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S C Phillips

Publications and source records attributed to S C Phillips.

53 records · Page 3Linked to original sources
PubMed1985

Representation of stimulus azimuth by low-frequency neurons in inferior colliculus of the cat.

The responses to changes in stimulus azimuth of 204 neurons in the inferior colliculus of the cat with best frequencies of less than 3 kHz were studied. Three main unit classes were identified: omnidirectional units uninfluenced by speaker azimuth (39%); multipeaked units with several azimuthal regions at which peak firing occurred (9%); and azimuth-selective units that showed clear preferences for a discrete range of sound-source azimuths (52%). Alterations in stimulus intensity produced little change in the shapes of profiles relating firing rate to stimulus azimuth (azimuth functions), but the peaks of these functions could shift by up to 20 degrees. Similar observations were made for a small sample of units, each of which was examined with a variety of stimulus frequencies. The pinnae were removed bilaterally in 11 cats, and azimuth functions for 35 units were measured both binaurally and with the ipsilateral or contralateral ear occluded. Evidence was found for facilitative or suppressive interactions, as a function of stimulus azimuth, between monaural inputs. The sharpness of an azimuth function was expressed by the half-width of the function, i.e., the number of degrees of azimuth between the peak of the function and the point at which 50% of maximum firing occurred on the medial side of the peak. When half-widths were plotted as a function of best frequency, it was found that the sharpest azimuth functions occurred for units with best frequencies between 1.1 and 1.5 kHz. Most units in the lowest two octaves (0.1-0.4 kHz) or having best frequencies between 2 and 3 kHz were omnidirectional. The relationship between half-width and the azimuth at which peak firing occurred (best azimuth) revealed that a range of best azimuths between 10 and 40 degrees contralateral contained the sharpest azimuth functions. When best frequency was plotted against best azimuth, it was observed that the majority of units (93%) had best azimuths in the contralateral hemifield. For frequencies between 0.7 and 1.7 kHz, best azimuths occurred relatively evenly between 10 and 60 degrees contralateral. These data suggested that for frequencies between 1.2 and 1.4 kHz, at least, the best azimuths of different units with the same best frequency collectively provide information about stimulus location across much of the contralateral hemifield.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

The interconnections of the inferior colliculi through their commissure.

Much is known of the sources and manner of termination of ascending and descending input to the inferior colliculus (IC) but its commissural connections are less well understood. Most studies of the commissure have utilized small lesions or tracer deposits; while all agree that commissural axons terminating in the IC do so in its superficial and dorsomedial sectors, it is not clear where projecting cell bodies are located in the IC. The present study attempted total infiltration of the commissure of the cat IC with horseradish peroxidase (HRP) in an effort to label all neuronal somas whose axons cross in the commissure. The distribution of labeled cells after the brachium of the IC (BIC) was cut unilaterally and infiltrated with HRP was also examined to enable comparison of the locations and approximate proportions of cells projecting to the contralateral IC and medial geniculate body (MGB). The cells giving rise to commissural axons form an array tilted dorsally from caudal to rostral that spreads mediolaterally through the central nucleus into the external nucleus of the IC, but largely excludes the dorsomedial sector at posterior levels. A similar distribution of labeled cells, but with reduced numbers, is found when large HRP deposits are made in the contralateral BIC. These results, in conjunction with those from studies of the terminations of commissural axons made by others, suggest that the interconnections of the inferior colliculi through their commissure are complementary, rather than reciprocal.

Animals↗
PubMed1984

Is the inferior colliculus an obligatory relay in the cat auditory system?

The status of the inferior colliculus of the cat as an obligatory relay in the ascending auditory pathway was examined by attempting to infiltrate totally the fibres of the brachium of the inferior colliculus on one side with horseradish peroxidase. Following a transport time of 24 h, alternate sections from thalamus to caudal brainstem were reacted with a sensitive histochemical method to reveal tracer reaction product. Results for three cats revealed that the inferior colliculus is an obligatory relay for the overwhelming majority of axons comprising the lateral lemniscus and originating in the cochlear nucleus and superior olive.

Animals↗
PubMed1984

Blood-brain barrier dysfunction in thiamine-deficient, alcohol-treated rats.

Rats maintained on a thiamine-deficient diet for 38 days loss weight and showed neurological symptoms. The PA value, representing the permeability of the blood-brain barrier to 14C-sucrose, was significantly increased whether urethane or ethanol was used as anaesthetic. This increase was prevented by giving rats on the same diet injections of thiamine twice weekly. Barrier function was normalised by injecting thiamine into deficient rats for just 3 days before biopsy. The brains of the thiamine-deficient rats were stained by the Fink-Heimer method but showed no degenerating axons except for silver grains in the glomeruli of the olfactory bulb. Other rats were maintained on the same diet for 38 days and additionally exposed to ethanol vapour for 16 h per day. This resulted in a similar loss of weight but a greater leakage of the blood-brain barrier. The latter was normalised by a thiamine injection only 24 h before biopsy, but was not reduced by withdrawal of ethanol for 3 days before biopsy. Axonal degeneration was present in the olfactory glomeruli. However, no lesions or extravasated blood cells were seen in any brains, there was no change in brain water indicative of oedema and no degeneration in retina, distal peripheral nerves or leg muscles. The relation of these and other experimental findings to alcohol-related brain damage is considered.

Animals↗
PubMed1984

Responses of neurons in inferior colliculus to variations in sound-source azimuth.

This study aimed to classify the responses of single units in the auditory midbrain to acoustic stimuli presented in the free field in order to characterize those units likely to have a role in sound localization in the horizontal plane. The responses of 131 single units in the inferior colliculus of the cat and the brush-tailed possum were studied using tone and noise-burst stimuli presented from a speaker capable of movement at any point along a plane 10 degrees above the horizontal plane. Speaker positions along this plane are referred to as speaker azimuths; those on the same side as the recorded inferior colliculus as ipsilateral, and on the opposite side as contralateral, azimuths. For each unit, spike counts were measured as a function of azimuth either at the best frequency (BF) or using noise bursts. These functions are referred to as azimuth functions and were usually measured for at least two intensities, between 10 and 70 dB above threshold. The recording sites of most units were identified histologically with the aid of microlesions and were related to the major subdivisions of the inferior colliculus: the central nucleus (ICC), the lateral part of the external nucleus (ICX), and the rostroventral process (R-ICX). Two units were located in the pericentral nucleus and two in the dorsal nucleus of the lateral lemniscus. Two major classes of neuron were identified: omnidirectional and directionally sensitive. Omnidirectional units exhibited azimuth functions that were either flat or that declined gradually at progressively ipsilateral azimuths. For the latter units, discharge rates at all points monotonically increased with stimulus intensity. There was no indication, for either type of omnidirectional unit, of significant binaural interaction. A good correlation was found between the summed proportions of excitatory-excitatory (EE) and monaural (EO) units observed in dichotic studies (46-55%) and the proportion of omnidirectional units in the present study (47%). A subgroup of directionally sensitive units (36% of the total) displayed azimuth functions for which the azimuthal position of the discharge border or peak firing azimuth remained essentially unaltered over a range of stimulus intensities. These azimuth-selective units are likely to have a role in the detection of the location of stimuli in the horizontal plane and appear to include units that would be considered excitatory-inhibitory (EI) or delay sensitive in dichotic studies. The azimuths over which directionally sensitive units showed their marked directional effects were influenced by the position of the contralateral pinna.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Alcohol withdrawal causes a loss of cerebellar Purkinje cells in mice.

Mice received a liquid diet containing alcohol for 4 months, after which half of them were sacrificed and the others given a 4-month recovery period before being sacrificed. They were compared with similar mice receiving the diet with alcohol replaced isocalorically by sucrose. No damage was detected in the cerebellum during alcohol consumption, but the number of Purkinje cells was significantly reduced in the recovery period. The experiment was repeated twice with mice consuming a normal diet but exposed to alcohol vapor. The first group was exposed to alcohol vapor 24 hr/day for 3 weeks and then given alternating 1-week periods of recovery and exposure 24 hr/day until a total of 6 weeks of exposure to alcohol vapor and 4 one-week recovery periods had been experienced. They were compared with similar mice exposed to alcohol vapor 24 hr/day for 6 weeks without a recovery period. The second group was exposed to alcohol vapor 9 hr/day for 3 weeks, when part of the group was given a 3-week recovery period. In both experiments, damage was not detected in the cerebellum during alcohol exposure, but in mice withdrawn from alcohol, the number of Purkinje cells was reduced and qualitative evidence of neuronal degeneration was found with a silver stain. In a further group of mice, exposure to alcohol vapor was tapered off gradually, and no evidence of neuronal loss was found. Indications in the literature that withdrawal from alcohol can cause brain damage are briefly reviewed.

Aerosols↗
PubMed1983

Chronic consumption of alcohol by adult mice: effect on hippocampal cells and synapses.

For 4 months C57 black mice were fed a nutritionally complete diet containing 9% alcohol or isocaloric sucrose and killed then or after 4 months recovery on standard food pellets. The number of cells in a thin plastic section of hippocampus was unchanged in field CA1 by alcohol exposure but was reduced 9% during withdrawal from alcohol. Electron microscopy was used to count synapses among the basal dendrites and no significant change was found in any treatment group. The spine heads were measured and found to be smaller in the alcohol group than in the sucrose group; many of the spines (in the alcohol group) were too small to be visible with the light microscope.

Alcoholism↗
PubMed1982

Weakening of the blood-brain barrier by alcohol-related stresses in the rat.

The product of the permeability x vascular surface area (PA) of the blood-brain barrier to [14C]sucrose has been measured in rats maintained for 3 weeks in a chamber, the air supply to which carried a controlled concentration of ethanol vapour. No statistically significant difference was found between the permeability measurements in rats inhaling ethanol vapour for 3 weeks and non-alcohol exposed rats. The PA value was found to be significantly increased (115%) in rats given the same ethanol exposure when additionally subject to starvation during the last 3 days of this treatment. If the ethanol supply was also withdrawn at the same time as the food, a similar significant increase (116%) in PA value was found. In the absence of any ethanol exposure, 3 days' starvation did not significantly alter the measured PA value. Finally, when rats are given 200 mg/kg disulfiram every second day during a 2-week period of ethanol inhalation, the PA value was not significantly altered, although the concentration of acetaldehyde in the blood was up to 129 microM. The results indicate that while ethanol or acetaldehyde alone do not cause a weakening in the blood-brain barrier, the additional stress of food withdrawal after alcohol exposure does reduce barrier function, and this could be significant in human binge drinking.

Acetaldehyde↗
PubMed1982

The blood-brain barrier in rats fed on diets high or low in saturated/unsaturated fat ratio.

The product of the permeability x vascular surface rate area (PA) of the blood-brain barrier to [14C]sucrose has been measured in rats raised on synthetic diets in which the saturated/unsaturated fat constitution was controlled at high or low levels. Gas-liquid chromatography demonstrated marked differences in brain fatty acid constitution between the dietary groups. No statistically significant differences was found between the permeability measurements in rats maintained on any of the synthetic diets, nor was there any difference from rats raised on a standard laboratory pellet food. The opportunity was taken to look at 3 other properties of brain that might be affected by lipid constitution. There was no change in the form of the membranous intracellular inclusions that can be induced by intracerebral injections of suramin, and Fink-Heimer staining of degenerating axons, which is inhibited by fat extraction, worked equally well on each diet group. The sleep time after an anaesthetic injection of alcohol was not significantly changed.

Animals↗
PubMed1981

Sexual transmission of enteric protozoa and helminths in a venereal-disease-clinic population.

We examined the prevalence of enteric protozoan and helminthic infections and the associations between infection and gender, sexual preference, and sexual practices in 180 consecutive patients at a venereal-disease clinic. Of 163 men, 29 were infected with one or more enteric parasites. None of the 17 women had an enteric infection. The prevalence of infections with Entamoeba histolytica or Giardia lamblia (or both) was 21.5 per cent in homosexual men, 6.2 per cent in bisexual men, and 0 in heterosexual men. There were significant associations between oral-anal sex and infection with E. histolytica (P less than 0.01) or with helminths (P less than 0.05). Homosexuality and oral-anal sex were the most important risk factors in E. histolytica, G. lamblia, and helminthic infections. We conclude the "hyperendemic" enteric protozoan infection rates in homosexual men are related to three factors: the original endemic level in the general population; the prevalence of sexual acts that facilitate transmission; and the frequency of exposure to an infected person.

Entamoebiasis↗
PubMed1981

The short-term toxicity of ethanol to neurons in rat cerebral cortex tested by topical application in vivo, and a note on a problem in estimating ethanol concentrations in tissue.

In rats anesthetized with ethanol 4.0 g/kg i.p. the dura overlying the parietal cortex was exposed and superfused with 100% ethanol for 1 h. After 6 days survival the underlying cortex was stained with a silver method that is selective for degenerating axons and their terminals. No degeneration was found in the superfused cortex, although heat-lesioned tissue stained concurrently showed axonal degeneration and so validated the technique. Electron microscopy after 3-20 days survival did not show any degeneration, and synapses of normal appearance were present immediately beneath the cortical surface. In other rats the ethanol concentration in the superfused tissue was assayed in 0.4 mm thick discs sectioned with a vibratome from a 4-mm diameter core cut with a trocar from the cortex immediately after 1 h of superfusion. The ethanol was eluted in 2% TCA, and an aliquot assayed enzymatically. A second elution of the tissue disc contributed a further 5% of the ethanol content indicating a partition coefficient for ethanol between wet brain tissue and 2% TCA of about 10. The total concentration of ethanol in the superficial cortex was found to be about 0.82 M or 3.8%. This estimation was confirmed by superfusion with 14C-labelled ethanol and scintillation counting. Thus neurons in the cerebral cortex did not degenerate after exposure for 1 h to a concentration of ethanol that was 3 times greater than the concentration that causes death in a rat by paralysis of the respiratory centre (1.2%).

Administration, Topical↗
PubMed1981

Does ethanol damage the blood--brain barrier?

The permeability of the blood--brain barrier has been measured using a technique which is independent of blood flow and is sufficiently accurate to monitor the penetration of weakly permeant substances. The permeability of the blood--brain barrier to [14C]sucrose has been measured in rats anaesthetised with either urethane or pentobarbitone (Nembutal). The values obtained from urethane-anaesthetised untreated rats were slightly lower, thus demonstrating the suitability of urethane as an anaesthetic for blood--brain barrier experiments. The permeability of the barrier has been measured in rats which had been drinking 7.5% ethanol for 6 months, or had been administered an anaesthetic dose of ethanol, or both. No statistically significant difference was found between the permeability measurements in rats subjected to any of these treatments. Positive controls in which 0.3 ml of a 30% ethanol solution was injected into the internal carotid artery demonstrated the sensitivity of the employed technique. Thus it was found that the blood--brain barrier does not weaken with respect to sucrose when the blood ethanol concentration reaches an anaesthetic level.

Alcohol Drinking↗
PubMedDate not supplied

The toxicity to rat cerebral cortex or topical applications of acetaldehyde, ammonia or bilirubin.

The relative toxicity of acetaldehyde, ammonia and bilirubin to cerebral cortex of rats has been tested by superfusion of the intact dura for 1 h with each toxin separately. The cortex was examined histologically after 6 days survival using a silver strain which selectively impregnates degenerating axons and their synaptic terminals. A tissue concentration of 30 mM acetaldehyde was found to cause axonal and terminal degeneration, whereas 11 mM acetaldehyde was not toxic, and did not produce any structural changes detectable by electron microscopy. In terms of tissue concentrations, acetaldehyde was at least 27 times more toxic than ethanol on a molar basis. However, the acetaldehyde concentration necessary to produce neuronal degeneration in a 1 h exposure is many times greater than ever reported in CSF in human alcoholism. Both ammonia and bilirubin are capable of causing neuronal degeneration, but we have not measured the tissue concentrations that are toxic. Comparison of molar concentrations in the superfusing fluids showed that ammonia is at least 39 times more toxic than acetaldehyde, and at least 1000 times more toxic than ethanol. Superfusion with an ethanolic solution of bilirubin (2.5mM) was strongly toxic, but this solution diluted to 50% with saline was not toxic. The possibility exists that ammonia or bilirubin may reach concentrations toxic to neurons in alcoholism, especially in the presence of liver damage.

Acetaldehyde↗
PubMedDate not supplied

A change in susceptibility of rat cerebellar Purkinje cells to damage by alcohol during fetal, neonatal and adult life.

The sensitivity of rat cerebellar Purkinje cells to ethanol exposure during fetal, neonatal or adult life was assessed by histological techniques. Pregnant female rats were exposed to ethanol vapour during the last 2 weeks of gestation. Purkinje cells were counted 5 days after the pups were born. The number of Purkinje cells in lobe VIII was reduced by 45%, and the linear density of Purkinje cells in lobe I was 47% less than in controls not exposed to ethanol. Smaller reductions were found in other lobes. The weight of the cerebellum was reduced by 34%. Neonatal rats were exposed to ethanol vapour briefly during daylight hours on the third and fourth days after birth. Purkinje cells were counted on the fifth day after birth, and losses similar to those described above were found, with additional significant reductions of cell numbers in lobe I and of Purkinje cell density in lobe VIII. The weight of the cerebellum was reduced by only 4%. Adult male rats were exposed to ethanol vapour for 3 weeks and no Purkinje cell losses were subsequently found. The dura overlying the cerebellum of separate adult male rats was superfused with 100% ethanol for 1 h and no abnormalities were detected with electron microscopy in the exposed cortex 6 days later. It is remarkable that the brief neonatal treatment caused a more widespread loss of Purkinje cells than the 10 days of exposure to ethanol in utero, whereas the Purkinje cells present in adult animals show a great resistance to ethanol. The neonatal period seems to be a time of high susceptibility of Purkinje cells to ethanol.

Animals↗
PubMedDate not supplied

A review of the non-neoplastic kidney effects of hydrocarbon exposure in humans.

This review has demonstrated that there is a considerable amount of information in the medical literature concerning hydrocarbon-associated kidney effects. The existing data lends itself to a variety of divergent interpretations. Ravnskov has stated that "glomerulonephritis should be recognized legally as an occupational disease," yet there is no mention of hydrocarbon exposure in the differential diagnosis of glomerulonephritis in two standard American textbooks of internal medicine. Two recently published textbooks of occupational medicine state without reservation that "studies have linked hydrocarbon exposure to glomerulonephritis" and base this conclusion on the previously cited studies of Beirne and Brennan, Zimmerman, and Ravnskov. Based on this review, the following conclusions have been reasonably substantiated: 1. Massive exposure to petroleum distillates on rare occasions may cause acute renal failure due to tubular necrosis. This appears to be a reversible lesion which, depending on the level of exposure, the medical care and support available, and pre-existing renal function, may be without chronic sequelae. 2. Case reports linking Goodpasture's syndrome and other types of glomerulonephritis to hydrocarbon exposure are based on circumstantial evidence and cannot be used to establish a causal association. 3. The evidence from the eight case-control studies of hydrocarbon exposure and glomerulonephritis is inconclusive. Six of the eight published case-control studies show a positive association between hydrocarbon exposure and glomerulonephritis, but four of the six studies have methodologic flaws that could explain the observed effect. The findings in the one positive study that is methodologically acceptable were not replicated in a subsequent study utilizing a similar design. 4. Studies of hydrocarbon-exposed occupational cohorts have generally revealed a lower than expected risk of death from renal causes. As with most historical cohorts, the specific exposures, intensities and durations of exposure have been poorly defined. Effects of mortality that may occur among highly exposed subsets of these occupational cohorts may be diluted by a relatively large proportion of workers with minimal or no exposure to the class of hydrocarbons in question. 5. Studies of renal biochemistry and renal function effects have been uniformly negative in groups of workers from several industries with relatively high exposures of long duration to a variety of hydrocarbon solvents. The statistically significant differences in proteinuria and cell excretion observed in one of the studies should not be confused with clinical significance.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗