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Biomedical subjects

Robert Greene

Publications and source records attributed to Robert Greene.

4 recordsLinked to original sources
PubMed2006

The role of CA3 hippocampal NMDA receptors in paired associate learning.

The hippocampus is necessary for declarative memory in humans and episodic memory in rodents. Considerable current research is focused on the role of plasticity within specific subfields of the hippocampus. Here, using a viral vector to temporally control a focal deletion of the NR1 gene, we show that learning novel paired associations between specific cues and their context is dependent on CA3 NMDA receptors. Deletion of CA3 NR1 genes in <30% of the dorsal hippocampus was sufficient to disrupt new learning, whereas the same treatment does not prevent expression of previously acquired paired associates and does not affect the ability to discriminate contexts or paired associate learning when either the cues or the context is familiar. The findings suggest that CA3 NMDA receptors specifically support the encoding of new experiences to involve incidental and contingent associations.

Animals↗
PubMed2005

Adenosine mediation of presynaptic feedback inhibition of glutamate release.

Conditions of increased metabolic demand relative to metabolite availability are associated with increased extracellular adenosine in CNS tissue. Synaptic activation of postsynaptic NMDA receptors on neurons of the cholinergic brainstem arousal center can increase sufficient extracellular adenosine to act on presynaptic A1 adenosine receptors (A1ADRs) of glutamate terminals, reducing release from the readily releasable pool. The time course of the adenosine response to an increase in glutamate release is slow (tau > 10 min), consistent with the role of adenosine as a fatigue factor that inhibits the activity of cholinergic arousal centers to reduce arousal.

Adenosine↗
PubMed2004

Sleep: a functional enigma.

Although continued total sleep deprivation is fatal, the function of sleep remains a mystery. Shorter durations of sleep deprivation are followed by rebound increases in non-rapid eye movement (non-REM) sleep, suggesting a homeostatic control. Measurements of the power spectrum of the electroencephalograph (EEG) suggest that a more accurate marker of the homeostasis may be delta frequency power, because it most closely reflects the duration of the preceding sleep deprivation. Several lines of evidence suggest a link with complex metabolic processes. These include a local homeostatic factor, adenosine, that inhibits neuronal activity in response to increases in the ratio of energy demand to metabolite availability. Other evidence derives from the relationship of circadian genes, NPAS2 and Clock, to metabolism. Additionally, at a systems level, hypocretin/Orexin may coordinate motor activity with feeding. A loss of hypocretin neurons or a mutation of the genes controlling this peptide system can result in the sleep disorder narcolepsy. Finally, evidence for a role of non-REM sleep in developmental central nervous system (CNS) plasticity, as well as learning and memory, is discussed.

Adenosine↗