Brief exposure to the G-protein activator NaF/AlCl3 induces prolonged enhancement of synaptic transmission in area CAl of rat hippocampal slices

Publicover, Stephen J.

doi:10.1007/bf00230983

Cited by 16 publications

(3 citation statements)

References 24 publications

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“…(Cain, 1989). The G protein activator (NaF/AlCI,) induces an LTP-like prolonged enhancement of synaptic transmission in hippocampal slices (Publicover, 1991). On the other hand, intrahippocampal administration of PTX inhibits generation of LTP Pennefather, 1989, 1990).…”

Section: Discussionmentioning

confidence: 99%

Amygdaloid Kindling Elicits Persistent Changes in Pertussis Toxin‐Catalyzed ADP‐Ribosylation

Iwasa

Hasegawa

Kikuchi³

et al. 1994

Epilepsia

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We examined the changes in pertussis toxin (PTX)-catalyzed ADP-ribosylation in amygdaloid-kindled rats to clarify the role of G proteins in the basic mechanisms of epilepsies. Autoradiographic analysis showed a remarkable increase in PTX-catalyzed ADP-ribosylation in 39-41-kDa proteins in hippocampus and cerebral cortex of kindled animals. The 39- to 41-kDa proteins were shown to be alpha-subunits of Gi and Go by immunoblotting with specific anti-Gi alpha and anti-Go alpha. The increase in ADP-ribosylation of these proteins was observed on stimulated and unstimulated sides of brains 24 h after the last generalized seizure and persisted for at least 3-4 weeks. These results suggest that persistent alterations in signal transduction through Gi and Go might be related to acquisition of long-lasting epileptogenesis.

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Section: Discussionmentioning

confidence: 99%

Amygdaloid Kindling Elicits Persistent Changes in Pertussis Toxin‐Catalyzed ADP‐Ribosylation

Iwasa

Hasegawa

Kikuchi³

et al. 1994

Epilepsia

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“…Upon washout, spike amplitude recovered beyond control values and in half of the preparations a prolonged enhancement of spike amplitude occurred. If AlCl 3 was omitted from fluoride-containing saline, enhancement of spike amplitude, when observed, was brief [192]. Brief bath application of AlFx in standard saline consistently induced a long lasting potentiation in area CA1 of rat hippocampus [193].…”

Section: Other Effectsmentioning

confidence: 96%

Fluoride Interactions: From Molecules to Disease

Strunecká¹,

Patočka²,

Blaylock³

et al. 2007

CST

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Fluoride has long been known to influence the activity of various enzymes in vitro. Later it has been demonstrated that many effects primarily attributed to fluoride are caused by synergistic action of fluoride plus aluminum. Aluminofluoride complexes have been widely used as analogues of phosphate groups to study phosphoryl transfer reactions and heterotrimeric G proteins involvement. A number of reports on their use have appeared, with far-reaching consequences for our understanding of fundamental biological processes. Fluoride plus aluminum send false messages, which are amplified by processes of signal transduction. Many investigations of the longterm administration of fluoride to laboratory animals have demonstrated that fluoride and aluminofluoride complexes can elicit impairment of homeostasis, growth, development, cognition, and behavior. Ameliorative effects of calcium, vitamins C, D, and E have been reported. Numerous epidemiological, ecological, and clinical studies have shown the effects of fluoride on humans. Millions of people live in endemic fluorosis areas. A review of fluoride interactions from molecules to disease is necessary for a sound scientific assessment of health risks, which may be linked to the chronic intake of small doses of fluoride and aluminum from environmental and artificial sources.

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“…Many different mechanisms have been connected to aluminium neurotoxicity. Aluminium accumulation in the brain can lead to neurofibrillary degeneration (Good and Perl 1993), damage of the cholinergic system (Gulya et al 1990;Zubenko and Hanin 1989), impairment in brain energy balance (Cho and Joshi 1988;Cho and Kim 1991;Octive et al 1991;Walker et al 1989) and disturbances in second messenger systems (Franceshetti et al 1992;Publicover 1991;Yamamoto et al 1990). Also, epidemiological studies on Al in drinking water have shown some positive relations between Al and AD (Flaten 2001).…”

Section: Introductionmentioning

confidence: 96%

Evaluation of the effects of aluminium, ethanol and their combination on rat brain synaptosomal integral proteins in vitro and after 90-day oral exposure

Kohila

Parkkonen

Tähti

2004

Archives of Toxicology

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The effects of aluminium lactate (Al-lactate) on the rat cerebral synaptosome integral proteins adenosinetriphosphatase (ATPase) and acetylcholinesterase(AChE) were studied in vitro and in vivo. Coexposure with ethanol (EtOH) was studied in both situations. Isolation of synaptosomes was carried out using isoosmotic Percoll gradients. In in vitro experiments, the synaptosomes were exposed to different concentrations of Al-lactate in the incubation mixture. Al-lactate caused decreases in total ATPase and AChE activities concentration dependently. The decrease in ATP activity started at 0.2 mM concentration, and concentration for the 50% decrease of the enzyme activity (EC50 ) was 1.1 mM. The decrease in AChE activity started at 5-10 mM concentration, and the EC50 value was 15.8 mM. Coexposure with ethanol (2 mM) increased the EC50 values similarly in both cases. After 90-day oral exposure of rats to Al-lactate (91.8 mg/kg/day), the serum aluminium level was 0.9-1.3 ptM/l. Coexposure with EtOH(3.0 g/kg/day) did not significantly increase the blood Al(0.7 2.2 pM/l). Aluminium exposure caused a decrease in the blood EtOH concentration (0.6 mM/1) compared with blood EtOH (12.3 mM/1) in the rats exposed to ethanol only. In the rats studied 2 weeks after the Al exposure, the activities of ATPase and AChE were significantly lower than in the rats studied immediately after the exposure. Correspondingly, a significant decrease in AChE activity was found in Al and EtOH-exposed rats, but in the control rats there were no differences between the study groups. Immediately after the 90-day dosing, the exposed rats did not differ significantly from the control rats. Based on the in vitro results, the neural membrane integral proteins ATPase and AChE may be considered as targets for the effects of aluminium and ethanol. Ninety-day in vivo exposure of rats to aluminium caused decrease in ATPase and AChE activities, detectable 2 weeks after the exposure.

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Brief exposure to the G-protein activator NaF/AlCl3 induces prolonged enhancement of synaptic transmission in area CAl of rat hippocampal slices

Cited by 16 publications

References 24 publications

Amygdaloid Kindling Elicits Persistent Changes in Pertussis Toxin‐Catalyzed ADP‐Ribosylation

Amygdaloid Kindling Elicits Persistent Changes in Pertussis Toxin‐Catalyzed ADP‐Ribosylation

Fluoride Interactions: From Molecules to Disease

Evaluation of the effects of aluminium, ethanol and their combination on rat brain synaptosomal integral proteins in vitro and after 90-day oral exposure

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