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PubMed1991

Reversal of age-related increase in brain protein oxidation, decrease in enzyme activity, and loss in temporal and spatial memory by chronic administration of the spin-trapping compound N-tert-butyl-alpha-phenylnitrone.

Oxygen free radicals and oxidative events have been implicated as playing a role in bringing about the changes in cellular function that occur during aging. Brain readily undergoes oxidative damage, so it is important to determine if aging-induced changes in brain may be associated with oxidative events. Previously we demonstrated that brain damage caused by an ischemia/reperfusion insult involved oxidative events. In addition, pretreatment with the spin-trapping compound N-tert-butyl-alpha-phenylnitrone (PBN) diminished the increase in oxidized protein and the loss of glutamine synthetase (GS) activity that accompanied ischemia/reperfusion injury in brain. We report here that aged gerbils had a significantly higher level of oxidized protein as assessed by carbonyl residues and decreased GS and neutral protease activities as compared to young adult gerbils. We also found that chronic treatment with the spin-trapping compound PBN caused a decrease in the level of oxidized protein and an increase in both GS and neutral protease activity in aged Mongolian gerbil brain. In contrast to aged gerbils, PBN treatment of young adult gerbils had no significant effect on brain oxidized protein content or GS activity. Male gerbils, young adults (3 months of age) and retired breeders (15-18 months of age), were treated with PBN for 14 days with twice daily dosages of 32 mg/kg. If PBN administration was ceased after 2 weeks, the significantly decreased level of oxidized protein and increased GS and neutral protease activities in old gerbils changed in a monotonic fashion back to the levels observed in aged gerbils prior to PBN administration. We also report that old gerbils make more errors than young animals and that older gerbils treated with PBN made fewer errors in a radial arm maze test for temporal and spatial memory than the untreated aged controls. These data can be interpreted to indicate that oxidation of cellular proteins may be a critical determinant of brain function. Moreover, it also implies that there is an age-related increase in vulnerability of tissue to oxidation that can be modified by free radical trapping compounds.

Aging↗
PubMed1996

Distinctions between hippocampus of mouse and rat: protein F1/GAP-43 gene expression, promoter activity, and spatial memory.

We began these experiments as an attempt to replicate in the mouse the induction by kainate (KA) of F1/GAP-43 mRNA we observed in adult rat hippocampal granule cells [Mol. Brain Res., 33 (1995) 22-28]. However, even though KA induced behavioral seizures in the mouse similar to those in the rat, neither induction of F1/GAP-43 mRNA nor subsequent mossy fiber sprouting observed in the rat was detected in three different mouse strains. It was also surprising that the distribution of constitutive levels of F1/GAP-43 mRNA in mouse and rat hippocampus was qualitatively different. Indeed, F1/GAP-43 expression in CA3 pyramidal cells was significantly greater in rat than mouse, while F1/GAP-43 expression in CA1 cells of rat and mouse was equivalent using densitometric analysis. Thus, F1/GAP-43 expression in rat is quantitatively higher in CA3 and CA1 pyramidal cells. In mouse, expression was equivalent in these two subfields. In a transgenic mouse bearing a rat F1/GAP-43 promoter-reporter (lacZ) construct (line 252), in-vivo promoter activity of F1/GAP-43 was studied in hippocampal cells. Transgene expression in hippocampal pyramidal subfields, high in CA3, low in CA1 pyramidal cells, paralleled the distribution of rat F1/GAP-43 mRNA levels, not mouse. Differences in the constitutive F1/GAP-43 expression pattern in hippocampus between rat and mouse may therefore be determined by different recognition elements present on the F1/GAP-43 promoter. KA injected into the line 252 transgenic mouse did not activate the rat F1/GAP-43 promoter in mouse hippocampal granule cells. The absence of both F1/GAP-43 mRNA expression induction and promoter activation in mouse granule cells after KA is likely related to genera differences in transcriptional regulatory mechanisms, though post-transcriptional mechanisms cannot be excluded. Since the different hippocampal chemistry of F1/GAP-43 in rat and mouse likely extends to other molecular species, behaviors in rat and mouse that depend on hippocampal function might be different as well. We therefore evaluated spatial memory ability in a delayed matching-to-sample task. In contrast to rat, we were surprised to find no evidence of the ability to learn this task in three different mouse strains. Since interest in mouse genetics in relation to behavior and memory functions of hippocampus is growing, generalizations concerning hippocampal function from studies carried out on the mouse need to be made with caution considering the specific behavioral, pharmacological, and general molecular differences observed here. One can also be opportunistic and exploit the natural variations between these two genera to gain insight into the molecular mechanisms underlying information storage.

Animals↗
PubMed1999

Estrogen replacement enhances acquisition of a spatial memory task and reduces deficits associated with hippocampal muscarinic receptor inhibition.

A delayed matching-to-position (DMP) T-maze task was used to examine the effects of estrogen replacement on spatial learning and memory, as well as the ability of estrogen replacement to reduce performance deficits produced by acute systemic and intrahippocampal muscarinic cholinergic inhibition. Two experiments were performed. In Experiment 1, ovariectomized animals were trained to criterion on the DMP task and then tested with increased intertrial delays and following systemic scopolamine administration. The animals then received either continuous estrogen replacement or sham surgery and were retested beginning 10 days later. In Experiment 2, ovariectomized animals received guide cannulae implanted bilaterally into the hippocampus. Half of these animals also began receiving continuous estrogen replacement. Two months later, the animals were trained on the DMP task and then tested with increased intertrial delays and following systemic as well as intrahippocampal scopolamine administration. Animals received the same test battery 8 months later and were then immediately trained on a reversal task. The results indicate that estrogen-treated animals acquired the DMP task at a significantly faster rate than the ovariectomized, non-estrogen-treated controls. In addition, estrogen replacement significantly reduced deficits in DMP performance produced by intrahippocampal, but not systemic, scopolamine administration. This occurred when animals were tested after 3.5 months, as well as after 12 months, of continuous estrogen replacement. No evidence for an effect of estrogen replacement on spatial working memory or reversal learning was detected. These findings demonstrate that estrogen replacement can enhance acquisition of a spatial memory task and reduce performance deficits associated with hippocampal cholinergic impairment.

Analysis of Variance↗
PubMed1997

Spatial memory is related to hippocampal subcellular concentrations of calcium-dependent protein kinase C isoforms in young and aged rats.

Relationships were examined between spatial learning and hippocampal concentrations of the alpha, beta2, and gamma isoforms of protein kinase C (PKC), an enzyme implicated in neuronal plasticity and memory formation. Concentrations of PKC were determined for individual 6-month-old (n = 13) and 24-month-old (n = 27) male Long-Evans rats trained in the water maze on a standard place-learning task and a transfer task designed for rapid acquisition. The results showed significant relationships between spatial learning and the amount of PKC among individual subjects, and those relationships differed according to age, isoform, and subcellular fraction. Among 6-month-old rats, those with the best spatial memory were those with the highest concentrations of PKCgamma in the particulate fraction and of PKCbeta2 in the soluble fraction. Aged rats had increased hippocampal PKCgamma concentrations in both subcellular fractions in comparison with young rats, and memory impairment was correlated with higher PKCgamma concentrations in the soluble fraction. No age difference or correlations with behavior were found for concentrations of PKCgamma in a comparison structure, the neostriatum, or for PKCalpha in the hippocampus. Relationships between spatial learning and hippocampal concentrations of calcium-dependent PKC are isoform-specific. Moreover, age-related spatial memory impairment is associated with altered subcellular concentrations of PKCgamma and may be indicative of deficient signal transduction and neuronal plasticity in the hippocampal formation.

Aging↗
PubMed2000

Remote spatial memory in an amnesic person with extensive bilateral hippocampal lesions.

The hippocampus may have a time-limited role in memory, being needed only until information is permanently stored elsewhere, or this region may permanently represent long-term allocentric spatial information or cognitive maps in memory. To test these ideas, we investigated remote spatial memory in K.C., a patient with bilateral hippocampal lesions and amnesia for autobiographical events. In his spatial knowledge, general aspects were preserved, but details were lost, a pattern that resembled his memory loss in other domains. K.C. performed normally on allocentric spatial tests of his neighborhood and the world. He had difficulty, however, in recognizing and identifying non-salient neighborhood landmarks, and in recognizing city locations on world maps. This suggests that the hippocampus is not crucial for maintenance and retrieval of remotely formed spatial representations of major landmarks, routes, distances and directions, but is necessary for specifying location details, regardless of when they were acquired.

Amnesia↗
PubMed1994

Reversal of spatial memory impairments in aged rats by nerve growth factor and neurotrophins 3 and 4/5 but not by brain-derived neurotrophic factor.

Aged rats, displaying impairments in spatial learning and memory associated with marked cellular atrophy of forebrain cholinergic neurons, received intracerebroventricular infusions of one of the four neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), or a combination of NGF and BDNF, or vehicle. During the 4-week infusion period rats receiving NGF, NT-3, or NT-4/5 showed improved acquisition and retention of spatial memory. With NGF and NT-3, but not NT-4/5, this was accompanied by a significant reduction in cholinergic neuron atrophy in septum, nucleus basalis, and striatum. BDNF, in contrast, was without effect either alone or in combination with NGF. These results show that memory deficits associated with aging can be reversed by several members of the neurotrophin family and that this effect may be mediated through activation of multiple neurotrophin receptors associated with cholinergic and possibly noncholinergic systems in the brain.

Aging↗
PubMedDate not supplied

Features of participation of spatial memory in choice reactions of white rats.

A study was made of the behavior of rats preliminarily trained to return to the same reinforcement site when that site was changed periodically. It was determined that after finding the new reinforcement site, the rats are able to optimize their behavior to correspond to the new location. Optimization of behavior consisted in shifting the direction of the course toward the new location of reinforcement and (or) in selective shifts before the blinds to correspond to the locations of obtaining reinforcement in the experiment. The increased role of the working memory and of the apparatus of probable prediction in selection is proposed as the basis for optimization of behavior.

Animals↗
PubMed2000

Glutamatergic influences on the nucleus paragigantocellularis: contribution to performance in avoidance and spatial memory tasks.

Stimulation of the locus coeruleus (LC) and the subsequent release of norepinephrine contribute to memory consolidation processes. Excitatory input to the LC is derived primarily from neurons in the nucleus paragigantocellularis (PGi). The authors examined the effects of activating the pathway between PGi and the LC on memory. Rats received vehicle or the excitatory amino acid glutamate (25, 50, or 100 nmol/0.5 microl) into PGi after training in an inhibitory avoidance (IA) or delayed matching-to-sample (DMS) task. Rats given the 100-nmol dose had significantly longer retention latencies on a 48-hr IA retention test. Rats treated with the 50- or 100-nmol dose made significantly more correct responses than controls on an 18-hr DMS retention test. Results suggest that encoding and storage of memory for emotional and spatial events may be enhanced by activation of neuronal circuits afferent to the LC.

Afferent Pathways↗
PubMed2000

Fos imaging reveals differential patterns of hippocampal and parahippocampal subfield activation in rats in response to different spatial memory tests.

We compared neuronal activation, as measured by Fos staining, during different spatial tasks in two experiments. The counts of Fos-stained neurons in the hippocampus increased as the spatial demands of the tasks increased, the tasks having been carefully matched for other factors. In Experiment 1, matched groups of rats either ran a standard eight-arm radial maze task or were trained to run up and down just one arm of the maze; the number of runs and rewards was identical in both conditions. In Experiment 2, rats were trained on the eight-arm maze but in different rooms. On the critical test day, both groups were run in the same room so that one group now performed with novel landmarks. All hippocampal subfields (dentate gyrus, CA3, CA1, dorsal, ventral, and caudal subiculum) showed a relative increases in c-fos activation in the eight-arm (Experiment 1) and novel room (Experiment 2) conditions, the sole exception being the ventral subiculum in Experiment 2. Although increased c-fos activation was found in both dorsal and ventral hippocampus, in Experiment 2 the relative increase was significantly greater in the dorsal hippocampus. Parahippocampal cortices responded heterogeneously: the perirhinal cortex failed to show increased activation in both experiments, in contrast to the entorhinal and postrhinal cortices. Subsequent comparisons confirmed that the perirhinal and postrhinal cortices responded in qualitatively different ways, the perirhinal cortex differing from the rest of the hippocampal formation. These experiments, which provide the first analysis of hippocampal Fos production during tests of allocentric spatial working memory, reveal that all components of the hippocampus are activated, but that under certain conditions the dorsal hippocampus is disproportionately involved.

Animals↗
PubMed1997

Spatial memory in transgenic mice with impaired glucocorticoid receptor function.

Spatial learning and memory function of transgenic mice with impaired glucocorticoid receptor function was assessed in the Morris water maze and the radial arm maze. Transgenic mice took longer to find a submerged and a visual platform in the water maze task than did mice from the parent strain (B6C/3F1), although performance was improved in the visible platform condition relative to the submerged platform task. In the radial arm maze, transgenic mice made significantly more errors than B6C/3F1 mice. In both tasks, the behavioural strategies adopted by transgenic mice were non-optimal for correct performance. It is suggested that the impaired performance displayed by transgenic mice in both tests is largely attributable to these altered behavioural strategies.

Animals↗
PubMed1989

Effects of fornix transection and cingulate cortical ablation on spatial memory in rhesus monkeys.

This study, together with a parallel study in rats (Markowska et al. 1988), attempted to relate the effects of hippocampal-system damage on similar tasks in both rats and monkeys. Not only were monkeys given a task (Experiment 1) which was of the sort usually used with rats, but in the companion study rats were given tasks (Experiment 2) like those usually used with monkeys. Experiment 1 examined the performance of rhesus monkeys with hippocampal-system damage on a spatial working memory task. Monkeys were trained preoperatively on delayed nonmatching-to-sample in a T-maze, placed into groups matched for their preoperative learning scores, and then received one of three treatments: 1) transection of the fornix; 2) ablation of the cingulate cortex; or 3) a sham operation. Monkeys with fornix transection were severely and significantly impaired, but monkeys with cingulate cortical ablations were not significantly impaired, relative to the controls. The results demonstrate that monkeys with fornix transection are severely impaired on a spatial working memory task requiring locomotion and, taken together with earlier work, suggest that the effect of fornix transection in both rodents and nonhuman primates is at least qualitatively similar (see Markowska et al. 1988). Experiment 2 assessed the role of the fornix and cingulate cortex in three conditional tasks in which the monkeys were provided with various spatial cues to indicate which one of two objects was rewarded. Both experimental groups were unimpaired, relative to the control group, on all three tasks, indicating that fornix transection does not produce a general impairment in place learning.

Animals↗
PubMed2002

Spatial memory dissociations in mice lacking GluR1.

Gene-targeted mice lacking the AMPA receptor subunit GluR1 (GluR-A) have deficits in hippocampal CA3-CA1 long-term potentiation. We now report that they showed normal spatial reference learning and memory, both on the hidden platform watermaze task and on an appetitively motivated Y-maze task. In contrast, they showed a specific spatial working memory impairment during tests of non-matching to place on both the Y-maze and an elevated T-maze. In addition, successful watermaze and Y-maze reference memory performance depended on hippocampal function in both wild-type and mutant mice; bilateral hippocampal lesions profoundly impaired performance on both tasks, to a similar extent in both groups. These results suggest that different forms of hippocampus-dependent spatial memory involve different aspects of neural processing within the hippocampus.

Animals↗
PubMed1999

In mice tonic estrogen replacement therapy improves non-spatial and spatial memory in a water maze task.

We investigated the effects of estrogen replacement therapy on water maze non-spatial and spatial navigation in mice. Three groups of mice were ovariectomized and two of these groups being implanted with s.c. pellets that produce blood levels of estrogen close to those found in estrous (estrogen low, 75-100 pg/ml blood) or proestrous (estrogen high, 300-400 pg/ml). The behavioral assessment was initiated 7 days after pellet implantation. Non-spatial navigation to a clearly visible platform was stimulated by low and high levels of estrogen. However, spatial navigation to a hidden platform was improved by low estrogen levels. We found that estrogen improves two different types of memory processes that depend on striatal (non-spatial navigation) and hippocampal (spatial) memory systems.

Animals↗
PubMed2000

Chronic [D-Ala2]-growth hormone-releasing hormone administration attenuates age-related deficits in spatial memory.

The age-related decline in growth hormone is one of the most robust endocrine markers of biological aging and has been hypothesized to contribute to the physiological deficits observed in aged animals. However, there have been few studies of the impact of this hormonal decline on brain aging. In this study, the effect of long-term subcutaneous administration of [D-Ala2]-growth hormone-releasing hormone (GHRH) on one measure of brain function, memory, was investigated. Animals were injected daily with 2.3 microg of [D-Ala2]-GHRH or saline from 9 to 30 months of age, and the spatial learning and reference memory of animals were assessed by using the Morris water maze and compared with those of 6-month-old animals. Results indicated that spatial memory decreased with age and that chronic [D-Ala2]-GHRH prevented this age-related decrement (24% improvement in the annulus-40 time and 23% improvement in the number of platform crossings compared with saline treated, age-matched controls; p < .05 each). No changes were noted in sensorimotor performance. [D-Ala2]-GHRH attenuated the age-related decline in plasma concentrations of insulinlike growth factor-1 (IGF-1) (p <.05). These data suggest that growth hormone and IGF-1 have important effects on brain function, that the decline in growth hormone and IGF-1 with age contributes to impairments in reference memory, and that these changes can be reversed by the chronic administration of GHRH.

Aging↗
PubMed1999

Sex dimorphisms in the rate of age-related decline in spatial memory: relevance to alterations in the estrous cycle.

The present experiments demonstrate the existence of sex differences in the rate of development and the magnitude of age-dependent impairments in cognitive and sensorimotor abilities. Although no sex differences were found in spatial reference memory at a young age, the mnemonic ability of female rats deteriorated more rapidly than that of male rats. A major drop in reference memory of the females occurred at the age of 12 months, whereas in the males the onset of impairments occurred later, at the age of 18 months. In spatial working memory, on the other hand, the magnitude of decline was greater in females than in males, although the onset of these impairments occurred at the age of 24 months in both sexes. A sexual dimorphism-aging interaction also was observed in sensorimotor performance. Up to the age of 18 months the females outperformed the males. Subsequently, by the age of 24 months, the performance of the females declined to a level similar to that of the males. The deficits observed in reference and working memory seem to be cognitive in origin and not attributable to alterations in sensory and motor abilities. In addition, the earlier onset of reference memory impairments in females generally coincides with the onset of alterations in the estrous cycle, suggesting that a decline in the estrogenic milieu of the females could be a factor in accelerating the rate of age-related cognitive impairments in the female rat.

Aging↗
PubMed1998

Aging of glutamate receptors: correlations between binding and spatial memory performance in mice.

C57B1/6 mice aged 3, 10, and 26 months were tested for spatial learning in the Morris water maze. Ten and 26 month old mice were ad libitum-fed or diet restricted (60% of ad libitum-fed calories). Diet restriction significantly improved memory performance among the 10 and 26 month olds. In age/diet group comparisons, aged ad libitum-fed mice had significantly higher average proximity scores, indicating poorer performance, in probe trials for place learning than the 3 month olds and diet restricted 10 month olds. Diet restricted 26 month olds did not differ significantly from 3 month olds or any other groups in probe trial measures. The group means for average proximity scores were significantly correlated with binding densities for the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors in the frontal cortex and CA1 region of the hippocampus. Alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) binding correlated with group proximity scores in frontal and parietal cortices and within the CA1 and CA3 regions of the hippocampus. Kainate and metabotropic binding sites showed no significant correlations with behavior. These results suggest that there is a sparing of spatial memory with diet restriction in aging C57B1/6 mice and that the effects of aging on NMDA and AMPA receptors may be associated with age-related declines in spatial learning.

Aging↗
PubMed2002

Role of the anterodorsal and anteroventral nuclei of the thalamus in spatial memory in the rat.

This study tests the hypothesis that the anterior thalamic nuclei play a significant role in spatial learning and memory. Adult, male Sprague-Dawley rats with bilateral ibotenic acid lesions of the anterior thalamus were tested for 5 days in a repeated acquisition water maze task. Compared with Controls, rats with nearly complete lesions of both anterodorsal (AD) and anteroventral (AV) thalamic nuclei (AD/AV) were only mildly impaired in their spatial learning and memory. Larger lesions that extended into the anteromedial (AM) thalamic nucleus (AD/AV+) caused a more severe impairment and complete lesions of all three anterior nuclei (AD/AV/AM) resulted in even greater impairment that extended to all aspects of the task. In probe trials, only the Control animals had a preference for the correct quadrant. Approximately one-half of the rats were tested for a second week to determine if the impaired groups would benefit from further training. AD/AV/AM rats showed little improvement, but the other groups all improved significantly in all aspects of the task except the probe trial. Together, these data indicate that the anterior thalamic nuclei contribute to spatial learning and memory, but neither AV nor AD independently plays a dominant role.

Animals↗
PubMed1996

Effect of intraventricular injections of dihydro-beta-erythroidine (DH beta E) on spatial memory in the rat.

The analysis of the behavioral effect of the nicotinic acetylcholine receptor (nAChR) antagonists has been generally based on drugs which act at the associated ion channel. In contrast dihydro-beta-erythroidine (DH beta E) is a competitive antagonist at the nAChR. Using rats, DH beta E was injected intraventricularly prior to training in two spatial tests, the Morris Water Maze and a Win-Stay radial maze. In addition DH beta E 300 nmol was used to reverse the effect of (-)-nicotine on locomotor activity. In the Morris Water Maze DH beta E (300 nmol) disrupted memory of the platform location as measured by crosses of the area in a probe trial. At 300 nmol DH beta E showed no sensorimotor effects in a visible platform test. In the Win-Stay task there was a significant, dose dependent disruption of spatial memory. A dissociation of nicotine's effects on locomotor activity was observed, in that DH beta E 300 nmol was able to significantly attenuate (-)-nicotine enhancement of horizontal motor activity, but did not affect the initial reduction of vertical activity. Nicotinic processing of memory appears to be involved in these tests of spatial memory.

Animals↗