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Biomedical subjects

S Barron

Publications and source records attributed to S Barron.

At least 55 records · Page 3Linked to original sources
PubMed1986

Spontaneous fetal behavior after maternal exposure to ethanol.

Acute and chronic intubations of ethanol to pregnant rats produced changes in spontaneous fetal behavior four hours later. Fetuses from mothers in intermediate alcohol groups (4 and 6 g/kg) were substantially less active than controls (0 g/kg), but fetuses from low (2 g/kg) and high (8 g/kg) alcohol groups showed little indication of behavioral suppression. Circulating levels of alcohol in maternal blood, fetal homogenate and amniotic fluid at the time fetuses were observed confirmed that fetuses were exposed to alcohol in utero, but the measured concentrations of alcohol were not predictive of fetal activity. We suggest that some of the developmental consequences of Fetal Alcohol Syndrome may be the consequence of fetal inactivity induced by alcohol in utero.

Amniotic Fluid↗
PubMed1986

The effect of prenatal alcohol exposure on umbilical cord length in fetal rats.

Umbilical cord length is reported to be a good indicator of fetal movement. This study was designed to examine the effects of chronic alcohol exposure on umbilical cord length in fetal rats. Exposure to alcohol during prenatal development was associated with shortened umbilical cord length, relative to controls. This finding was not a function of body weight differences alone and provides evidence that fetal movements may be decreased as a consequence of maternal alcohol consumption. The possible role of suppressed fetal movements in some of alcohol's teratogenic actions is also discussed.

Animals↗
PubMed1984

Taste aversion learning in preweanling rats exposed to alcohol prenatally.

The effects of prenatal alcohol exposure on the development of a conditioned taste aversion were examined in preweanling rat pups. Mothers of these pups were fed isocaloric liquid diets containing either 35 or 0% ethanol-derived calories (EDC) from gestation days 6 through 20. A pair-feeding procedure was employed, and an ad lib lab chow control group was also included. At 5, 10, or 15 days of age, pups were infused with a saccharin solution through a cannula implanted in the oral cavity. Half of the pups in each group were then injected with lithium chloride (LiCl), which served as the poisoning agent, and the other half with sodium chloride (NaCl) as a control. Animals were subsequently tested for a conditioned aversion to the saccharin solution. At 15 days of age, all of the pups in the LiCl-poisoned group demonstrated a conditioned taste aversion to the saccharin solution, but the degree of this aversion was less in alcohol-exposed offspring. At 10 days of age, a taste aversion was learned, although it was not as strong as that shown by 15-day-old pups, and it appeared to be learned equally well by all of the prenatal treatment groups. At 5 days of age, there was marginal support for taste aversion learning. Again, it did not interact with prenatal treatment. The ontogenic differences in taste aversion learning exhibited by alcohol-exposed offspring relative to controls are discussed in terms of altered hippocampal development.

Animals↗
PubMed1978

Aerodynamic studies of cleft-palate speech.

The aerodynamic oral-nasal factors related to the speech of two groups of cleft-palate children were evaluated. One group presented hypernasality and the other group presented normal nasal resonance. The aerodynamic parameters evaluated were oral pressure, nasal flow, and flow-pressure ratio (nasal flow/oral pressure). Oral temperature readings were also obtained. These parameters were evaluated under three conditions (1) blowing, (2) vocalizing the vowel /i/, and (3) reading eight sentences representing two different rhythm patterns, two types of consonant loadings, and two conditions of syllable stress. The findings revealed significant differences between the hypernasal and normal resonance groups in flow-pressure ratio, oral pressure, and nasal flow while subjects were reading sentences. However, only a small proportion of the variability in these aerodynamic measurements could be accounted for based on the classification of hypernasality or normal nasal resonance. Oral-nasal aerodynamic studies done during speaking activity are more useful clinically than blowing activity or saying vowel sounds. No aerodynamic differences were noted between the two groups for the different rhythm and stress patterns and phonemic loadings within the sentences used.

Adolescent↗
PubMed1977

Extracorporeal membrane oxygenation for massive pulmonary thromboembolism.

This study was undertaken to determine whether extracorporeal membrane oxygenation (ECMO) could modify the effects of massive lethal thromboembolism and prevent death. Twenty anesthetized dogs were prepared for venoarterial perfusion with a demand pump and membrane lung and were perfused slowly for 1 1/2 hours to lessen homologous blood shock; 1 ml per kilogram of 24-hour-old tantalum-impregnated thrombus was injected intravenously. The dogs had profound systemic hypotension with an elevated mean pulmonary artery pressure (62.9 +/-4.5 mm Hg) immediately after embolization. Control animals generally died within 15 minutes. Four of the 10 ECMO-supported animals lived for six days, at which time they were restudied and killed. Not only can ECMO maintain an animal that would otherwise die quickly of massive pulmonary thromboembolism, but such support, even though temporary, can greatly improve the chances of survival.

Animals↗
PubMed1966

Actin-myosin interaction: inhibition of the myosin adenosine triphosphatase by actin.

In the absence of magnesium ion, the addition of actin to myosin in a 1 :4 ratio has a strong inhibitory effect on the adenosine triphosphatase activity, in contrast to the well-known activating effect of actin in the presence of magnesium ion. This finding suggests that both effects result from a conformational change in the active site of the myosin adenosine triphosphatase.

Adenosine Triphosphatases↗
PubMedDate not supplied

Hyperactivity in preweanling rats following postnatal alcohol exposure.

Neonatal alcohol exposure in rats has been used as a model to study the effects of third-trimester alcohol consumption in humans. In the present research, male and female rat pups were artificially reared (AR) and received condensed alcohol exposure (6 g/kg/day or 4 g/kg/day) on postnatal days (PNs) 4 through 9. Controls consisted of both artificially reared animals receiving maltose-dextrin substituted for alcohol and normally reared animals. These rats were tested for open-field activity at 18 days of age for four days. Both male and female rat pups that received the high dose of alcohol (6 g/kg/day) evidenced overactivity relative to pups in both control groups. These findings extend previous work and indicate that neonatal alcohol exposure can induce hyperactivity in young male rats.

Animals↗
PubMedDate not supplied

The effects of prenatal alcohol exposure on odor associative learning in rats.

Alcohol was administered to pregnant females via a liquid diet that contained either 35% ethanol-derived calories (35% EDC) or 0% EDC on gestation days 6-20. An ad lib lab chow group (LC) was also included. In Experiment 1, odor-aversion learning was examined in 10-day-old offspring. While both the 0% EDC and LC groups displayed odor aversions, the 35% EDC offspring did not. In Experiment 2, learning was assessed in an appetitive paradigm in three-day-old offspring. Once again, the 35% EDC offspring showed no evidence of learning. Experiment 3 examined odor-aversion learning in adults. Both alcohol-exposed offspring and controls learned the odor association equally well. These findings suggest that odor associative learning is a sensitive indicator for alcohol-related learning deficits in rat pups although these deficits may dissipate as the offspring matures. Since odor associations play a critical role in neonatal behaviors, these deficits may help explain other behavioral anomalies noted following prenatal alcohol exposure.

Age Factors↗
PubMedDate not supplied

Passive avoidance performance following neonatal alcohol exposure.

Prenatal alcohol exposure has been associated with deficits in response inhibition in both human and nonhuman studies. In this study, we investigated the effects of neonatal alcohol exposure on passive avoidance, a task that requires response inhibition. Neonatal alcohol exposure has been used to examine the effects of alcohol during a period of CNS development that is equivalent to the human third trimester "brain growth spurt." Subjects were 23-day-old rats that were artificially reared (AR) from gestation day (GD) 26-32 through gastrostomy tubes. The AR groups included two ethanol doses; 6 g/kg and 4 g/kg and an isocaloric control. A sham surgery group was also included. Subjects were tested for acquisition and 24-hr retention of the passive avoidance task. The 6 g/kg females required more trials to reach the criterion during both acquisition and retention relative to all other groups. These findings suggest that neonatal alcohol exposure can produce deficits in response inhibiton, but that there may be differential sensitivity across sexes to some of alcohol's effects.

Animals↗
PubMedDate not supplied

The effect of prenatal cocaine exposure on umbilical cord length in fetal rats.

Umbilical cord length has been considered a reliable indicator of fetal movement. In this study, the effect of prenatal cocaine exposure on umbilical cord length was examined in rats. Pregnant rats were intubated with either 0 or 60 mg/kg cocaine hydrochloride daily from gestation day (GD) 14-21. Fetuses were removed via Caesarean section on GD 21 and umbilical cord length, placental weight and fetal body weight were measured. Fetuses exposed to cocaine in utero had significantly shorter umbilical cords than intubated controls, although there were no differences in placental or fetal body weights. These data suggest that prenatal cocaine exposure suppresses fetal movement, which could contribute to some of the long-term effects observed in cocaine-exposed offspring.

Animals↗
PubMedDate not supplied

The effects of prenatal alcohol exposure on behavioral and neuroanatomical components of olfaction.

Prenatal alcohol exposure is associated with deficits in odor-associative learning in very young rat pups. One alternative explanation for these findings is that rather than a learning deficit per se, alcohol-exposed pups may display a sensory deficit. The present study was designed to examine the effects of prenatal alcohol exposure on behavioral and neuroanatomical components involved in olfaction. The subjects in this study were pups exposed to 35% ethanol-derived calorie (EDC) liquid diet from gestation days (GD) 6-20. Two control groups were included, a 0% EDC pair-fed and an ad lib lab chow group. In Experiment 1, respiratory response to a novel odor was examined in pups tested at either 3, 4, or 10 days of age. The 35% EDC offspring clearly detected the odor. Furthermore, there was an apparent alcohol-related development delay in respiratory rate as shown by a lower baseline respiratory rate at PN 3 relative to controls which was no longer apparent by PN 4. Experiment 2 examined the volume of two neuroanatomical structures involved in olfaction, the main olfactory bulb (MOB) and the vomeronasal organ (VNO) in 3-day-old pups. Prenatal alcohol exposure was associated with a decreased volume of the MOB although the VNO was unaffected.

Animals↗
PubMedDate not supplied

Effects of neonatal cocaine exposure on two measures of balance and coordination.

This study examined the effects of third trimester cocaine exposure on motor coordination and balance using a rodent model. The subjects were Sprague-Dawley rats that had been artificially reared (AR) and fed through gastrostomy tubes from postnatal days (PND 4-11). The AR groups included two groups given either 20 mg/kg/day or 60 mg/kg/day cocaine hydrochloride and a control group. A suckled control group raised by its natural dam was also included to control for artificial rearing. In Experiment 1, neonatal exposure to the high dose of cocaine resulted in impaired performance on parallel rods at 19-21 days of age. Exposure to the lower dose of cocaine impaired parallel rod performance on 20 and 21 days of age. In Experiment 2, walking gait was examined in 38-48-day-old subjects. Neonatal cocaine exposure was associated with a narrower stance width, however, there were no differences across neonatal treatment groups on step angle or stride length. These data suggest that third trimester cocaine exposure results in balance and coordination impairments. These findings support preliminary data suggesting motor impairments in infants with prenatal cocaine histories.

Animals↗
PubMedDate not supplied

Neonatal cocaine exposure, activity, and responsivity to cocaine in a rodent model.

This study examined the effects of neonatal cocaine exposure on running wheel activity and subsequent responsivity to cocaine using a rodent model. Subjects were artificially reared from postnatal (PND) days 4-10 via an intragastric cannula. The four treatment groups included two cocaine doses (20 mg/kg/day and 40 mg/kg/day), an artificially reared control and a normally reared suckled control. Subjects were tested at either PND 21 through PND 24 (Experiment 1) or PND 60 through PND 70 (Experiment 2) for 2 consecutive days. Testing consisted of a 30-min habituation period followed by injection of either saline (Day 1) or cocaine (Day 2) and an additional 60-min test session. Neonatal treatment had little effect on baseline activity or activity following saline injection at either age. All subjects showed an activation with cocaine injections, however, the activation was more pronounced in juveniles. Again, neonatal treatment did not interact with response to cocaine. These findings suggest that neonatal cocaine exposure does not alter activity or long-term responsivity to 20 mg/kg cocaine as measured in the running wheel apparatus.

Aging↗
PubMedDate not supplied

The behavioral teratogenic potential of fenbendazole: a medication for pinworm infestation.

Fenbendazole (FBZ) is a benzimidazole currently used for anthelmintic treatment of pinworm populations in numerous animal species although it is not currently approved for laboratory rodents in the U.S. It has received considerable interest for treating rodent populations due to its low toxicity, wide safety margin and apparent absence of gross teratogenic effects. The purpose of this study was to assess the behavioral teratogenic potential of FBZ. Pregnant rats were administered either FBZ-medicated feed at a therapeutic level or normal rat chow throughout pregnancy and gestation. FBZ had no effect on pregnancy indicators such as maternal weight gain or water consumption, number of pups born or pup birth weights. Offspring were examined in a variety of paradigms including righting reflex, negative geotaxis, running wheel activity, Morris water maze (MWM) performance and digging maze performance. FBZ offspring did show delayed righting reflex, some modest changes in locomotor activity in a running wheel and minor alterations in performance during the probe session of the MWM relative to controls. However, the effects of FBZ on behavior were subtle and many of the behaviors examined were unaffected. These results suggest that FBZ may be an effective and relatively safe anthelmintic treatment for use in breeding colonies.

Analysis of Variance↗
PubMedDate not supplied

Neonatal cocaine and/or ethanol exposure: effects on a runway task with suckling reward.

This experiment employed a rodent model to examine the effects of neonatal exposure to cocaine, ethanol, or both drugs in combination on acquisition and extinction of an appetitive runway task. After implantation with an intragastric cannula, subjects were artificially reared (AR) from postnatal days (PND) 4-10. There were five treatment groups, including: cocaine (20 mg/kg/day), ethanol (4 g/kg/ day), cocaine/ethanol (20 mg/kg/day cocaine and 4 g/kg/day ethanol), stock (an AR control), and sham (a suckled control). Subjects were tested on PND 13-14. The runway task consisted of traversing a runway for nonnutritive suckling on an anesthetized dam and a subsequent milk reward, given manually by the experimenter. Pups from all treatment groups acquired and extinguished the runway task; however, pups exposed to cocaine had longer latencies to leave the start box than controls. Pups exposed to cocaine or ethanol, but not cocaine/ethanol, were impaired on the nipple attachment measures compared to sham controls. These results provide further support that the "third trimester" is a sensitive period for developmental drug exposure.

Analysis of Variance↗
PubMedDate not supplied

The effects of clonidine on rat pups neonatally exposed to cocaine.

This study examined the effects of neonatal cocaine exposure on responsivity to the alpha2 noradrenergic agonist clonidine in 11-day-old rat pups. On postnatal day (PND) 4 neonatal rats were assigned to one of four treatment groups: artificially reared (AR) receiving 40 mg/kg/day cocaine hydrochloride, AR receiving 20 mg/kg cocaine, AR control receiving no drug, and a normally reared control group. Pups were maintained in this fashion from PND 4 to 9 and received no drug on PND 10. On PND 11 subjects received an IP injection of either 0, 0.25, or 1.0 mg/kg clonidine hydrochloride and were observed for locomotor activity and wall-climbing during a 15-min test session. Subjects exposed to the 40 mg/kg dose of cocaine demonstrated an enhanced sensitivity to the locomotor stimulating effects of clonidine relative to both control groups. This cocaine-related enhanced sensitivity was not observed on the wall-climbing measure. All groups showed evidence of wall-climbing, although this behavior was somewhat dampened among AR groups. The 20 mg/kg cocaine-exposed males also took longer to display wall-climbing behavior than their respective females regardless of clonidine dose, although this sex difference was not apparent for any other treatment group. These findings suggest that neonatal cocaine exposure may alter response of the noradrenergic system.

Adrenergic alpha-Agonists↗