Effects of fetal hippocampal field grafts on ischaemic-induced deficits in spatial navigation in the water maze

Netto, Carlos Alexandre; Hodges, Helen; Sinden, John D.; Peillet, E. Le; Kershaw, T. R.; Sowiński, P.; Meldrum, Brian S.; Gray, Jeffrey A.

doi:10.1016/0306-4522(93)90384-r

Cited by 191 publications

(81 citation statements)

References 47 publications

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“…The latency and distance swum, required to locate the hidden platform, were recorded as above. The difference between latency scores on trials 2 and 3, expressed as percentage of trial 1, provided an additional measure of working memory performance ("savings") (see also Netto et al, 1993). The same analysis was also performed on animals' performance between trials 3 and 4 to rule out the possible adoption of unrelated across-day trajectory strategies that would be more dependent on striatal, rather than hippocampal, mechanisms (see also White, 1997;Jog et al, 1999;Cassel et al, 2002).…”

Section: Methodsmentioning

confidence: 99%

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Functional Convergence of Dopaminergic and Cholinergic Input Is Critical for Hippocampus-Dependent Working Memory

Wisman¹,

Şahin²,

Maingay³

et al. 2008

J. Neurosci.

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Although Parkinson's disease is a movement disorder, in many patients cognitive dysfunction is an important clinical sign. It is not yet clear whether this is attributable solely to a decrease in dopamine levels, or whether other neurotransmitter systems might be involved as well. In the present study, the importance of the mesocorticolimbic dopamine pathway and a possible convergence with forebrain cholinergic projections to neocortex and hippocampus in the regulation of learning and memory abilities were investigated by using specific lesion paradigms in one or both systems. Lesioning of dopaminergic neurons in the ventral tegmental area resulted in an impaired performance in the reference memory task, whereas the execution of the working memory tasks appeared to be unaffected in the Morris water maze. Analysis of the swim paths revealed that the dopamine-depleted animals were capable of adapting a search strategy on a given testing day but failed to transfer this information to the next day, suggesting a deficit in information storage and/or recall. In contrast, cholinergic lesions alone were without effect in all test paradigms. However, when both dopamine and acetylcholine were depleted, animals were also impaired in the working memory task, indicating that a functional convergence of the inputs from these systems was critical for acquisition of spatial memory. Interestingly, such an additional acquisition deficit appeared only after hippocampal cholinergic depletion regardless of a concurrent disruption of basalocortical cholinergic afferents. Thus, further analyses of cholinergic alterations may prove useful in better understanding the cognitive symptoms in Parkinson's disease.

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Section: Methodsmentioning

confidence: 99%

“…4 B) and between trials 1 and 3 (Fig. 4C) were analyzed and plotted in terms of savings (Netto et al, 1993). Under these conditions, control rats were seen to reduce their latency to reach the platform by ϳ50 -70%.…”

Section: Combined Loss Of Dopaminergic and Cholinergic Inputs To The mentioning

confidence: 99%

Functional Convergence of Dopaminergic and Cholinergic Input Is Critical for Hippocampus-Dependent Working Memory

Wisman¹,

Şahin²,

Maingay³

et al. 2008

J. Neurosci.

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“…For example, cerebral ischemia produces a lesion of the CA1 cell field of the hippocampus, with corresponding learning and memory deficits in the water and radial maze tasks (Auer et al, 1989;Davis and Volpe, 1991). These deficits can be reversed by the transplantation of either fetal hippocampal (H) tissue or fetal CA1 cells into the lesioned hippocampus, but not by the grafting of other cell types (Onifer and Low, 1990;Netto et al, 1993). Thus, only homologous and not heterologous neural tissue transplants appear to be successful in ameliorating cognitive deficits produced in these Hf lesion models.…”

Section: Abstract: Learning and Memory; Neural Transplantation; Hippmentioning

confidence: 99%

Hippocampal Tissue Transplants Reverse Lesion-Induced Spatial Memory Deficits in Zebra Finches (Taeniopygia guttata)

1997

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The avian hippocampal formation (Hf ) plays an important role in spatial memory for food storing. Here we examined the effects of excitotoxic lesions of the Hf and subsequent neural transplantation on a one-trial associative memory task in zebra finches. The results showed (1) that small ibotenic acid lesions of the dorsal Hf of zebra finches produced significant spatial memory impairments compared with controls, sham-lesioned birds, and prelesion performance; and (2) that Hf-lesioned birds given transplants of embryonic hippocampal (H) tissue, but not those given transplants of embryonic anterior telencephalon (AT ) tissue, showed a significant reversal of the performance deficits on the spatial memory task. Lesioned-only birds and lesioned birds given H or AT transplants that did not survive did not show behavioral improvement. Sham-lesioned and untreated control birds maintained good performance throughout the experiment. The H and AT transplants were found to be growing partially within the Hf and partially within the underlying ventricle. The transplants appeared healthy and contained neurons with beaded and unbeaded fibers (shown by immunohistochemistry with antibodies to parvalbumin, substance P, and a 200 kDa neurofilament protein). Blood vessels and erythrocytes were also present within the transplants. The results show that neural transplants can survive within the bird brain and that small lesions of the Hf produce significant spatial memory deficits that can only be reversed by surviving homologous H transplants, and not by heterologous telencephalon transplants.

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“…Microsphere embolism is considered to induce small widespread emboli and multiple infarct areas in the brain, which may be comparable with the pathogenesis of multi-infarct dementia (24). It has been shown that a variety of deficits in learning and memory function are induced in animals with ischemic brain damage, such as in rats with four vessel ligation (25), middle cerebral artery occlusion (26), and microsphere embolism (27). It becomes an important objective to determine the nature of intracellular signal transduction pathways via mAChR, particularly the M 1 receptor, and how they are modulated by cerebral ischemia.…”

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confidence: 99%

Altered Extracellular Signal-regulated Kinase Signal Transduction by the Muscarinic Acetylcholine and Metabotropic Glutamate Receptors after Cerebral Ischemia

Takagi¹,

Miyake-Takagi²,

Takagi³

et al. 2002

Journal of Biological Chemistry

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To determine whether muscarinic acetylcholine receptors (mAChR) in the post-ischemic hippocampus may be involved in altered extracellular signal-regulated kinases (ERK) signal transduction, we have investigated changes in the activity of ERK1/2 induced by a muscarinic agonist, carbachol. Cerebral ischemia was produced in the rat by injecting 900 microspheres (48 m in diameter) into the right internal carotid artery. Applying carbachol to the contralateral hippocampal slices from ischemic rats increased the phosphorylation of ERK1/2 but did not increase phosphorylation in the ipsilateral hippocampus. Analysis of M 1 mAChR binding showed that there was no significant difference in the number and K d values between the hippocampi from naïve and ischemic rats. Immunoblotting analysis showed no significant difference in the amount of M 1 mAChR in both hemispheres. In contrast to carbachol stimulation, the protein kinase C activator induced an activation of ERK1/2 in the ipsilateral hippocampus. This increase was shown to occur in neurons by immunofluorescence colocalization study. Carbachol-stimulated tyrosine phosphorylation of the G␣ q/11 , inositol 1,4,5-trisphosphate formation, and association of G␣ q/11 with phospholipase C␤1 were attenuated in the ipsilateral hippocampus. We also found that stimulation of group I metabotropic glutamate receptors, which are linked to G␣ q/11 , failed to increase in phosphorylation of ERK1/2 in the ipsilateral hippocampus. These results suggest that failure in receptor-mediated tyrosine phosphorylation of the G␣ q/11 subunit and a defect in receptor-G␣ q/11-effector coupling in the ischemic hippocampus may be involved in alterations of ERK signal transduction.

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Effects of fetal hippocampal field grafts on ischaemic-induced deficits in spatial navigation in the water maze

Cited by 191 publications

References 47 publications

Functional Convergence of Dopaminergic and Cholinergic Input Is Critical for Hippocampus-Dependent Working Memory

Functional Convergence of Dopaminergic and Cholinergic Input Is Critical for Hippocampus-Dependent Working Memory

Hippocampal Tissue Transplants Reverse Lesion-Induced Spatial Memory Deficits in Zebra Finches (Taeniopygia guttata)

Altered Extracellular Signal-regulated Kinase Signal Transduction by the Muscarinic Acetylcholine and Metabotropic Glutamate Receptors after Cerebral Ischemia

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