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Antoine Mudakikwa - One of the best experts on this subject based on the ideXlab platform.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Antoine Mudakikwa, Timothy G Bromage, Matthew W Tocheri, Michael R. Cranfield
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3–4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population. Am. J. Primatol. 75:450-463, 2013. © 2012 Wiley Periodicals, Inc.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Timothy G Bromage, Matthew W Tocheri, Patrick R Hof, Antoine Mudakikwa
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3-4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population.

Shelby Carley Mcfarlin - One of the best experts on this subject based on the ideXlab platform.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Antoine Mudakikwa, Timothy G Bromage, Matthew W Tocheri, Michael R. Cranfield
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3–4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population. Am. J. Primatol. 75:450-463, 2013. © 2012 Wiley Periodicals, Inc.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Timothy G Bromage, Matthew W Tocheri, Patrick R Hof, Antoine Mudakikwa
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3-4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population.

James R West - One of the best experts on this subject based on the ideXlab platform.

  • zinc supplementation does not attenuate alcohol induced cerebellar purkinje cell loss during the Brain Growth spurt period
    Alcoholism: Clinical and Experimental Research, 2001
    Co-Authors: Weijung A Chen, Eve C Berryhill, James R West
    Abstract:

    Background: Alcohol-induced zinc deficiency is one of the mechanisms proposed as a cause of developmental Brain damage associated with fetal alcohol syndrome. It is known that alcohol exposure during the Brain Growth spurt period leads to cerebellar Purkinje cell loss. Therefore, this study examined whether zinc supplementation was capable of preventing alcohol-induced Purkinje cell loss in the cerebellar vermis in a neonatal rat model system. Methods: Sprague-Dawley rat pups were given alcohol (EtOH; 4.5 g/kg/day), zinc (Zn; 0.54 mg/ml diet; [10 times the regular diet Zn concentration]), or both from postnatal days (PD) 4 through 9 using the artificial-rearing paradigm. A gastrostomy control (GC) and a suckle control group (SC) also were included. All pups were killed on PD 10. Following perfusion, the cerebellar vermis was dissected and processed for stereological cell counting. The total number of Purkinje cells and the volume of the cerebellar vermis were determined. Results: Alcohol produced a significant loss of Purkinje cells compared with that in the GC group (no EtOH and no Zn supplement). The zinc supplementation had no effect in attenuating alcohol-induced Purkinje cell loss in the cerebellar vermis. In fact, the serum zinc concentration data indicated higher zinc concentrations following either EtOH or Zn treatment. Interestingly, the GC group showed a significantly lower zinc concentration compared with the SC group, even though no significant difference in Purkinje cell numbers was observed between these two control groups. Conclusion: These findings indicate that alcohol exposure during the third trimester equivalent did not result in zinc deficiency in this neonatal rat model system, nor did zinc supplementation rescue the alcohol-induced Purkinje cell loss in the cerebellar vermis. These findings showed clearly that the serum zinc concentration was not correlated with Purkinje cell loss, suggesting that alcohol-induced loss of cerebellar Purkinje cells in this neonatal rat model system is independent of the availability of serum zinc.

  • cocaine exposure during the Brain Growth spurt failed to produce cerebellar purkinje cell loss in rat pups
    Teratology, 1996
    Co-Authors: Weijung A Chen, Robert E Mcalhany, Susan E Maier, James R West
    Abstract:

    Previous studies in our laboratory indicated that cocaine exposure during the Brain Growth spurt period, a developmental stage vulnerable to various teratogens, did not produce microencephaly (gross Brain weight measures). However, neonatal cocaine exposure has been shown to affect motor coordination and balance, which are both sensitive to cerebellar damage. The purpose of this study was to investigate whether cocaine exposure during the Brain Growth spurt period could result in the loss of cerebellar Purkinje cells, a neuronal population known to be vulnerable to other teratogenic insults. Sprague-Dawley rat pups were randomly assigned to either cocaine-treated groups (40, 80 mg/kg s.c.) or a gastrostomy control group, and were reared using an artificial-rearing method from postnatal days (PDs) 4 through 9. On PD 10, these animals were perfused and the cerebella were extracted and processed for cell counts. Estimates of Purkinje cell numbers were obtained using a 3-dimensional optical dissector method. The results using this stereological method demonstrated no significant Purkinje cell loss in response to cocaine treatment, even at a dose which has been shown to result in high mortality. The failure of cocaine to produce significant Purkinje cell loss (present finding) or microencephaly (previous finding) odds to the evidence indicating that cocaine is not a potent neuroteratogen.

  • permanent neuronal cell loss in the cerebellum of rats exposed to continuous low blood alcohol levels during the Brain Growth spurt a stereological investigation
    The Journal of Comparative Neurology, 1995
    Co-Authors: James R West, Ruth M A Napper
    Abstract:

    This study demonstrates that exposure to an alcohol regimen that resulted in low, uniform blood alcohol concentrations during a period of rapid Brain Growth can lead to a permanent deficit in the number of Purkinje cells and granule cells in the floccular-parafloccular region of the cerebellum. Sprague-Dawley rat pups were artificially reared and were administered alcohol over postnatal days 4 through 9, a period of Brain development similar to that of the human third trimester. Two groups received a daily alcohol dose of 4.5 g/kg, administered either as a 10.2% solution in two of the 12 daily feedings (10.2% group) or as a 5.1% solution in four of the 12 feedings (5.1% group). A third group received a daily dose of 6.6 g/kg administered as a 2.5% solution in every feeding (2.5% group). The condensed patterns of alcohol administration resulted in high peak blood alcohol concentrations with near total clearance while the higher daily dose (6.6 g/kg), administered continuously, resulted in low but continuous blood alcohol concentrations. Pups were allowed to grow to adulthood and killed on postnatal day 115. The total number of Purkinje cells and granule cells in the floccular-parafioccular region of the cerebellum was estimated using unbiased stereological methods. Exposure to alcohol resulted in significant deficits in the number of both Purkinje cells and granule cells at 115 days of age in all three treatment groups. Most importantly a significant deficit of Purkinje cells and granule cells was found following continuous exposure to low blood alcohol concentrations, i.e., in the 2.5% group. The total number of Purkinje cells in the 2.5% group was 2.33 ± 0.31 x 104 compared with 3.18 ± 0.30 x 104 in the artificially reared controls. The total number of granule cells in the 2.5% group and the controls was 1.24 ± 0.10 x 107 and 1.64 ± 0.19 x 107 respectively. These results support the hypothesis that exposure to a continuous, low blood alcohol concentration can result in the death of developing neurons and lead to permanent neuronal deficits. The degree of neuronal loss does not correlate with the magnitude of the peaks of blood alcohol concentration © Wiley-Liss, Inc.

  • permanent neuronal cell loss in the inferior olive of adult rats exposed to alcohol during the Brain Growth spurt a stereological investigation
    Alcoholism: Clinical and Experimental Research, 1995
    Co-Authors: Ruth M A Napper, James R West
    Abstract:

    The purpose of this study was to examine whether exposure of rat pups to alcohol postnatally over a period of Brain development similar to that of the human 3rd trimester results in a permanent loss of cells in the inferior olivary nucleus. It was hypothesized that a deficit of neurons in the inferior olive, the sole source of climbing fibers, may contribute to the cerebellar dysfunction observed following exposure to alcohol during development. Sprague-Dawley rat pups were artificially reared and administered alcohol over postnatal days 4–9. One artificially reared group received a daily alcohol dose of 4.5 g/kg, administered as a 10.2% solution in 2 of 12 daily feedings (10.2% group). This pattern of alcohol administration resulted in high peak blood alcohol concentrations with near total clearance. The other artificially reared group was fed a diet made isocaloric to the alcohol-containing diet (gastrostomy control group). Pups were allowed to grow to adulthood and killed on postnatal day 115. The total number of neurons in the inferior olivary nucleus was estimated using unbiased stereological methods. Exposure to alcohol resulted in a significant deficit in the number of neurons in the inferior olive at 115 days of age. The total number of neurons in the alcohol-exposed group was 40.12 ± 8.7 ± 103, compared with 53.37 ± 3.7 ± 103 in the artificially reared controls. These results indicate that there is a permanent deficit of neurons in the inferior olive after postnatal exposure to alcohol. This supports the hypothesis that cerebellar dysfunction after exposure to alcohol during the Brain Growth spurt may be the result of more extensive neuronal deficits than previously thought.

  • 4 methylpyrazole an alcohol dehydrogenase inhibitor exacerbates alcohol induced microencephaly during the Brain Growth spurt
    Alcohol, 1995
    Co-Authors: Weijung A Chen, Robert E Mcalhany, James R West
    Abstract:

    Whether alcohol-induced microencephaly occurs as a result of the effect of alcohol or acetaldehyde remains an unanswered, yet important, question. The present study addressed this issue by using an alcohol dehydrogenase (ADH) inhibitor, 4-methylpyrazole (4-MP), that works by blocking the metabolism of alcohol to its primary metabolite acetaldehyde, thereby prolonging the actions of alcohol while minimizing the generation of acetaldehyde. Four groups of artificially reared Sprague-Dawley rat pups were treated with alcohol treatment (3.3 g/kg EtOH or isocalorically matched control formula from postnatal days 4 through 9) and 4-MP administration (IP, 50 mg/kg or saline). A suckle control group was introduced to control the effects of the artificial rearing procedure. On postnatal day 10, all pups were perfused. Alcohol in combination with 4-MP treatment produced a marked microencephaly, as assessed by Brain weights or Brain to body weight ratios, compared with other artificially reared groups. The peak BACs in the pups that received both alcohol and 4-MP were increased at least twofold compared with those that received alcohol alone. These findings indicate that 4-MP is an effective nontoxic ADH inhibitor and that microencephaly is associated with BAC levels. Most importantly, these results support the hypothesis that alcohol is a causative agent for alcohol-induced microencephaly and implicates the importance of functional ADH activity in attenuating alcohol-induced neuroteratogenicity.

Michael R. Cranfield - One of the best experts on this subject based on the ideXlab platform.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Antoine Mudakikwa, Timothy G Bromage, Matthew W Tocheri, Michael R. Cranfield
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3–4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population. Am. J. Primatol. 75:450-463, 2013. © 2012 Wiley Periodicals, Inc.

Jason S Massey - One of the best experts on this subject based on the ideXlab platform.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Antoine Mudakikwa, Timothy G Bromage, Matthew W Tocheri, Michael R. Cranfield
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3–4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population. Am. J. Primatol. 75:450-463, 2013. © 2012 Wiley Periodicals, Inc.

  • early Brain Growth cessation in wild virunga mountain gorillas gorilla beringei beringei
    American Journal of Primatology, 2013
    Co-Authors: Shelby Carley Mcfarlin, Tara S. Stoinski, Katie A Fawcett, Sarah K Barks, Jason S Massey, Amandine B Eriksen, Timothy G Bromage, Matthew W Tocheri, Patrick R Hof, Antoine Mudakikwa
    Abstract:

    Understanding the life history correlates of ontogenetic differences in hominoid Brain Growth requires information from multiple species. At present, however, data on how Brain size changes over the course of development are only available from chimpanzees and modern humans. In this study, we examined Brain Growth in wild Virunga mountain gorillas using data derived from necropsy reports (N = 34) and endocranial volume (EV) measurements (N = 86). The youngest individual in our sample was a 10-day-old neonatal male with a Brain mass of 208 g, representing 42% of the adult male average. Our results demonstrate that Virunga mountain gorillas reach maximum adult-like Brain mass by 3-4 years of age; adult-sized EV is reached by the time the first permanent molars emerge. This is in contrast to the pattern observed in chimpanzees, which despite their smaller absolute Brain size, reportedly attain adult Brain mass approximately 1 year later than Virunga mountain gorillas. Our findings demonstrate that Brain Growth is completed early in Virunga mountain gorillas compared to other great apes studied thus far, in a manner that appears to be linked with other life history characteristics of this population.