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PubMed1995

The effects of frontal- or temporal-lobe lesions on susceptibility to interference in spatial memory.

Patients with unilateral frontal- or temporal-lobe lesions and normal control subjects studied multiple arrays of pictures and were tested for recall of the locations of the pictures. One condition consisted of three trials of the same pictures in different spatial arrangements, recall being tested immediately after each presentation. In a second condition (using different stimuli), the subject was given two trials with one set of pictures, but a new set of pictures was viewed on the third trial. All groups showed a build-up of proactive interference across trials using the same pictures, and a release of proactive interference when they studied new pictures. Patients with frontal-lobe lesions were more susceptible to proactive interference than were the other groups.

Adolescent↗
PubMed2002

Spatial memory and choice behavior in the radial arm maze after fornix transection.

In the radial arm maze task, it is well established that performance of rats with hippocampal damage is severely impaired on the place version, which relies heavily, if not exclusively, on spatial information. However, very little is known about the effects of hippocampal damage on actual choice behavior. To address this issue, sham-operated (SH) and fornix-transected (FX) rats were trained and tested on the place task in the eight-arm radial maze. The following measures were recorded: the frequency of re-entry errors, the number of choices separating repeated visits to the same arm, the latency to arm re-entry, the distribution and targets of microchoices defined as orientations toward an arm or entries in the proximal portion of an arm [Brown, M.F., 1992. Does a cognitive map guide choices in the radial arm maze? J. Exp. Psychol., Anim. Behav. Processes 18, 56-66]. These measures were used as indexes of performance, within-trial retroactive intrusion, memory trace decay and choice behavior, respectively. As generally observed in the literature, the frequency of errors was higher in rats of the FX group than in rats of the SH group; the impairment persisted even after the training criterion was reached. The analysis of latency to arm re-entry and of the number of choices separating re-entries suggested that this impairment was the result of faster memory decay rather than retroactive interference. Both FX and SH groups exhibited a systematic pattern of microchoices, but the frequency of microchoices was higher in FX lesioned rats than in SH controls. Moreover, in lesioned animals, relatively fewer of the initial microchoices were directed toward the baited arms during training-to-criterion. Some of the results provide support to the working memory theory [Olton, D.S., Becker, J.T., Handelmann, G.E., 1979. Hippocampus, space, and memory. Behav. Brain Sci. 2, 313-365], whereas others look more consistent with the cognitive map view [O'Keefe, J., Nadel, L., 1978. The Hippocampus as a Cognitive Map. Clarendon Press, Oxford]. The discussion suggests that both theories and a distinction between prospective and retrospective memory may be required to account for the function of the hippocampal formation in memory.

Animals↗
PubMed2004

Increase of the RNA-binding protein HuD and posttranscriptional up-regulation of the GAP-43 gene during spatial memory.

Neuronal ELAV-like proteins (HuB, HuC, and HuD) are highly conserved RNA-binding proteins able to selectively associate with the 3' UTR of a subset of target mRNAs and increase their cytoplasmic stability and rate of translation. We previously demonstrated the involvement of these proteins in learning, reporting that they undergo a sustained up-regulation in the hippocampus of mice trained in a spatial discrimination task. Here, we extend this finding, showing that a similar up-regulation occurs in the hippocampus of rats trained in another spatial learning paradigm, the Morris water maze. HuD, a strictly neuron-specific ELAV-like protein, is shown to increase after learning, with a preferential binding to the cytoskeletal fraction. HuD up-regulation is associated with an enhancement of GAP-43 mRNA and protein levels, with an apparently increased HuD colocalization with the GAP-43 mRNA and an increased association of neuronal ELAV-like proteins with the GAP-43 mRNA. These learning-dependent biochemical events appear to be spatiotemporally controlled, because they do not occur in another brain region involved in learning, the retrosplenial cortex, and at the level of protein expression they show extinction 1 month after training despite memory retention. By contrast, HuD mRNA levels still remain increased after 1 month in the CA1 region. This persistence may have implications for long-term memory recall.

Animals↗
PubMed2006

Effect of chronic angiotensin converting enzyme inhibition on spatial memory and anxiety-like behaviours in rats.

Angiotensin converting enzyme inhibitors (ACEis) are widely used anti-hypertensive agents that are also reported to have positive effects on mood and cognition. The present study examined the influence of the ACEi, perindopril, on cognitive performance and anxiety measures in rats. Two groups of rats were treated orally for one week with the ACEi, perindopril, at doses of 0.1 and 1.0mg/kg/day. Learning was assessed by the reference memory task in the water maze, comparing treated to control rats. Over five training days both perindopril-treated groups learnt the location of the submerged platform in the water maze task significantly faster than control rats. A 60s probe trial on day 6 showed that the 1.0mg/kg/day group spent significantly longer time in the training quadrant than control rats. This improved performance in the swim maze task was not due to the effect of perindopril on motor activity or the anxiety levels of the rats as perindopril-treated and control animals behaved similarly in activity boxes and on the elevated+maze. These results confirm the anecdotal human studies that ACEis have a positive influence on cognition and provide possibilities for ACEis to be developed into therapies for memory loss.

Administration, Oral↗
PubMedDate not supplied

Temporally graded, age-related impairments in spatial memory in the rat.

We report here on the analysis of data from 6-, 12-, and 24-month-old Long-Evans rats tested in the Morris water maze. The animals were given 18 trials over a 5-day period with the platform submerged (spatial condition); 3 trials on the first day, 4 trials on each of the subsequent 3 days, followed by 3 trials on the fifth day. On the sixth day, the animals were given five trials in which the platform was elevated above the water level (cued condition). Over the 18 trials in the spatial condition, the 24-month-old animals took significantly longer to find the platform than did the 6-month-old animals; the performance of the 12-month-day animals lay between the older and younger groups. We then analyzed the latency data depending on the position of the trial in that day of testing: The first trial of each day followed the preceding trial by 20-22 hours, whereas the last trial of each day followed the preceding trial by only 20 minutes. The performance of the 12-month-old animals on the first trial of the second, third, and fourth days of testing was indistinguishable from that of the 24-month-old animals. Whereas, the performance of the 12-month-old animals on the last trial of the second, third, and fourth days of testing was indistinguishable from that of the 6-month-old animals. An analysis of the distance data (distance covered before locating the platform) revealed the same pattern of results.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed2003

Detailed behavioral analysis reveals both task strategies and spatial memory impairments in rats given bilateral middle cerebral artery stroke.

Middle cerebral artery occlusion (MCAO) impairs performance in the water maze task by rats. The purpose was to evaluate the effect of bilateral MCAO in naive and strategies-pretrained rats using a detailed behavioral analysis to further develop a water maze model of stroke. Rats were trained in either a simple swim-to-visible platform task or in a conventional spatial version with a hidden platform in the pool. In the visible platform task naive stroked rats were impaired because of a marked tendency to swim thigmotaxically on most trials. For the spatial learning experiment, some rats received Morris' water maze strategies pretraining prior to MCAO and subsequent spatial training to familiarize them with the general behavioral strategies required in the task. In the spatial learning task naive stroked rats had both strategies and spatial learning impairments but pretrained stroked rats were indistinguishable from sham controls on all behavioral measures. All stroked rats had comparable bilateral brain damage measured using a computerized volumetric measuring technique. These results indicate that in naive rats bilateral MCAO causes behavioral strategies impairments in the visible and hidden platform versions of the water maze as well as specific spatial learning impairments in the hidden platform version. The results also indicate that behavioral strategies pretraining allows stroked rats to acquire and remember sufficient strategies skills and spatial information to perform as well as sham controls during subsequent spatial training. These techniques appear to be capable of quantifying the effects of potentially protective treatments for stroke.

Adaptation, Psychological↗
PubMed1998

D1 receptor modulation of hippocampal-prefrontal cortical circuits integrating spatial memory with executive functions in the rat.

Dopamine (DA) within the prefrontal cortex (PFC) plays an important role in modulating the short-term retention of information during working memory tasks. In contrast, little is known about the role of DA in modulating other executive aspects of working memory such as the use of short-term memory to guide action. The present study examined the effects of D1 and D2 receptor blockade in the PFC on foraging by rats on a radial arm maze under two task conditions: (1) a delayed task in which spatial information acquired during a training phase was used 30 min later to guide prospective responses, and (2) a nondelayed task that was identical to the test phase of the delayed task but lacked a training phase, thereby depriving rats of previous information about the location of food on the maze. In experiment 1, microinjections of the D1 antagonist SCH-23390 (0.05, 0.5, or 5 microg/&microl), but not the D2 antagonist sulpiride (0.05, 0.5, or 5 microg/microl), into the prelimbic region of the PFC before the test phase disrupted performance of the delayed task without affecting response latencies. In contrast, neither drug affected performance of the nondelayed task. In the present study, we also investigated the role of D1 receptors in modulating activity in hippocampal-PFC circuits during delayed responding. Unilateral injections of SCH-23390 into the PFC in the hemisphere contralateral to a microinjection of lidocaine into the hippocampus severely disrupted performance of the delayed task. Thus, the ability to use previously acquired spatial information to guide responding 30 min later on a radial arm maze requires D1 receptor activation in the PFC and D1 receptor modulation of hippocampal inputs to the PFC. These data suggest that D1 receptors in the PFC are involved in working memory processes other than just the short-term active retention of information and also provide direct evidence for DA modulation of limbic-PFC circuits during behavior.

Animals↗
PubMed2007

Aged SOD overexpressing mice exhibit enhanced spatial memory while lacking hippocampal neurogenesis.

The recent finding that hippocampal slices from aged mice overexpressing the gene for superoxide dismutase (SOD) exhibit long-term potentiation (LTP) of reactivity to afferent stimulation that is significantly larger than that produced in aged wild-type (wt) mice has encouraged the exploration of the effects of reactive oxygen species (ROS) on learning in aged mice. In addition, young-adult and aged wt and SOD transgenic mice were used in an attempt to correlate adult neurogenesis with spatial learning. Aged wt and SOD mice exhibited a 90% reduction in doublecortin-labeled new dentate gyrus neurons as compared to young mice, with no significant difference between genotypes. In addition, aged SOD mice exhibited better performance than wt controls in both reference and working memory tasks in a water maze. These findings provide a behavioral measure to demonstrate that excessive production of H2O2 is beneficial in aged mice.

Aging↗
PubMed2005

Heterozygous mice with Ric-8 mutation exhibit impaired spatial memory and decreased anxiety.

Ric-8 is a guanine nucleotide exchange factor for a subset of Galpha proteins and it is required to maintain Galpha(q) and the Galpha(s) pathways in functional state. In adult mice Ric-8 is expressed in regions involved in the regulation of behavior (neocortex, cingulate cortex and hippocampus). As Ric-8 is shown to regulate neuronal transmitter release, the aim of present study was to perform behavioral analysis of ric-8 mutant. Homozygous (-/-) ric-8 mutant mice are not viable and die in early embryonic development, therefore for behavioral analysis heterozygous (+/-) ric-8 mutant mice were used. We found decreased anxiety of ric-8 heterozygous mice in light-dark compartment test where mutant mice significantly avoided the light compartment. In spatial learning paradigm (Morris water maze) the performance of ric-8 (+/-) mice was impaired. Namely, in the reversal test, ric-8 (+/-) mice exhibited significant delay to find the hidden platform compared to wild-type (wt) littermates. We did not find differences in the behavioral tests reflecting the motor abilities of mice (motor activity, rota-rod). Therefore, described alterations seem to be specific for anxiety and spatial learning. Based on these results we can conclude the importance of ric-8 in the regulation of memory and emotional behavior.

Animals↗
PubMed2004

BetaCCM enhances retrieval of serial contextual but not of serial spatial memory in mice.

The effects of inverse agonists of the gamma-aminobutyric acid (GABA)/benzodiazepine receptors such as beta-carboline-3-carboxylate (betaCCM) on retrieval processes have not been studied extensively. This study investigates the effects in mice of an acute betaCCM injection on retrieval of previously acquired serial discriminations, involving distinct contextual cues (Contextual Serial Discrimination, CSD) or identical cues (Serial Spatial Discrimination, SSD) in a four-hole board. Animals submitted to CSD were also evaluated for emotional reactivity in an elevated-plus maze. In both the CSD and the SSD tasks, mice were injected with saline before the learning session began. Twenty-four hours later, mice were replaced on the hole-board following a single dose of saline or betaCCM (0.5 mg/kg or 1.5 mg/kg) injected 20 min before testing. The highest dose of betaCCM improved performance of the first discrimination in the contextual task but not in the spatial task. Moreover, the higher dose of betaCCM produced anxiety-like reactivity in an elevated-plus maze, and scores of 'anxiety' were positively correlated with memory scores. Overall, the data show that the betaCCM enhancement of memory processes depends on: (1) the cues associated with the to-be-remembered information; and (2) the emotional effects of the drug.

Animals↗
PubMed1998

Unilateral hippocampal lesions in newborn and adult rats: effects on spatial memory and BDNF gene expression.

Subcortical damage at birth often produces more severe deficits than similar lesions in an adult. In the present study, effects of unilateral electrolytic hippocampal ablations made on postnatal day 1 or in 3-month-old adult rats, were compared. Exploratory behavior and spatial navigation in the Morris water maze (MWM) were assessed 8 and 20 weeks after hippocampal damage. Rats with neonatal damage did not respond to novelty in the environment and did not learn to find the hidden platform in the MWM. Rats lesioned as adults did learn the water maze task, but slower than controls. We hypothesized that behavioral deficits observed in rats lesioned at birth, may be due, in part, to neurochemical dysfunction of the contralateral hippocampus. Specifically, cholinergic and GABAergic neurotransmission were assessed by measuring choline-acetyltransferase (ChAT) and GABAdecarboxylase (GAD) activity. In addition, nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) mRNA levels were assayed in the remaining (contralateral) hippocampus. Of these molecules, only BDNF gene expression was significantly reduced (by 30%) at 8 and 20 weeks after neonatal and adult unilateral ablation. The similar reduction in BDNF mRNA in both treatment groups does not correspond with the lesion's differential effect on memory function. However, the more severe learning impairment after neonatal lesion may reflect increased dependence on trophins during development.

Aging↗
PubMed1992

Prenatal irradiation and spatial memory in mice: investigation of critical period.

Pregnant CD1 mice were exposed on various gestational or postnatal days to 1 Gy of 250 kV X-rays. Ten adult, male offspring from each exposure condition were tested in a radial arm maze. Compared to sham-exposed control mice, acquisition of spatial information was unimpaired in animals exposed on gestational days 13 or 15, or on postnatal day 10, but animals exposed on gestational day 18 or postnatal day 1 showed sustained deficits in acquisition. These results appear consistent with the known time-course for the proliferation and migration of the dentate granule cells of the hippocampus in the mouse, and are discussed in relation to the dependence on hippocampal integrity of the acquisition and use of spatial information. The results suggest that comparable deficits in mental function might be expected in humans similarly exposed to ionizing radiation during periods of proliferation and migration of the dentate granule cells.

Animals↗
PubMed2000

[Nphe(1)]-Nociceptin (1-13)-NH(2), a nociceptin receptor antagonist, reverses nociceptin-induced spatial memory impairments in the Morris water maze task in rats.

1. The present study was undertaken to investigate the effects of the novel nociceptin receptor antagonist, [Nphe(1)]-Nociceptin (1-13)-NH(2) (bilateral intrahippocampal injection, 50 nmole rat(-1)) on purported nociceptin-induced (bilateral intrahippocampal injection, 5 nmole rat(-1)) deficits in spatial learning in the rat Morris water maze task. In addition, experiments were performed in an 'open field' to investigate possible peptide-induced changes in exploratory behaviour. 2. Nociceptin significantly impaired the ability of the animal to locate the hidden platform throughout training (P<0.001 versus control group). 3. Pretreatment with [Nphe(1)]-Nociceptin (1-13)-NH(2) significantly blocked nociceptin-induced impairment of spatial learning (P<0.001 versus nociceptin group). 4. A probe trial revealed that vehicle-treated animals spent more time in the quadrant that had previously contained the hidden platform, whereas nociceptin-treated animals did not spend more time in any one quadrant. 5. Learning impairments were not attributable to non-specific deficits in motor performance or change in exploratory behaviour. 6. Taken together, our results reveal that [Nphe(1)]-Nociceptin (1-13)-NH(2) represents an effective and useful in vivo antagonist at the nociceptin receptors involved in learning and memory.

Animals↗
PubMed2004

NMDA receptors and voltage-dependent calcium channels mediate different aspects of acquisition and retention of a spatial memory task.

Activity dependent calcium entry into neurons can initiate a form of synaptic plasticity called long-term potentiation (LTP). This phenomenon is considered by many to be one possible cellular mechanism underlying learning and memory. The calcium entry that induces this phenomenon can occur when N-methyl-D-aspartate receptors (NMDARs) and/or voltage-dependent calcium channels (VDCCs) are activated. While much is known about synaptic plasticity and the mechanisms that are triggered by activation of these two Ca(2+) channels, it is unclear what roles they play in learning. To better understand the role activation of these channels may play in learning we systemically administered pharmacological antagonists to block NMDARs, VDCCs, or both during training trials and retention tests in a radial arm maze task. Wistar rats injected with the NMDAR antagonist MK-801 (0.1mg/kg) were impaired in the acquisition of this task. In contrast, rats injected with verapamil (10mg/kg), an antagonist to VDCCs, acquired the task at the same rate as control animals, but were impaired on a 10-day retention test. A group of animals injected with both antagonists were unable to learn the task. The results suggest that each of the calcium channels and the processes they trigger are involved in a different stage of memory formation or expression.

Animals↗
PubMed1998

Effects of lesions of thalamic intralaminar and midline nuclei and internal medullary lamina on spatial memory and object discrimination.

Male Sprague-Dawley rats received either radiofrequency lesions of the lateral internal medullary lamina (IML) or ibotenic acid lesions of the lateral intralaminar nuclei (ILN) and midline nuclei (MLN) or sham treatment. Neither lesion group was impaired in the retention of 3 object pair discriminations acquired before surgery nor in the acquisition of a new object pair after surgery. Rats with ILN, but not IML, lesions were impaired in acquiring an initial and 5 subsequent hidden platform locations in a water maze task. These results suggest that damage to both ILN and MLN are needed to produce spatial learning deficits and that extensive damage to the IML or ILN has no detectable effects on retrograde or anterograde memory of object discriminations.

Animals↗
PubMed1999

Spatial memory improvement by levodopa in parkinsonian MPTP-treated monkeys.

RATIONALE: The ameliorative effects of levodopa (L-3,4-dihydroxy-phenylalanine) on the motor impairment in Parkinson's disease patients is well established, but characterization of its effects on the associated cognitive deficits is still incomplete. OBJECTIVE: The present study determined the effect of different doses of levodopa on performance on a test of working memory in MPTP-treated rhesus monkeys, an animal model of Parkinson's disease. METHODS: Four MPTP-treated monkeys and their age-matched controls with the same experimental history as the MPTP-treated monkeys were tested on a spatial delay response task. Each daily session consisted of five trials at each of seven randomly presented delays (0, 10, 20, 30, 40, 50 and 60 s). Training was continued for 5 days in each of five different conditions. In the first condition, control and MPTP-treated animals performed the task without levodopa. In the second condition, both groups were tested with a dose of 100 mg of levodopa. In the third and fourth conditions, in which the doses of levodopa were increased to 250 and 500 mg, respectively, only the MPTP-treated animals were tested. In the final condition, the MPTP-treated animals where retested without levodopa. RESULTS: Significant improvement was observed at all doses tested (range 100-500 mg). CONCLUSIONS: Levodopa can ameliorate memory impairments in this parkinsonian model.

Animals↗
PubMed2003

Severe hypoglycemia and long-term spatial memory in children with type 1 diabetes mellitus: a retrospective study.

Performance on long delays of delayed response tasks is associated with medial temporal function, a region of the brain affected by severe hypoglycemia. A previous study showed that children with type 1 diabetes mellitus (T1DM) with higher risk for severe hypoglycemia performed worse than controls on long delays of a spatial delayed response (SDR) task. We tested the more specific hypothesis that frequency of severe hypoglycemia would relate to long delay SDR performance. Children with T1DM (n = 51) and controls (n = 32) performed the SDR task with short and long delays. Information was collected on children's past severe hypoglycemia. In children with T1DM, number of past severe hypoglycemic episodes accounted for a significant portion of the variance in long delay SDR after controlling for age and age of onset. This relationship was not seen with short delay SDR or with other tasks (verbal or object memory, attention, motor speed). These results support the hypothesis that severe hypoglycemia has specific, negative effects on memory skills in children. If this relationship is extrapolated to children with higher frequency of severe hypoglycemia, due to longer duration of disease or poorer glucose control, it may affect daily functioning and thus need to be considered in treatment decisions.

Adolescent↗