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At least 55 records · Page 3Linked to original sources
PubMed1979

Metabolic and EEG alterations during the early phase of triethyltinsulphate (TET) intoxication.

EEG changes as well as the mechanisms of the hyperglycaemic effect of triethyltinsulphate (TET), a compound known to induce brain oedema, were investigated in cats and rabbits, respectively. Considerable EEG alterations characterized by slow waves appeared in some minutes after TET administration. The hyperglycaemic effect of TET like that of epinephrine could be prevented by the administration of 1 mg/kg of the beta blocker, pindolol. It is suggested that the hyperglycaemic effect of TET is brought about by sympathetic activation.

Action Potentials↗
PubMed1984

Trimethyltin inhibits the activity of hippocampal neurons recorded in vitro.

The effects of trimethyltin (TMT) on hippocampal CA1 pyramidal cell activity was studied using an in vitro brain slice preparation. TMT (0.6 micron) reduced the orthodromic population spike and increased the threshold for population spike generation. The excitatory postsynaptic potentials (EPSP) were reduced by TMT (0.6-1.1 micron) in a dose dependent manner. The antidromically driven population spike was attenuated by TMT (0.8 micron). These results indicate that TMT alters hippocampal synaptic transmission by depression of the postsynaptic CA1 neuron. An increased perfusion time decreased the TMT dose which produced a depressive effect.

Animals↗
PubMed1984

Cerebral antioedematous effect of Teproside and of some vincamine derivatives.

Alkyltin compounds are known to produce in the rat a selective oedema of the CNS, especially of the white matter. Vincamine and vincamine derivatives, among which Teproside is the most potent, are able to prevent the occurrence of such an oedematous reaction whereas xanthine derivatives and papaverine fail to prevent this oedema. It is suggested that there may be a potentiation of the effect of vincamine by the xanthine part of the Teproside chemical structure.

Animals↗
PubMed1982

Postpartum exposure to triethyl tin produces long-term alterations in responsiveness to apomorphine.

Male and female rat pups were exposed to a single dose of triethyl tin (TET) or ethanol vehicle on day 5 postnatally and tested for responsiveness to apomorphine as adults. TET-exposed animals displayed an increased response to the stereotypic effects of 1 mg/kg of apomorphine. Female rats exposed neonatally to TET had decreased baseline rates of responding on a food reinforced variable interval (VI) 15 sec. schedule, while TET-exposed males were found to have increased baseline rates relative to controls. The rats maintained on a VI 15 sec. schedule were given various doses of apomorphine (0.0312-0.25 mg/kg, s.c.). Neonatal exposure to TET had no effect on the disruptive effects of apomorphine on VI 15 sec. responding. These data show an altered responsiveness of TET-exposed animals to higher doses of apomorphine (1 mg/kg), but not to lower doses of apomorphine (0.0312-0.25 mg/kg). The present data are in accord with the hypothesis that one of the long-term consequences of neonatal exposure to TET might be an alteration in the responsiveness of the dopamine system.

Animals↗
PubMedDate not supplied

Behavioral toxicology of acute trimethyltin exposure in the mouse.

Adult BALB/c mice were injected IP with trimethyltin . HCl (TMT), and the effects of TMT were studied on gross behavior, lethality, spontaneous motor activity (SMA), and responding under a multiple fixed-ratio 30, fixed-interval 600 sec (mult FR30 FI600) schedule of reinforcement. Following doses of 4, 5, and 6 mg/kg, the cumulative 48-hr lethality was 10% at 4 mg/kg, IP, and 100% at 5 and 6 mg/kg, IP. No deaths were observed during the first 48 hrs following 3 mg/kg TMT. This non-lethal dose produced whole body tremors. The SMA of mice receiving 3 mg/kg was reduced to 70% during the first 24-hr period following TMT and some recovery of total activity was observed during the second 24-hr period. The reduction in SMA was accompanied by a change in the normal circadian cycle of activity. Responding under the mult FR30 FI600 schedule was severely disrupted. Three hours after TMT administration and rate of responding in both components was decreased and the decrease became progressively larger over the next 48 hrs. In addition to the rate of FI600 responding being reduced, the normal pattern of FI responding was altered with an increase in responding observed in the early portions of the FI. These results suggest that the mouse is much more sensitive to the effects of TMT than the rat and may have potential as an animal model in the study of the neurotoxicity of TMT.

Animals↗
PubMed1981

The effects of postpartum exposure to triethyl tin on the neurobehavioral functioning of rats.

Male and female Fischer rat pups received sc injections of 1.5 or 3 mg/kg of triethyl tin bromide (TET), ethanol vehicle or distilled water on day 5 postpartum. At 21, 28, 60, and 90 days of age, the rats were weighed and assessed in a battery of tests which included fore- and hindlimb grip strength, negative geotaxis, startle responsiveness and spontaneous motor activity. Animals at 60 days of age were also tested in a two-way shuttle box avoidance procedure. Exposure to TET did not affect body weight at any time during testing, nor did it affect negative geotaxis of grip strength, Startle response to an air puff stimulus was decreased in males and females at 21 and 60 days of age, while no effects were observed at 28 or 90 days of age. Responsiveness to an acoustic stimulus was decreased at 60 days of age only. Spontaneous motor activity of males was increased at 21, and 28 and 60 days of age, while females had elevated activity at 28 and 60 days of age. Relative to ethanol controls, rats of both sexes were significantly hypoactive at 90 days of age. In a two-way shuttle box procedure, latencies to emerge prior to the first trial were elevated in TET exposed male and female rats. The number of discriminated avoidance responses made during a 60 trial session was decreased in females receiving the 3 mg/kg dose. Activity during the intertrial interval was not affected. A single postnatal exposure to TET can produce long-term alterations in the sensorimotor capabilities of rats; the effect appears to occur equally in both sexes and is independent of toxicant-induced body weight changes.

Aging↗
PubMed1976

[Electroencephalographic study on experimental brain edema induced by triethyltinsulfate (author's transl)].

The electroencephalographic effects of several doses of a brain edema inducing agent, triethyltinsulfate (TET), was studied by implanted epidural electrodes in cats. The effect of TET on the central nervous system was found to have two phases: 1. a six hours' acute toxic phase following TET administration, 2. An edematic phase developing on the 2nd to the 4th day. Similarly to our earlier observations brain edema induced by TET was found to be dose-dependent, as shown by EEG-s, and their analysis performed by computation.

Animals↗
PubMed1984

Behavioral toxicity of trialkyltin compounds: a review.

Triethyltin (TET) and trimethyltin (TMT) are neurotoxic organotin compounds which produce different patterns of toxicity in adult animals. Exposure to TET produces behavioral toxicity (decreased motor activity, grip strength, operant response rate and startle response amplitude) which reflects impaired neuromotor function. These deficits are consistent with the reported myelin vacuolation and cerebral edema produced by TET, and with its direct effects on muscle. Exposure to TMT produces both hyperactivity and impaired learning and performance. These impairments are consistent with reported neuronal cell death produced by TMT, particularly in limbic system structures. While the behavioral deficits produced by repeated exposure to TET are reversible when dosing is terminated, the behavioral impairments produced by a single exposure to TMT appears to be irreversible.

Animals↗
PubMedDate not supplied

Reversible neuronal damage in hippocampal pyramidal cells with triethyllead: the role of astrocytes.

A single dose (19 mg kg-1) of triethyllead given to weanling rats produces necrosis in a small number of hippocampal pyramidal (CA3) and hilar neurons with reversible changes in the remaining neurons of this region. The sequence of events has been studied by light and electron microscopy over a period from 12 h to 14 days after dosing. Early changes resemble those previously described for trimethyltin, with the formation of characteristic tubulo-vesicular dense bodies by 12 h accompanied by vacuolation of Golgi and smooth surfaced endoplasmic reticulum (SER) elements which became generalized by 24 h. Large numbers of secondary dense bodies, formed from tubulo-vesicular dense bodies as well as from autophagosomes, were present by 48 h, whilst very little rough surfaced endoplasmic reticulum (RER) and few polyribosomes remained and vacuolation was much reduced. In those animals which did not die from seizures, the majority of hippocampal pyramidal cells were able to recover from these changes with astrocytes playing a significant role in the elimination of the dense bodies. This involved astrocytes inserting processes into the neuronal perikaryon from where the secondary dense bodies were selectively transferred into the astrocyte cytoplasm. This activity was first seen at 48 h, reached a peak at 4 days, when most CA3 neurons contained one or more astroglial intrusions and subsided soon after. The surviving neurons returned to apparent normality over the period from 3 to 7 days with a gradual return of polyribosomes. Golgi elements and RER.

Animals↗