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Query: UMLS:C0022116 (
ischemia
)
91,303
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The goals of this research were to develop a within-subject test of spatial working memory and performance for the rat in a T-maze, based on a delayed alternation, or "win-shift" foraging strategy. Using this model, specific aims were to compare the effects of: (1) age, (2) basal forebrain, medial septal, and amygdala lesions, (3) four vessel occlusion (4-VO), forebrain
ischemia
, and (4) physostigmine, scopolamine, arecoline, piracetam, and clonidine on memory and performance of young middle-aged, and old rats. Aging significantly impaired working memory and performance of Long-Evans rats. Memory of septal and basal forebrain, but not of amygdala lesioned rats was significantly impaired without effects on performance. Transient, 4-VO forebrain
ischemia
produced significant memory impairment, without effects on performance, and highly selective CA1 cell loss in the hippocampus. Physostigmine enhanced working memory in middle-aged and old rats.
Scopolamine
impaired memory in young, middle-aged, and old rats. Physostigmine reversed the scopolamine impairments of working memory. Arecoline enhanced memory in old rats without effects on performance. Piracetam and clonidine had no direct effects on memory, but piracetam increased and clonidine decreased speed of performance. From the aging, lesion,
ischemia
, and drug studies it was concluded that there was a convergence of evidence from 4 different approaches for a critical role for the hippocampus, particularly the CA1 fields, in spatial working memory.
...
PMID:An animal model of human-type memory loss based on aging, lesion, forebrain ischemia, and drug studies with the rat. 306 74
Effects of bifemelane hydrochloride (MCI-2016) on acetylcholine (ACh) level in the cerebral cortex and hippocampus of rats and Mongolian gerbils were examined. In normal rats, MCI-2016 (30 mg/kg, i.p.) slightly increased ACh content in the cerebral cortex.
Scopolamine
(1 mg/kg, i.p.) or hypoxia (95% N2 +5% O2, 9 min) decreased ACh level and pretreatment of MCI-2016 attenuated the decrement of ACh level in the rats. ACh level in the brain of Mongolian gerbils was significantly decreased following ligation of bilateral carotid arteries. In this case, MCI-2016 also attenuated the decrement of ACh level. These results suggest that improvement by MCI-2016 of behavioral impairment observed in the animals treated with scopolamine, hypoxia or
ischemia
may be, at least partly, attributed to the amelioration of decreased ACh level in the brain.
...
PMID:Effects of bifemelane hydrochloride (MCI-2016) on acetylcholine level reduced by scopolamine, hypoxia and ischemia in the rats and mongolian gerbils. 406 78
The neurodegeneration in the CA1 subfield of hippocampus exhibited a dorsal-ventral gradient of susceptibility in global
ischemia
(82% dorsoseptally and only 16% ventrotemporally).
Scopolamine
(
SCOP
) did not improve the neuronal damage caused by the global ischemic challenge in rats and did not reduce the infarct area after the focal MCA-occlusion in mice. No differences were observed between saline and
SCOP
-treated animals in the physiologic parameters, except for a slight increase in rectal temperature. In contrast, treatment of hippocampal cultures with increasing concentrations of
SCOP
(1 nM to 1 mM) under glutamate incubation had a beneficial effect on neuronal viability. These data show that (1) there is substantial gradient of vulnerability of the hippocampus from dorsal to ventral in global
ischemia
and (2) that interactions between the NMDA, muscarinic receptors and their corresponding neurotransmitter inputs to hippocampal neurons are evident in vitro and may play a crucial role in neuronal neurodegeneration. However, the mechanisms underlying the high vulnerability of dorsal hippocampus still remain enigmatic.
...
PMID:Differential effects of scopolamine on neuronal survival in ischemia and glutamate neurotoxicity: relationships to the excessive vulnerability of the dorsoseptal hippocampus. 931 69