Amy Morin

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We evaluated the neuroprotective effect of MK-801, a noncompetitive, selective N-methyl-D-aspartate receptor antagonist, in a neonatal hypoxic-ischemic animal model. Seven-day-old rats underwent bilateral ligation of the carotid arteries followed by exposure to an 8% oxygen atmosphere for 1 hr. We sacrificed the animals 72 hrs later and assessed the(More)
[3H]MK-801 binding sites are present in neonate rat brain as early as 3 days after birth. Immature hippocampus and cortex contain approximately one sixth the concentration of binding sites of the adult, while brainstem concentration is twice as high as that of adult. [3H]MK-801 binding is stimulated by glutamate and glycine and blocked by phencyclidine and(More)
The regulation of serotonin synthesis was investigated in the serotonergic neurons, which provide afferents to the dorsolateral hypothalamus (DLH). The origin of the DLH projection neurons within the raphe nucleus was identified by retrograde transport of Cholera toxin (CTb) and their serotonergic nature confirmed by tryptophan hydroxylase (TPH)(More)
To determine the biochemical basis of decreased brain uptake of glucose with age, the brain influx of 3-O-methylglucose (3-O-MG) was measured in male Fischer 344 rats at various ages using the arterial injection-tissue sampling technique of Oldendorf. The Vmax of 3-O-MG transport in the 24-month-old rats (0.22 +/- 0.14 mumol/min/g) was significantly lower(More)
Measurement of cholinergic muscarinic receptor binding in various rat brain areas using the ligand [3H]quinuclidinyl benzilate indicates that receptor binding is decreased in striatum and cerebellum of aged female rats (22 months old) as compared to younger rats (4 months old). Decreases were not observed in cortex, hippocampus, hypothalamus, or amygdala(More)
Oxidative stress is a major contributing factor in neurodegeneration and can arise from dietary, environmental, and genetic sources. Here we examine the separate and combined impact of deprivation of folate and vitamin E, coupled with dietary iron as a prooxidant, on normal mice and transgenic mice lacking apolipoprotein E (ApoE-/- mice). Both mouse strains(More)
Nitric oxide synthase (NOS) is present within cerebrovascular endothelial cells in a distinct membrane-bound juxtanuclear location. The enzyme product, nitric oxide, causes vasodilation as well as stimulation of ADP-ribosylations of some proteins. The activity of specific stimulatory ADP-ribosylation factors, associated with the Golgi complex (GC), has been(More)
Cultured cells derived from the cerebromicrovasculature can be shown to contain the enzyme nitric oxide synthase (NOS) by NADPH diaphorase staining. NOS is located largely as a distinct crescent adjacent to the nuclear membrane. NOS in these cells appears to be associated with the microtubule and microfilament structures and the Golgi apparatus of the cell(More)