Functional Neurogenesis
neurogenesis survival timecourses
From here:
New neurons are born and then many die. The survival timecourse answers the questions: How many new neurons are born? Where are they born and where do they end up, anatomically? How many of them survive and can their survival be altered? Survival timecourses are typically performed by injecting animals with a mitotic marker that will label new neurons as they’re being born, e.g. ³H-thymidine (old school), BrdU (tried and true – example), or a GFP-expressing retrovirus (new school). At a later date one can then detect these birthdated new neurons and count them, see where they’re located etc.
What do these survival timecourses tell us?
many newborn neurons die between 1w and 4w of age but after that they all survive
neurons born during infancy are an exception as they DO die off many months after their birth (Dayer 2003), lending support to the sexy-but-underexplored idea that neuronal turnover might underlie memory turnover in the hippocampus
the number of new cells labeled with a birthdating marker (e.g. BrdU) grows between 2 hours and several days after the birthdating marker is administered
this is caused by continued division of the stem cell or precursor cell that took up the marker in the first place (see expression timecourse, below). After a few cell divisions the marker gets diluted to undetectable levels.
the general timecourse of cell death is similar in young and aged animals (McDonald 2005) and in mice and rats, although more cells die in mice (Snyder 2009)
the addition and culling of newborn neurons in the monkey hippocampus (Gould 2001) follows a delayed timecourse compared to rodents
CREB signalling is critical for neurons to survive between 5-7 days old (Jagasia 2009), NMDA receptors are critical for survival from 14-21 days (Tashiro 2006)
thus, CREB signalling would appear to regulate survival before new neurons have formed excitatory connections and are functional (see below) and NMDA receptors regulate survival during the early phase of excitatory synapse formation, when new neurons are just beginning to be able to contribute to behavior. Knowing how to regulate neuronal survival has obvious implications for disorders where reduced neurogenesis might be a causative factor.
learning increases the survival of new neurons (Leuner 2004)
learning does not increase the survival of new neurons (Snyder 2005)
neurogenesis survival timecourses
From here:
New neurons are born and then many die. The survival timecourse answers the questions: How many new neurons are born? Where are they born and where do they end up, anatomically? How many of them survive and can their survival be altered? Survival timecourses are typically performed by injecting animals with a mitotic marker that will label new neurons as they’re being born, e.g. ³H-thymidine (old school), BrdU (tried and true – example), or a GFP-expressing retrovirus (new school). At a later date one can then detect these birthdated new neurons and count them, see where they’re located etc.
What do these survival timecourses tell us?
many newborn neurons die between 1w and 4w of age but after that they all survive
neurons born during infancy are an exception as they DO die off many months after their birth (Dayer 2003), lending support to the sexy-but-underexplored idea that neuronal turnover might underlie memory turnover in the hippocampus
the number of new cells labeled with a birthdating marker (e.g. BrdU) grows between 2 hours and several days after the birthdating marker is administered
this is caused by continued division of the stem cell or precursor cell that took up the marker in the first place (see expression timecourse, below). After a few cell divisions the marker gets diluted to undetectable levels.
the general timecourse of cell death is similar in young and aged animals (McDonald 2005) and in mice and rats, although more cells die in mice (Snyder 2009)
the addition and culling of newborn neurons in the monkey hippocampus (Gould 2001) follows a delayed timecourse compared to rodents
CREB signalling is critical for neurons to survive between 5-7 days old (Jagasia 2009), NMDA receptors are critical for survival from 14-21 days (Tashiro 2006)
thus, CREB signalling would appear to regulate survival before new neurons have formed excitatory connections and are functional (see below) and NMDA receptors regulate survival during the early phase of excitatory synapse formation, when new neurons are just beginning to be able to contribute to behavior. Knowing how to regulate neuronal survival has obvious implications for disorders where reduced neurogenesis might be a causative factor.
learning increases the survival of new neurons (Leuner 2004)
learning does not increase the survival of new neurons (Snyder 2005)