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F Samson

Publications and source records attributed to F Samson.

49 records · Page 3Linked to original sources
PubMed1983

Soman-induced depression of brain activity in TAB-pretreated rats: 2-deoxyglucose study.

Administration of large doses of Soman (2xLD50) to rats protected with TAB, a mixture of trimedoxime (TMB-4), atropine and benactyzine, results in approximately 2-fold reductions of local cerebral glucose utilization (LCGU) in most brain regions. This is in contrast to the marked increase in LCGU that is observed in conjunction with the seizures associated with an LD50 dose of Soman given to unprotected rats. This study reveals that TAB is effective in protecting against Soman-induced seizures, but only at the expense of a severe decrease in LCGU after Soman exposure.

Animals↗
PubMed1983

An inverse relationship between serum immunoglobulin-G and intellectual functioning.

Serum immunoglobulin levels for IgA, IgE, IgG, and IgM were measured in 13 institutionalized, profoundly mentally retarded individuals and for 20 retarded and 29 intellectually average noninstitutionalized individuals. A significant elevation in IgG was observed for the retarded groups as compared with the intellectually average group. There was a significant inverse relationship between IgG and level of intellectual functioning. The elevated IgG is suggestive of the findings with auto-immune diseases and warrants further investigation.

Adolescent↗
PubMed1982

Superior colliculus activation by retinal nicotinic ganglion cells: a 2-deoxyglucose study.

Systemic injection of the acetylcholinesterase inhibitor, di-isopropylfluorophosphate, in rats causes a marked increase in glucose use in the superficial layers of the superior colliculus. This activation of the superior colliculus is largely a retinal effect. Furthermore, since this response can be blocked by intraocular as well as systemic injections of mecamylamine, it is postulated that retinal nicotinic receptors are involved.

Animals↗
PubMed1982

Influence of chloralose on brain regional glucose utilization.

Choralose, a widely used anesthetic in neurophysiology, produces a unique pattern of anesthesia characterized by both an excitant (myoclonic jerks and startle response) and depressant (sedation and anesthesia) action. We investigated the influence of chloralose on the rate of regional brain glucose metabolism to determine if chloralose produces anesthesia by hyperexciting certain brain regions. That is, does chloralose act as an 'epileptoid anesthetic'. Rats were anesthetized with either 60 or 120 mg/kg chloralose and regional brain glucose utilization rates quantitated by the 2-deoxyglucose method. In chloralose-anesthesized rats, glucose consumption rates decreased in the frontal and auditory cortex, reticular nucleus of thalamus, superior colliculus, medial geniculate body, midbrain reticular formation and hippocampus. Rates of glucose use were not decreased in the lateral lemniscus and a zone in the vicinity of the oculomotor nucleus, medial longitudinal fasciculus and surrounding reticular formation. Since chloralose did not induce any discernible focal points of high activity, chloralose appears not to be an epileptogen. Rather, chloralose appears to act as a general depressant except in certain gray areas of the midbrain and lower brain stem. Retained and possibly increased functional activity in the vicinity of the oculomotor nucleus and medial longitudinal fasciculus may represent active reflex pathways involved in mediating the paradoxical startle response and myoclonic activity observed in chloralose-anesthetized animals.

Analysis of Variance↗
PubMed1982

The influence of droperidol, diazepam, and physostigmine on ketamine-induced behavior and brain regional glucose utilization in rat.

Diazepam and droperidol are used clinically with ketamine anesthesia to reduce emergence hallucinations, vivid unpleasant dreams, and hyperexcitability. Also, there are reports that the recovery time from ketamine anesthesia is shortened after administration of physostigmine. The authors investigated the influence of diazepam, droperidol, and physostigmine pretreatment on ketamine anesthesia by measuring the brain local regional activity and behavioral responses in rat. The 2-deoxyglucose brain local metabolic mapping method was used to determine regional brain functional activity. The recovery of tail flick response and righting reflex from ketamine anesthesia were prolonged by diazepam and by droperidol pretreatment, but the duration of agitation was shortened; physostigmine caused no significant change in any of these responses. Ketamine alone caused a statistically significant (P less than 0.05) increase in the rate of glucose utilization along the hippocampal molecular layer (control 87 mumol . 100 g-1 . min-1; ketamine 166 mumol . 100 g-1 . min-1) and a decrease in medial geniculate (25%), inferior colliculus (37%), and lateral habenula (18%). Diazepam, droperidol, and physostigmine pretreatment did not significantly alter any ketamine-induced glucose use changes, except for a decreased activity in hippocampal molecular layer with diazepam pretreatment (20%) and an increased activity in the lateral habenula with droperidol pretreatment (94%, P less than 0.05). These findings corroborate the "epileptogenic" character of ketamine anesthesia and implicate the hippocampus as a major focus. The reduced activity in the hippocampus induced by diazepam retreatment and the increased activity in the lateral habenula induced by droperidol pretreatment may be factors in the clinical reduction of ketamine hyperexcitability and hallucination by these drugs.

Animals↗
PubMed1980

Ketamine-induced changes in regional glucose utilization in the rat brain.

Ketamine appears to induce both excitatory and depressant actions in the brain; however, it is not clear which regions are affected. The 2-deoxyglucose functional mapping method of Sokoloff et al. was used to determine regional variations in metabolic activity of rat brain caused by injection of ketamine, 25-75 mg, intramuscularly. To compare the effects of ketamine with those of hippocampal-induced seizures, the 2-deoxyglucose method was used, following injection of penicillin G, 400-800 units, into the hippocampus. The findings from five control, seven ketamine-treated, and three penicillin G-treated rats are given. Ketamine caused a significant increase of metabolic activity in the hippocampal sulci and a decrease of activity in the medial geniculate and the inferior colliculus. Similar changes were found with hippocampal seizures caused by penicillin. The inhibition of the regions associated with sensory systems (medial geniculate and inferior colliculus) may account in part for the anesthetic action of ketamine, while the intense activity of the hippocampus may be related to the excitatory manifestations. The results indicate that ketamine produces seizures in the hippocampus, which in turn inhibit auditory and visually associated nuclei. Thus, the anesthesia may follow from the sensory depression and the cataleptic phenomena may be related to the hippocampal excitation.

Animals↗
PubMed1979

Nocodazole action on tubulin assembly, axonal ultrastructure and fast axoplasmic transport.

The action of a synthetic antitubulin agent, nocodazole, on tubulin self-assembly, preformed microtubules, fast axoplasmic transport and axonal ultrastructure was studied. Nocodazole completely blocks the self-assembly of tubulin containing or lacking associated proteins. This inhibition is readily reversible. At similar concentrations, nocodazole also depolymerizes preformed microtubules in vitro. Fast axoplasmic transport in cat vagus nerve is disrupted by bathing the nerve fivers in a medium containing 10 micrometer nocodazole for periods of 2.5 hr or longer. A 4-hr exposure results in extensive inhibition. The nocodazole action on fast axoplasmic transport appears to be reversible but with a high degree of variability. After 2.5 hr of exposure to 10 micrometers nocodazole, there is a slight decrease in axonal microtubules and an increase in 10 nm neurofilaments. A 4 hr exposure results in a marked reduction in microtubules. These results suggest that nocodazole has a mode of action similar to other antimicrotubule agents.

Animals↗
PubMed1977

Dimethylsulfoxide action on fast axoplasmic transport and ultrastructure of vagal axons.

The axonal microtubules (MT) are believed to be involved in fast axonal transport (FAXT). Dimethylsulfoxide (DMSO) has a strong stabilizing action on MT in vitro which may account for some of its reported biological effects. DMSO at concentrations of 5% disrupts the FAXT in a high percentage of axons emanating from the nodosum ganglion in the cat vagus nerve. Whereas 5% DMSO does not affect the FAXT in all axons, 10% DMSO blocks all the FAXT. The blockage is substantially, but not completely, reversed by washing the vagus for 2 h. DMSO at 2% caused no discernible change in either the FAXT or the axonal morphology, but some swelling of glial cells occurred. Ultrastructurally, 10% DMSO caused some axons to swell and others to shrink. The MT appeared normal and their total number per axon did not change. The spatial relationship of the axonal constituents is clearly altered by the DMSO and this may have contributed to the failure of the transport. It is suggested that the DMSO, through strengthening the forces involved in polymerization, renders them non-functional for FAXT.

Animals↗
PubMed1975

Isolation and polymerization of brain actin.

The studies presented here confirm earlier reports that an actin-like protein is abundant in brain. However, when the traditional procedures for isolating muscle actin are applied to brain, many different proteins are extracted. Tubulin, a major protein in brain with properties similar to actin, is the major constituent. A method is described for isolating the "brain actin" to a purity of 90-95%. The isolation method begins with an extraction of bovine brain in low ionic strength buffer with ATP and sucrose. The extract is treated with NH4SO4, MgCl, and KCl and incubated at 37 degrees C. A precipitate is formed which contains primarily tubulin and brain actin. Resolubilization of the brain actin is achieved with a low ionic strength buffer solution with sucrose and ATP. Further purification is accomplished by a cycle of polymerization-depolymerization. This "brain actin" shares with muscle actin the following properties: (1) Similar molecular weight and molecular charge as determined by SDS polyacrylamide gel and ordinary disc electrophoresis; (2) Polymerization to a filamentous form under the same conditions; (3) Contains 3-methylhistidine; (4) Vinblastine sulfate will induce filament formation.

Actins↗
PubMed1974

Stability of neuronal microtubules to high pressure in vivo and in vitro.

Neuronal microtubules in a variety of nerve cell types are unaffected by high hydrostatic pressures over a range of 1400-10,000 pounds/inch(2) and periods of 10-45 min. Similarly, purified tubulin polymerized to form microtubules in vitro were not depolymerized by the same range of pressures. The depolymerization of microtubules in several types of non-neuronal cells, which has been reported, may have been over-generalized with regard to the direct action of pressure on microtubule stability.

Animals↗