Short-Term Memory and Cerebral Ischemia: Pharmacological Application

Poncin-Lafitte, M. Le; C, Grosdemouge; Roy-Billon, C; Duterte, D; Potrat, P.; Lespinasse, Pierre; Rapin, J. R.

doi:10.1159/000115245

Cited by 15 publications

(7 citation statements)

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“…LES was thought to be extremely susceptible to an ischaemic insult, because of an almost complete lack of vertebral blood supply under normal conditions [23,43]. Although similar results were obtained in WS rats after cauterization of vertebral arteries [33], this study demonstrated that the LES was more resistant than the WS, following 10 minutes ischaemia.…”

Section: Difference Between the Strainssupporting

confidence: 70%

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats

Taşdemiroğlu

1996

Acta neurochir

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Anaesthetized male rats (n = 86) from both Long-Evans strain (LES) (n = 43) and Wistar strain (WS) (n = 43) were utilized for the experiments. While three animals from each strain were used as control, 40 rats from each strain underwent up to 10 minutes forebrain ischaemia by bilateral common carotid artery (CCA) occlusion combined with systemic hypotension [Mean Arterial Blood Pressure (MABP) = 50 mm/Hg]. The animals from each strain were divided into four (n = 10) groups. In both strains, groups (n = 10) 1 and 2, temporalis muscle (TM) and body temperatures of the animals were kept at 36-37 degrees C during the experiments. The groups 1 and 2 were killed in 3 and 7 days after the ischaemic insult, respectively. The groups 3 and 4 were also killed 3 and 7 days after the ischaemic insult, but the forebrain ischaemia was carried out under mild cerebral hypothermia (TM temperature = 33 degrees C). Pyramidal neurons of the hippocampal CA1 region from each group was evaluated semiquantitatively. In WS, groups 1 and 2 showed moderate and severe neuronal loss in the CA1 region, respectively. However, in LES while the group 1 (3 days survival) did not show any neuronal loss, group 2 showed moderate neuronal loss of the CA1 region. While in group 3 (3 days survival, hypothermia) WS and LES, hypothermia protected the CA1 region, group 4 of LES showed mild neuronal loss. However WS, group 4 (7 days survival, hypothermia) showed severe neuronal loss of the CA1 region. It was concluded that mild hypothermia during ischaemic insults did not prevent the delayed postischaemic neuronal damage of the hippocampal CA1 region of both strains, and following 10 minutes forebrain ischaemia, male LES rats were found more resistant than male WS rats to neuronal loss of the CA1 region.

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Section: Difference Between the Strainssupporting

confidence: 70%

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats

Taşdemiroğlu

1996

Acta neurochir

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“…Since the memory impairments induced by physical (cerebral ischemia, brain injury) or chemical (drugs, anoxic treatment) means in the mouse one-trial passive avoidance test are improved by the administration of various drugs including cholinergic drugs such as physostigmine and oxotremorine before the retention trial (28,(35)(36)(37)(38), these memory impairments are considered to be due to disturbance of the retrieval process of memory rather than of the consolidation of memory (39). In a similar experiment in mice using a light-dark box, the shortened latency in the retention trial 24 hours after exposure to CO-, gas immediately following the acquisition trial was dose-dependently prolonged by oral administration of TA-0910 60 min before the retention trial.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological study of TA-0910, a new thyrotropin-releasing hormone(TRH) analog. (IV). Effects on experimental memory impairment in mice and rats.

Yamamura¹,

Kawakami²,

Nakagawa³

et al. 1991

Jpn.J.Pharmacol

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ABSTRACT-The effects of a new TRH analog, TA-0910, orally administered, on experimental memory impairments for the one-trial passive avoidance response in anoxic mice (light-dark box), active avoidance response in basal forebrain (BF)-lesioned rats (shuttle box), and delayed alternation task in scopolamine-treated rats (T-maze) were studied. In mice, TA-0910 (3 -30 mg) administered 60 min before the retention trial dose-dependently prolonged the passive avoidance response latency reduced by C02-exposure that was given immediately after the acquisition trial, but not when it was given 60 min before the acquisition or just after the anoxic treatment. In rats, TA-0910 (0.3-3 mg/kg) administered 40-60 min before the test trial, dose-dependently prevented the reduction in mean avoidance rate caused by BF-lesioning and elevated the scopolamine (0.1 mg/kg, i.p.)-induced reduction in percent correct choice level in the alternation task. TRH (30 -300 mg/kg), on the other hand, produced no improvements in any of the above tests. These results suggest that TA-0910 improves impaired memory by correcting the retrieval process of memory.Thyrotropin-releasing hormone (TRH) is a hypothalamic hormone that stimulates secretion of thyrotropin and prolactin. However, radioimmunoassay has demonstrated that twothirds of the total TRH content of the brain is distributed widely in areas other than the hypothalamus (1). Also, autoradiographic studies have revealed that TRH receptors of the brain are concentrated in the cerebral cortex and the limbic system (2, 3). Based on these findings, TRH is considered to play an important role in the brain in the maintenance of consciousness and emotional or intellectual functions (4). Moreover, Yarbrough and Pomara (5) recommended the use of TRH for the treatment of dementia of the Alzheimer type (DAT) from the functional relationship between TRH and central cholinergic nervous system and the effectiveness of TRH in the treatment of dementia of patients with amyotrophic lateral sclerosis complicated by degeneration of cholinergic nerves, and by Metcalf (6) and Griffiths (7) from the effect of TRH to improve disturbance of consciousness (8) and its antidepressant effect (9, 10).Recently, improvements in mental symptoms (such as disturbances in impressibility, emotional disturbances, reduced ability to think, deduced spontaneity, inertia, and apathy) were reported in patients with Alzheimer's disease (AD) and cerebrovascular dementia after administration of TRH (11,12). Tem-

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“…This neurological dysfunction is naturally reflected in the deterioration of behavioral performance and memory function. In fact, cerebral ischemia induced by an injec tion of microspheres results in poor retention of the active avoidance response in rats (1,2). Pulsinelli and Brierley (3) have introduced a method for producing cerebral ische mia in unanesthetized rats by temporarily occluding the common carotid arteries and permanently interrupting the vertebral arteries.…”

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confidence: 99%

Characteristics of Transient Cerebral Ischemia-Induced Deficits on Various Learning and Memory Tasks in Male Mongolian Gerbils

Amano

Hasegawa

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-We examined the characteristics of 5-min cerebral ischemia-induced behavioral deficits in spontaneous locomotor activity and their effects on the performance of habituation (HAB), passive avoidance (PA) and 8-arm radial maze (RM) tasks in Mongolian gerbils. Performances in HAB, PA and RM were impaired within 2 days after occlusion, and gerbils showed hyperlocomotion during this period. Ten days after ischemia, the hyperlocomotion disappeared and performance in the HAB and PA was the same as that in the sham-operated group. Retention in the RM was impaired at that period, but this impair ment was overcome, and retention recovered easily to the sham-operated level with a few additional trials. When the acquisition trial in the RM began at 11 days after occlusion, severe learning impairment was found. Destruction of hippocampal CAI neurons appears from 2-3 days after ischemic insult, with most CAI neurons having disappeared by day 7. These findings suggest that the impairment of performance in the HAB and PA within 2 days after occlusion may be related to an early phase of CAI neuronal death and to hyperlocomotion, although the impairment of spatial learning and memory was clearly associated with CAI injury 10 days after ischemia.

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Short-Term Memory and Cerebral Ischemia: Pharmacological Application

Cited by 15 publications

References 0 publications

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats

Pharmacological study of TA-0910, a new thyrotropin-releasing hormone(TRH) analog. (IV). Effects on experimental memory impairment in mice and rats.

Characteristics of Transient Cerebral Ischemia-Induced Deficits on Various Learning and Memory Tasks in Male Mongolian Gerbils

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