decreased with hyperpolarization beyond about —60 mV.


1988 ◽  
Vol 8 (5) ◽  
pp. 733-741 ◽  
Author(s):  
John W. Phillis ◽  
Michael H. O'Regan ◽  
Gary A. Walter

The effects of the adenosine deaminase inhibitor, deoxycoformycin, on purine release from the rat cerebral cortex were studied with the cortical cup technique. Deoxycoformycin (5 and 500 μg/kg i.v.) enhanced the hypoxia/ischemia-evoked release of adenosine from the cerebral cortex, indicating a marked rise in the adenosine content of interstitial fluid in the cerebral cortex. Inosine and hypoxanthine release were attenuated at the higher dose of deoxycoformycin, acid release into the cortical perfusates was enhanced at the higher dose level. These results demonstrate that low doses of deoxycoformycin can be used to elevate interstitial levels of adenosine in the brain during hypoxia, and to depress the formation of some of its metabolites. The elevation of hypoxia/ischemia-evoked adenosine levels can account for the previously reported potentiation of hypoxia-evoked increases in rat cerebral blood flow after deoxycoformycin administration. The potential therapeutic utility of these findings is discussed.


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