James W. Fawcett, Anne E. Rosser, and Stephen B. Dunnett
- Published in print:
- 2002
- Published Online:
- March 2012
- ISBN:
- 9780198523376
- eISBN:
- 9780191724534
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198523376.003.0009
- Subject:
- Neuroscience, Techniques
The developing nervous system produces about twice as many neurons as will survive into adulthood, and then at the end of development, around the time of birth in mammals, there is a short period ...
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The developing nervous system produces about twice as many neurons as will survive into adulthood, and then at the end of development, around the time of birth in mammals, there is a short period termed the ‘period of ontogenetic cell death’ during which about half the neurones die. Trophic factors have a well-characterised role in the control of this process. The first trophic factor to be characterised was nerve growth factor (NGF): Rita Levi-Montalcini and Stanley Cohen received a Nobel prize for their pioneering work in the identification of this molecule. Subsequently, many other neuronal trophic factors have been discovered, many of them mentioned later in this chapter, but NGF has provided the prototype for all that followed.Less
The developing nervous system produces about twice as many neurons as will survive into adulthood, and then at the end of development, around the time of birth in mammals, there is a short period termed the ‘period of ontogenetic cell death’ during which about half the neurones die. Trophic factors have a well-characterised role in the control of this process. The first trophic factor to be characterised was nerve growth factor (NGF): Rita Levi-Montalcini and Stanley Cohen received a Nobel prize for their pioneering work in the identification of this molecule. Subsequently, many other neuronal trophic factors have been discovered, many of them mentioned later in this chapter, but NGF has provided the prototype for all that followed.
F. Bermúdez-Rattoni
- Published in print:
- 1998
- Published Online:
- January 2008
- ISBN:
- 9780198523475
- eISBN:
- 9780191712678
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198523475.003.0008
- Subject:
- Psychology, Neuropsychology
Removed insular cortex (IC – about 3 mm3) can be substituted 60 days later by homotopic fetal IC transplant allowing CTA relearning. Similar attempts to compensate the lesioned amygdala by ...
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Removed insular cortex (IC – about 3 mm3) can be substituted 60 days later by homotopic fetal IC transplant allowing CTA relearning. Similar attempts to compensate the lesioned amygdala by transplantation were less successful, probably because less HRP labelled cells regenerated in the Am than in the IC transplants. Recovery of CTA was absent after 15 days, poor after 30–45 days, and normal after 60 days following transplantation. Positive results were due to improved connectivity and to a higher content of trophic factors (NGF) and of acetyltransferase. In contrast, cholinergic blockade by scopolamine delayed the transplantation induced CTA recovery. Grafting fetal homotopic IC tissue allowed for a full recovery of the already learned CTA and learning CTA to novel taste. Grafting fetal occipital cortex into the lesioned IC allowed for recovery of the already established CTA but not any learning of new CTAs. This evidence indicates that the ‘reversibility’ of the ablation procedure is valid only when access to critical input and output centers remains preserved.Less
Removed insular cortex (IC – about 3 mm3) can be substituted 60 days later by homotopic fetal IC transplant allowing CTA relearning. Similar attempts to compensate the lesioned amygdala by transplantation were less successful, probably because less HRP labelled cells regenerated in the Am than in the IC transplants. Recovery of CTA was absent after 15 days, poor after 30–45 days, and normal after 60 days following transplantation. Positive results were due to improved connectivity and to a higher content of trophic factors (NGF) and of acetyltransferase. In contrast, cholinergic blockade by scopolamine delayed the transplantation induced CTA recovery. Grafting fetal homotopic IC tissue allowed for a full recovery of the already learned CTA and learning CTA to novel taste. Grafting fetal occipital cortex into the lesioned IC allowed for recovery of the already established CTA but not any learning of new CTAs. This evidence indicates that the ‘reversibility’ of the ablation procedure is valid only when access to critical input and output centers remains preserved.
