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PubMed2004

Preserved anterograde and retrograde memory of rapidly acquired olfactory discrminations after neurotoxic hippocampal lesions.

A forced-choice discrimination paradigm was used in two experiments, to evaluate retrograde and anterograde amnesia in rats after hippocampal ablation. In a within-subjects design (Experiment 1), rats were trained on a set of 10 olfactory discriminations 4 weeks before surgery and on a separate set of 10 discriminations 1 week before surgery. In a mixed design (Experiment 2), rats were trained on olfactory discriminations in one of three conditions: condition 1 (10 discriminations at 4 weeks before surgery); condition 2 (10 discriminations at 1 week before surgery); or condition 3 (10 discriminations at 4 weeks before surgery and 10 discriminations at 1 week before surgery). Discriminations in both experiments were rapidly learned, requiring 7-10 trials to reach criterion. After training, half of the rats in each condition received bilateral neurotoxic lesions of the hippocampus, and the other half received sham surgery. One week after surgery, all rats were given a retention test, consisting of a single critical trial for each discrimination. In both experiments, rats with selective hippocampal lesions exhibited preserved retention of these olfactory discriminations with no observable retention gradient. A postoperative acquisition test for two new discriminations indicated that anterograde memory was also preserved, while a postoperative test of spatial learning in the Morris water maze confirmed that the hippocampal lesions impaired spatial learning. Together, these experiments refute the contention that the hippocampus is requisite for (non-spatial) olfactory memory consolidation, storage, or access, despite the condition that the information be rapidly acquired.

Amnesia, Anterograde↗
PubMed2000

[Deficits of Morris water maze learning in rats with striatal kainic acid lesions].

This study investigated effects of intrastriatal kainic acid administration, which induces selective neuronal cell death in the striatum sparing passing nerve fibers and terminals, on the acquisition of spatial learning in Morris water maze. Rats treated with bilateral kainic acid (0.5-1.0 microgram) into the striatum were trained to escape to a hidden platform under the water. Compared with control rats, kainic acid (1.0 microgram)-lesioned rats showed significantly longer escape latency in the place navigation, and in the following probe test lower rate of swimming within the quadrant where the platform had been placed. In addition, kainic acid (1.0 microgram)-lesioned rats showed longer latency in the cue navigation in which rats were trained to escape to a visible platform above the water. These deficits were caused by their tendency to swim along the wall of pool before approaching the platform and not by their swim difficulty. Results suggest that striatal neurons or neural circuits containing these neurons play an important role in the acquisition of spatial learning task, and the nature of this performance impairment was discussed in terms of both learning and attention deficits.

Animals↗
PubMed2006

Analysis of the stress response in rats trained in the water-maze: differential expression of corticotropin-releasing hormone, CRH-R1, glucocorticoid receptors and brain-derived neurotrophic factor in limbic regions.

Glucocorticoids and corticotropin-releasing hormone (CRH) are key regulators of stress responses. Different types of stress activate the CRH system; in hypothalamus, CRH expression and release are increased by physical or psychological stressors while in amygdala, preferentially by psychological stress. Learning and memory processes are modulated by glucocorticoids and stress at different levels. To characterize the kind of stress provoked by a hippocampal-dependent task such as spatial learning, we compared the expression profile of glucocorticoid receptor (GR), pro-CRH and CRH-R1 mRNAs (analyzed by RT-PCR), in amygdala, hippocampus and hypothalamus and quantified serum corticosterone levels by radioimmunoassay at different stages of training. mRNA levels of brain-derived neurotrophic factor (BDNF) were also quantified due to its prominent role in learning and memory processes. Male Wistar rats trained for 1, 3 or 5 days in the Morris water-maze (10 trials/day) were sacrificed 5-60 min the after last trial. A strong stress response occurred at day one in both yoked and trained animals (increased corticosterone and hypothalamic pro-CRH and CRH-R1 mRNA levels); changes gradually diminished as the test progressed. In amygdala, pro-CRH mRNA levels decreased while those of BDNF augmented when stress was highest, in yoked and trained animals. Hippocampi, of both yoked and trained groups, had decreased levels of GR mRNA on days 1 and 3, normalizing by day 5, while those of pro-CRH and CRH-R1 increased after the 3rd day. Increased gene expression, specifically due to spatial learning, occurred only for hippocampal BDNF since day 3. These results show that the Morris water-maze paradigm induces a strong stress response that is gradually attenuated. Inhibition of CRH expression in amygdala suggests that the stress inflicted is of physical but not of psychological nature and could lead to reduced fear or anxiety.

Amygdala↗
PubMed2006

[Research of kingsbrain on improving the learning and memory ability of MCAO rats].

OBJECTIVE: To explore the influence of Kingsbrain (GETO) on the learning memory impairment of rats with cerebral ischemia. METHOD: Rats with cerebral ischemia were administered GETO orally once a day for one month. The ability of spatial-learning memory of rats was evaluated by Morris Water Maze (MWM). Duxil was used as a positive control. RESULT: the results of place navigation of MWM showed that at the 3rd time of swimming training, the escape latency of rats of the GETO group, Duxil group and Sham group were shorter than that of model group. The escape latency were (54.1 +/- 43.94), (55.9 +/- 43.49), (50.4 +/- 34.99) and (85.4 +/- 42.8) s, respectively; but there was no significantly difference. After the 6th time of swimming training, the escape latency of rats of the GETO group (37.8 +/- 38.69) s, the Duxil group (37.4 +/- 38.03) s and the sham group (26.9 +/- 21.63) s were significantly shorter than that of model rats (77.5 +/- 47.59) s, P < 0.05, respectively. Comparison of the swimming distance among groups were similar to the escape latency among groups. In the test of spatial probe, results of the ratio of the swimming time of platform quadrant (tP) vs the total swimming time (tT) and the ratio of the swimming distance of platform quadrant (dP) vs the total swimming distance (dT) indicated that the ratios of the GETO group (0.347 +/- 0.0662, 0.344 +/-0.055 1), the Duxil group (0.345 +/- 0.0984, 0.34 +/- 0.0934) and the sham group (0.35 +/- 0.0662, 0.349 +/- 0.0589) were significantly higher than those of the Model group (0.261 +/- 0.0689, 0.274 +/- 0.0544), P < 0.05, respectively. CONCLUSION: GETO can significantly improve the spatial learning and memory ability of rats with cerebral ischemia, which provides the pharmacodynamics evidence for its clinical application of improveing the learning and memory ability in poststroke patients.

Animals↗
PubMed1998

An essential role for retinoid receptors RARbeta and RXRgamma in long-term potentiation and depression.

Hippocampal long-term potentiation (LTP) and long-term depression (LTD) are the most widely studied forms of synaptic plasticity thought to underlie spatial learning and memory. We report here that RARbeta deficiency in mice virtually eliminates hippocampal CA1 LTP and LTD. It also results in substantial performance deficits in spatial learning and memory tasks. Surprisingly, RXRgamma null mice exhibit a distinct phenotype in which LTD is lost whereas LTP is normal. Thus, while retinoid receptors contribute to both LTP and LTD, they do so in different ways. These findings not only genetically uncouple LTP and LTD but also reveal a novel and unexpected role for vitamin A in higher cognitive functions.

Animals↗
PubMed2004

Effects of physical fatigue in mice on learning performance in a water maze.

We investigated the effects of physical fatigue produced by swimming exercise on learning the Morris water maze in BALB/c mice. We measured the escape latency in the maze immediately after the swimming exercise. The control group was soaked in the water but not fatigued. For easier tasks, like one with an obvious cue flag, the escape latency was not changed by exercise fatigue. However, escape latency was increased after exercise fatigue for more difficult tasks of spatial learning. These results appear to suggest that physical fatigue impaired learning performance. The effects of swimming exercise fatigue on learning efficiency were then investigated. Mice were continuously fatigued during the spatial learning period. This increased escape latency between the first and third sessions. The results suggest that learning efficiency was impaired by exercise fatigue. This system may be useful for screening new foods used to enhance brain function during exercise.

Animals↗
PubMed2004

Proof of the mysterious efficacy of ginseng: basic and clinical trials: effects of red ginseng on learning and memory deficits in an animal model of amnesia.

Ameliorating effects of red ginseng on learning and memory deficits due to hippocampal lesions and aging were reviewed; the performance of young rats with selective hippocampal lesions with or without red ginseng (p.o.), and aged rats with or without red ginseng (p.o.) in the spatial learning tasks was compared with that of sham-operated or intact young rats. Each rat was tested with 3 types of spatial learning tasks (distance movement task, DMT; random reward place search task, RRPST; and place learning task, PLT) in a circular open field using intracranial self-stimulation (ICSS) as reward. The results in the DMT and RRPST indicated that motivational and motor activity of young rats with hippocampal lesions with and without ginseng and aged rats with and without ginseng were not significantly different from that of control young rats. However, young rats with hippocampal lesions without ginseng and aged rats without ginseng displayed significant deficits in the PLT. Treatment with red ginseng significantly ameliorated place-navigation deficits in young rats with hippocampal lesions in the PLT. Similarly, red ginseng improved performance of aged rats in the PLT. The results, along with previous studies showing significant effects of red ginseng on the central nervous system, suggest that red ginseng ameliorates learning and memory deficits through effects on the central nervous system, partly through effects on the hippocampal formation. However, its mechanisms are still unclear, and further studies are required.

Aging↗
PubMed1998

Environmental enrichment results in higher levels of nerve growth factor mRNA in the rat visual cortex and hippocampus.

Evidence for structural modifications in the brain following environmental changes have been provided during the last decades. The most pronounced alterations following environmental manipulations have been found in the visual cortex. These plastic changes are supposed to reflect reorganization of neuronal connections involved in postnatal development and adult adjustments of connections involved in sensori-perceptual processing and learning. Potential candidates to mediate these changes are neurotrophins. Nerve growth factor (NGF) has been associated with cognitive functions and shown to improve the performance of aged rats in spatial learning and memory task. In the central nervous system, NGF is of importance for development and maintenance of cholinergic neurons and atrophy of cholinergic neurons is strongly correlated with learning and memory impairments. Exposure to enriched environmental conditions improves learning and problem-solving ability and results in plastic changes in the brain. This study examined the effect of environmental enrichment on expression of NGF mRNA in the rat visual cortex and hippocampus. Rats housed in groups in a stimulus-rich environment for 30 days had significantly higher levels of NGF mRNA than rats housed individually in single cages without stimulus-enrichment. We have recently presented results showing higher levels of neurotrophin-3 (NT-3) mRNA and improved spatial learning following environmental enrichment, and suggest that an interplay involving the neurotrophins NGF and NT-3 may be mediating experience-induced structural changes.

Animals↗
PubMed1998

Spatial Memory and Learning in Transgenic Mice: Fact or Artifact?

Spatial learning of transgenic mice is often assessed in the Morris watermaze, where mice must use distant cues to locate a submerged platform. Such learning is confounded by species-specific noncognitive swimming strategies. Factor analysis permits cognitive and noncognitive strategies to be disentangled and their association with electrophysiological phenomena to be investigated.

Journal Article↗
PubMed1996

Neural grafting of cholinergic neurons in the hippocampal formation.

The cholinergic septohippocampal system plays an important role in spatial learning and memory functions. Transections of the septohippocampal pathway have been shown to result in a near complete loss of cholinergic innervation in the hippocampus and induce severe spatial memory impairments. In this article, we have reviewed the studies which demonstrate the ability of intrahippocampal septal grafts to reinnervate the hippocampal formation and ameliorate spatial learning and memory deficits. Neuroanatomical studies suggest that grafts of cholinergic tissue can innervate the host hippocampal formation in a pattern that mimics that of the normal septohippocampal pathway. This innervation, in turn, is associated with the formation of graft-to-host synaptic connections. Neurochemical studies reveal that intrahippocampal grafts of septal cells can restore choline acetyltransferase activity, acetylcholine synthesis, and high affinity choline uptake in presynaptic terminals of grafted neurons. In addition, these grafts can normalize the upregulation of cholinergic muscarinic receptors seen postsynaptically in the hippocampus following lesions of the septohippocampal pathway. The functional nature of these grafts is also substantiated by electrophysiological recordings which demonstrate stimulus-evoked graft-to-host synaptic transmission as well as the reinstatement of EEG activity typical of septohippocampal connectivity. In addition to graft-to-host connections, behavioral and neurochemical studies also provide evidence for host-to-graft connections that can regulate the activity of grafted cholinergic neurons during the performance of specific behavioral tasks requiring spatial memory function. Together, these studies suggest that grafts of cholinergic neurons from the medial septal nucleus can become anatomically and functionally incorporated into the circuitry of the host hippocampal formation.

Animals↗
PubMed2004

Sleep deprivation impairs spatial memory and decreases extracellular signal-regulated kinase phosphorylation in the hippocampus.

Loss of sleep may result in memory impairment. However, little is known about the biochemical basis for memory deficits induced by sleep deprivation. Extracellular signal-regulated kinase (ERK) is involved in memory consolidation in different tasks. Phosphorylation of ERK is necessary for its activation and is an important step in mediating neuronal responses to synaptic activities. The aim of the present study was to determine the effects of total sleep deprivation (TSD) on memory and ERK phosphorylation in the brain. Rats were trained in Morris water maze to find a hidden platform (a spatial task) or a visible platform (a nonspatial task) after 6 h TSD or spontaneous sleep. TSD had no effect on spatial learning, but significantly impaired spatial memory tested 24 h after training. Nonspatial learning and memory were not impaired by TSD. Phospho-ERK levels in the hippocampus were significantly reduced after 6 h TSD compared to the controls and returned to the control levels after 2 h recovery sleep. Total ERK1 and ERK2 were slightly increased after 6 h TSD and returned to the control levels after 2 h recovery sleep. These alterations were not observed in the cortex after TSD. Protein phosphotase-1 and mitogen-activated protein kinase phosphatase-2, which dephosphorylates phospho-ERK, were also measured, but they were not altered by TSD. The impairments of both spatial memory and ERK phosphorylation indicate that the hippocampus is vulnerable to sleep loss. These results are consistent with the idea that decreased ERK activation in the hippocampus is involved in sleep deprivation-induced spatial memory impairment.

Animals↗
PubMed1994

A novel anticholinesterase THB013: biochemical and behavioural studies.

Clinical trials with tacrine (THA) have resulted in elevations of liver enzymes in Alzheimer patients that showed improvement. In an effort to minimize these side effects several THA analogues were synthesized. These analogues were compared to THA in biochemical as well as behavioural studies. In this study, the biochemical effects of THA and one of these analogs, THB 013, on plasma cholinesterase activity, cholinergic receptors as well as the effect of these drugs on spatial learning in adult rats were examined. THB 013 was, at lower concentration, more efficacious in inhibiting plasma cholinesterase as well as blocking the scopolamine induced disruption of spatial learning when administered 10 min before the scopolamine injection. It is possible that THB 013 with more potent cholinergic effects than THA might be useful in the treatment of Alzheimer's disease.

Alzheimer Disease↗
PubMedDate not supplied

Sleep deprivation selectively impairs memory consolidation for contextual fear conditioning.

Many behavioral and electrophysiological studies in animals and humans have suggested that sleep and circadian rhythms influence memory consolidation. In rodents, hippocampus-dependent memory may be particularly sensitive to sleep deprivation after training, as spatial memory in the Morris water maze is impaired by rapid eye movement sleep deprivation following training. Spatial learning in the Morris water maze, however, requires multiple training trials and performance, as measured by time to reach the hidden platform is influenced by not only spatial learning but also procedural learning. To determine if sleep is important for the consolidation of a single-trial, hippocampus-dependent task, we sleep deprived animals for 0-5 and 5-10 h after training for contextual and cued fear conditioning. We found that sleep deprivation from 0-5 h after training for this task impaired memory consolidation for contextual fear conditioning whereas sleep deprivation from 5-10 h after training had no effect. Sleep deprivation at either time point had no effect on cued fear conditioning, a hippocampus-independent task. Previous studies have determined that memory consolidation for fear conditioning is impaired when protein kinase A and protein synthesis inhibitors are administered at the same time as when sleep deprivation is effective, suggesting that sleep deprivation may act by modifying these molecular mechanisms of memory storage.

Analysis of Variance↗
PubMed2001

Clitoria ternatea (Linn) root extract treatment during growth spurt period enhances learning and memory in rats.

Neonatal rat pups (7 days old) were intubated with either 50 mg/kg body weight or 100 mg/kg body weight of aqueous root extract of Clitoria ternatea (CTR) for 30 days. These rats were then subjected to open field, two compartment passive avoidance and spatial learning (T-Maze) tests (i) immediately after the treatment and (ii) 30 days after the treatment, along with age matched normal and saline control rats. Results showed no change in open field behaviour, but showed improved retention and spatial learning performance at both time points of behavioural tests, indicating the memory enhancing property of CTR which implicates a permanent change in the brain of CTR treated rats.

Animals↗
PubMed2005

Galanin impairs performance on learning and memory tasks: findings from galanin transgenic and GAL-R1 knockout mice.

Galanin (GAL) impairs performance on cognitive tasks when administered centrally to rats. GAL transgenic (GAL-tg) mice overexpressing endogenous GAL show deficits on the probe trial of the Morris water maze spatial learning task, on the social transmission of food preference olfactory memory task, and on the trace cued fear conditioning emotional learning and memory task. Knockout mice deficient in the GAL-R1 receptor subtype were normal on most memory tasks, while showing a small deficit in trace cued fear conditioning, suggesting a selective role for the GAL-R1 in aversive memories, and implicating other GAL receptor subtypes in spatial learning and olfactory social memory. The growing body of rodent literature implicating excess GAL in cognitive impairment is relevant to the overexpression of GAL in the basal forebrain during the progression of Alzheimer's disease.

Animals↗
PubMed1994

The effects of general and restricted serotonergic lesions on hippocampal electrophysiology and behavior.

Depletion of the forebrain serotonergic system was found in previous studies to induce an increased excitability of the dentate gyrus (DG) granule cells and, when combined with a cholinergic deficiency, to impair spatial learning. We now compared the effects of general forebrain serotonergic lesions induced by intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT), to those of a more restricted injection of 5,7-DHT into fornix-fimbria and cingulum, to eliminate hippocampal serotonergic innervation. Control and lesioned rats were injected with atropine and tested in the spatial learning water-maze task. Following the behavioral tests, rats were anesthetized and the responsiveness of the DG to perforant path (PP) stimulation was measured. To assess the lesions functionally, responses to application of the serotonin releasing drug fenfluramine (FFA) were measured. Finally, the reduction, in the hippocampus, of serotonergic innervation was evaluated by [3H]imipramine binding. The effects of the lesions on the responsiveness to FFA confirmed that the ICV lesions were functionally more general than the FF lesions. [3H]Imipramine binding indicated that both lesions reduced the serotonergic innervation of the hippocampus significantly. Behaviorally, both lesioned groups were impaired in the water-maze. Electrophysiologically, in both DG excitability was higher than in controls and in both hyperexcitability was associated with an increase in feed-forward inhibition. The results suggest that the serotonergic innervation of the hippocampus proper is involved in cognitive functions associated with the hippocampus.

Action Potentials↗
PubMed1991

The histopathological, behavioral and neurochemical effects of intraventricular injection of ethylcholine mustard aziridinium (AF64A) in the neonatal rat.

This study investigated the histopathological, behavioral and neurochemical effects of bilateral injection of 2.0, 0.5 and 0.1 nmol/ventricle ethylcholine aziridinium (AF64A) on postnatal day (PND) 2. The rats showed a significant, but non-dose-related reduction of choline acetyltransferase (ChAT) in the hippocampus but not the cerebral cortex or the caudate nucleus when sacrificed on PND 16. No effect on ChAT was found in any region at PND 58. The group given 2 nmol/ventricle were hyperactive and showed a deficit in spatial learning when tested on the Morris water maze at PND 38-43. No such differences were observed for the rats injected with 0.1 or 0.5 nmol/ventricle AF64A. This spatial learning impairment in the 2 nmol group was associated with non-specific tissue damage seen only in animals from this group that were sacrificed at PND 40. This tissue damage was most evident in the left medial frontal cortex, the caudate nuclei and the anterior dorsal hippocampus.

Animals↗
PubMed1992

Loss of cholinergic neurons in the nucleus basalis induces neocortical electroencephalographic and passive avoidance deficits.

The present experiments were designed to examine the hypothesis that the degeneration of cholinergic nucleus basalis is related to the cognitive and neurophysiological deficits found in old age. Aged (26 months) rats were impaired both in the acquisition of spatial (water-maze) task and retention of passive avoidance task. During aging, neocortical electroencephalographic fast activity was decreased and high-voltage spindles increased. Loss of choline acetyltransferase-positive neurons correlated with the high-voltage spindle incidence and passive avoidance retention deficit. Unilateral ibotenate nucleus basalis lesioning decreased choline acetyltransferase activity in the cortex and produced a large nonspecific subcortical cell loss in young rats. Ibotenate-lesioned rats were impaired in spatial learning and passive avoidance retention in young rats. Quisqualic acid produced a greater decrease in cortical choline acetyltransferase activity and smaller nonspecific subcortical cell loss than ibotenate lesioning. Spatial learning was not impaired, but passive avoidance performance was disrupted. Slow waves and high-voltage spindles were increased and beta activity decreased on the side of either quisqualate or ibotenate nucleus basalis lesioning. These results demonstrate that age-related neurophysiological and cognitive deficits result partially from the loss of cholinergic neurons in the nucleus basalis and that quisqualic acid nucleus basalis-lesioning in young rats may be used as a pharmacological model of the age-related cholinergic neuron loss.

Acetylcholinesterase↗