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Biomedical subjects

John H Morrison

Publications and source records attributed to John H Morrison.

40 records · Page 3Linked to original sources
PubMed2002

Morphological alterations in neurons forming corticocortical projections in the neocortex of aged Patas monkeys.

Recent studies indicate that the cognitive processes mediated by the prefrontal cortex, such as working memory, are impaired during normal aging. These disturbances in cortical function may be a consequence of abnormalities in neocortical circuits, even though the numbers of cortical neurons are preserved in normal aging. We performed retrograde tract-tracing of cortical projections connecting the temporal cortex to the prefrontal cortex in combination with dye-filling and three-dimensional neuronal reconstructions in aged patas monkeys. Age-related changes affected the apparent complexity of the apical dendrites of projection neurons and caused a significant loss of dendritic spines at all levels of their dendritic trees. These results indicate that normal aging is accompanied by neuronal changes that are quite subtle, and possibly involves discrete cellular components of certain cortical neurons selectively rather than inducing major alterations such as cell death.

Aging↗
PubMed2002

Selective vulnerability of corticocortical and hippocampal circuits in aging and Alzheimer's disease.

Alzheimer's disease (AD), a classic neurodegenerative disorder, is characterized by extensive yet selective neuron death in the neocortex and hippocampus that leads to dramatic decline in cognitive abilities and memory. Crucial subsets of pyramidal cells and their projections are particularly vulnerable. A more modest disruption of memory occurs often in normal aging, yet such functional decline does not appear to be accompanied by significant neuron death. However, the same circuits that are devastated through degeneration in AD are vulnerable to sublethal age-related biochemical and morphologic shifts that alter synaptic transmission, and thereby impair function. For example, in the monkey neocortex, pyramidal cells that are homologous to those that degenerate in AD do not degenerate with aging, yet they lose spines, suggesting that an age-related synaptic disruption has occurred. Such age-related synaptic alterations have also been reported in hippocampus. For example, NMDA receptors are decreased in certain hippocampal circuits with aging. NMDA receptors are also responsive to circulating estrogen levels, thus interactions between reproductive senescence and brain aging may also affect excitatory synaptic transmission in the hippocampus. Thus, the aging synapse may be the key to age-related memory decline, whereas neuron death is the more prominent and problematic culprit in AD.

Aging↗
PubMed2002

Parvalbumin-containing interneurons in rat hippocampus have an AMPA receptor profile suggestive of vulnerability to excitotoxicity.

alpha-Amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors mediate excitatory neurotransmission in the central nervous system, and contain combinations of four subunits (GluR1-4). We developed a GluR3-specific monoclonal antibody and quantified the cellular distribution of GluR3 in rat hippocampus. GluR3 immunoreactivity was detected in all pyramidal neurons and most interneurons. In addition, we found a subset of parvalbumin (PV)-containing interneurons in the hippocampus and neocortex that was notable for its intense GluR3 immunoreactivity and lack of GluR2 immunoreactivity. Such an expression pattern of AMPA receptor subunits is likely to make these interneurons selectively vulnerable to excitotoxicity.

Animals↗