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PubMed2005

Cellular mechanisms underlying the effects of an early experience on cognitive abilities and affective states.

In the present study we investigated the effects of neonatal handling, an animal model of early experience, on spatial learning and memory, on hippocampal glucocorticoid (GR), mineralocorticoid (MR) and type 1A serotonin (5-HT1A) receptors, as well as brain derived neurotrophic factor (BDNF), and on circulating leptin levels, of male rats. METHOD: Spatial learning and memory following an acute restraint stress (30 min) were assessed in the Morris water maze. Hippocampal GR, MR and BDNF levels were determined immunocytochemically. 5-HT1A receptors were quantified by in vitro binding autoradiography. Circulating leptin levels, following a chronic forced swimming stress, were measured by radioimmunoassay (RIA). Data were statistically analyzed by analysis of variance (ANOVA). RESULTS: Neonatal handling increased the ability of male rats for spatial learning and memory. It also resulted in increased GR/MR ratio, BDNF and 5-HT1A receptor levels in the hippocampus. Furthermore, leptin levels, body weight and food consumption during chronic forced swimming stress were reduced as a result of handling. CONCLUSION: Neonatal handling is shown to have a beneficial effect in the males, improving their cognitive abilities. This effect on behavior could be mediated by the handling-induced increase in hippocampal GR/MR ratio and BDNF levels. The handling-induced changes in BDNF and 5-HT1A receptors could underlie the previously documented effect of handling in preventing "depression". Furthermore, handling is shown to prevent other maladaptive states such as stress-induced hyperphagia, obesity and resistance to leptin.

Journal Article↗
PubMed2002

Water maze performance, exploratory activity, inhibitory avoidance and hippocampal plasticity in aged superior and inferior learners.

In 28- to 30-month-old rats, in vitro short-term and long-term potentiation (STP and LTP) were measured in area CA1 of the hippocampus in seven superior and seven inferior learners, that were selected from a pool of 40 rats based on water maze escape performance over a period of 9 days. The aim was to examine whether levels of STP and LTP could account for group differences in learning of water maze escape, spatial preference and wall (thigmotaxis)-avoidance and in short-term retention of an inhibitory avoidance task. There was no significant group difference in open-field exploration, i.e. the number of rearings. In contrast to expectation, the superior and inferior learners did not differ significantly from each other in levels of STP and LTP. However, variability in escape and spatial learning, but not thigmotaxis-avoidance learning, was significantly predicted by variability in STP and LTP in the superior group. Also, open-field exploratory rearings were significantly correlated with STP and LTP as well as with maze escape learning in the superior group. The results show that, in the aged superior group, levels of CA1 STP and LTP coincided with residual water maze escape and spatial preference learning as well as open-field exploration, i.e. behavioural expressions known to be related to hippocampal functioning, but not with learning to avoid thigmotaxis in the maze. The lack of such correlations in the inferior group may be due to the severe impairment in escape and spatial preference learning and/or the influence of yet unknown third variables on these relationships.

Action Potentials↗
PubMed2006

Differential susceptibility following beta-amyloid peptide-(1-40) administration in C57BL/6 and Swiss albino mice: Evidence for a dissociation between cognitive deficits and the glutathione system response.

Considerable evidence supports the role of oxidative stress in the pathogenesis of Alzheimer's disease (AD). Previous studies suggest that the central nervous system (CNS) administration of beta-amyloid peptide, the major constituent of senile plaque in AD, induces oxidative stress in rodents which may contribute to the learning and memory deficits verified in the beta-amyloid model of AD. In the present study, we compared the effects of a single intracerebroventricular (i.c.v.) injection of aggregated beta-amyloid peptide-(1-40) (Abeta(1-40)) (400pmol/mouse) on spatial learning and memory performance, synaptic density and the glutathione (GSH)-dependent antioxidant status in adult male C57BL/6 and Swiss albino mice. Seven days after Abeta(1-40) administration, C57BL/6 and Swiss mice presented similar spatial learning and memory impairments, as evaluated in the water maze task, although these impairments were not found in Abeta(40-1)-treated mice. Moreover, a similar decline of synaptophysin levels was observed in the hippocampus (HC) and prefrontal cortex (PFC) of both Swiss and C57BL/6 mice treated with Abeta(1-40), which suggests synaptic loss. C57BL/6 mice presented lower levels of glutathione-related antioxidant defences (total glutathione (GSH-t) levels, glutathione peroxidase (GPx) and glutathione reductase (GR) activity) in the HC and PFC in comparison to Swiss mice. Despite the reduced basal GSH-dependent antioxidant defences observed in C57BL/6 mice, Abeta(1-40) administration induced significant alterations in the brain antioxidant parameters only in Swiss mice, decreasing GSH-t levels and increasing GPx and GR activity in the HC and PFC 24h after treatment. These results indicate strain differences in the susceptibility to Abeta(1-40)-induced changes in the GSH-dependent antioxidant defences in mice, which should be taken into account in further studies using the Abeta model of AD in mice. In addition, the present findings suggest that the spatial learning and memory deficits induced by beta-amyloid peptides in rodents may not be entirely related to glutathione-dependent antioxidant response.

Amyloid beta-Peptides↗
PubMed2004

What is learned in spatial contextual cuing--configuration or individual locations?

With the use of spatial contextual cuing, we tested whether subjects learned to associate target locations with overall configurations of distractors or with individual locations of distractors. In Experiment 1, subjects were trained on 36 visual search displays that contained 36 sets of distractor locations and 18 target locations. Each target location was paired with two sets of distractor locations on separate trials. After training, the subjects showed perfect transfer to recombined displays, which were created by combining half of one trained distractor set with half of another trained distractor set. This result suggests that individual distractor locations were sufficient to cue the target location. In Experiment 2, the subjects showed good transfer from trained displays to rescaled, displaced, and perceptually regrouped displays, suggesting that the relative locations among items were also learned. Thus, both individual target-distractor associations and configural associations are learned in contextual cuing.

Adolescent↗
PubMed1990

S-emopamil ameliorates ischemic brain damage in rats: histological and behavioural approaches.

Transient ischemia induced by 4 vessel occlusion (4VO) in rats is known to produce neuronal damage to particular brain structures such as the CA1 sector of the hippocampus. Behavioural changes associated with ischemic lesioning of this brain region are an impairment in spatial learning of rats tested in a water maze (14). In the present study, it was investigated whether pretreatment with S-emopamil, a Ca2(+)-channel blocker as well as a 5-HT2 antagonist, prevents the occurrence of hippocampal cell damage and/or spatial learning impairments in rats subjected to 4VO. Neuronal lesioning in the hippocampus was significantly reduced following pretreatment with S-emopamil in 4VO rats. In addition, S-emopamil treated animals showed an improved spatial learning ability compared to saline treated 4VO rats. It is suggested that S-emopamil may exert a protective effect under ischemic conditions. The possible mechanisms involved are discussed.

Animals↗
PubMedDate not supplied

Deficits in water escape performance and alterations in hippocampal cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice.

Mice treated neonatally with monosodium glutamate (MSG) were found to have learning and memory deficits in performing a non-spatial water escape task. Scopolamine impaired the water-escape performance of the control mice but not that of the MSG-treated mice. It was suggested that the water-escape performance deficit in the MSG-treated mice was a result of impaired central cholinergic mechanisms. As such, scopolamine was unable to further incapacitate an already impaired cholinergic system. This is strongly supported by the decreased affinity of the sodium-dependent high-affinity choline uptake observed in the hippocampus. D-Cycloserine, a partial agonist at the glycine site of the NMDA receptor, did not affect the water-escape performance of the MSG-treated and control mice; nor did it alter the effects of scopolamine. This lack of effect of D-Cycloserine may imply that the NMDA receptors are not involved in non-spatial learning, in contrast to their reported involvement in spatial learning.

Animals↗
PubMed2002

Theta-frequency synaptic potentiation in CA1 in vitro distinguishes cognitively impaired from unimpaired aged Fischer 344 rats.

Hippocampal-dependent learning and memory deficits have been well documented in aging rodents. The results of several recent studies have suggested that these deficits arise from weakened synaptic plasticity within the hippocampus. In the present study, we examined the relationship between hippocampal long-term potentiation (LTP) in vitro and spatial learning in aged (24-26 months) Fischer 344 rats. We found that LTP induced in the CA1 region using theta-frequency stimulation (5 Hz) is selectively impaired in slices from a subpopulation of aged rats that had shown poor spatial learning in the Morris water maze. LTP at 5 Hz in aged rats that did not show learning deficits was similar to that seen in young (4-6 months) controls. We also found that 5 Hz LTP amplitude strongly correlated with individual learning performance among aged rats. The difference in 5 Hz LTP magnitude among aged rats was not attributable to an altered response to 5 Hz stimulation or to differences in the NMDA receptor-mediated field EPSP. In addition, no performance-related differences in LTP were seen when LTP was induced with 30 or 70 Hz stimulation protocols. Finally, both 5 Hz LTP and spatial learning in learning-impaired rats were enhanced with the selective muscarinic M2 antagonist BIBN-99 (5,11-dihydro-8-chloro-11-[[4-[3-[(2,2-dimethyl-1-oxopentyl)ethylamino]propyl]-1-piperidinyl]acetyl]-6H-pyrido[2,3-b][1,4]benzodiazepin-6-one). These findings reinforce the idea that distinct types of hippocampal LTP offer mechanistic insight into age-associated cognitive decline.

Age Factors↗
PubMed1995

The antioxidant LY 231617 ameliorates functional and morphological sequelae induced by global ischemia in rats.

In this study the effect of LY 231617, an antioxidant, on spatial learning deficit and on neuronal damage following transient cerebral ischemia was evaluated. Global ischemia was induced by four-vessel-occlusion (4VO) for 20 min in rats. LY 231617 (20 mg/kg i.p.) was administered after onset of reperfusion. One week after surgery spatial learning was tested in the Morris water maze. LY 231617 reduced the increase in escape latency and in swim distance induced by 4VO. Neuronal damage in the CAI sector of the hippocampus produced by 4VO was significantly attenuated by LY 231617. The present data demonstrate that posttreatment with LY 231617 exerts a protective effect on hippocampal neuronal damage and deficits in spatial learning induced by 4VO.

Animals↗
PubMed2006

Muscarinic receptor-mediated GTP-Eu binding in the hippocampus and prefrontal cortex is correlated with spatial memory impairment in aged rats.

The present study examined muscarinic receptor/G-protein coupling in the hippocampus and the prefrontal cortex of young and aged Long-Evans rats characterized for spatial learning ability in the Morris water maze. In a highly sensitive time-resolved fluorometry GTP-Eu binding assay, muscarinic-mediated GTP-Eu binding was severely blunted in hippocampus (-32%) and prefrontal cortex (-34%) as a consequence of aging. Furthermore, the magnitude of decreased muscarinic-mediated GTP-Eu binding was significantly correlated with the severity of spatial learning impairment in hippocampus and prefrontal cortex of aged rats and was specifically decreased in the subset of aged rats that were spatial learning impaired when compared to the aged unimpaired and the young rats. Western blot data indicated a preservation of the membrane-bound M1 receptor and the Galphaq/11 protein in both brain regions. These data demonstrate that muscarinic signaling is severely impaired as a consequence of normal aging in a manner that is closely associated with age-related cognitive decline.

Age Factors↗
PubMed1996

Memantine reduces functional and morphological consequences induced by global ischemia in rats.

In this study the effect of memantine, an antagonist at the N-methyl-D-aspartate receptor, on spatial learning deficit and on neuronal damage following transient cerebral ischemia was evaluated. Global ischemia was induced by four-vessel-occlusion (4VO) for 20 min in rats. Memantine was administered 20 min before induction of ischemia at a dose of 10 or 20 mg/kg. One week after surgery spatial learning was tested in the Morris water maze. Treatment with the higher dose of memantine reduced the increase in escape latency and in swim distance induced by 4VO. Neuronal damage in the CA1 sector of the hippocampus and in the striatum produced by 4VO was significantly attenuated by 20 mg/kg memantine. Treatment with the lower dose of memantine had no influence on the deficit in spatial learning and the neuronal damage resulting from ischemia. The present data demonstrate that treatment with a neuroprotective agent like memantine can reduce functional as well as morphological sequelae induced by ischemia.

Animals↗
PubMed2005

Behavioral changes in metallothionein-null mice after the cessation of long-term, low-level exposure to mercury vapor.

The neurobehavioral changes in wild-type and metallothionein (MT)-null mice after the cessation of long-term, low-level exposure to Hg0 were investigated. MT-null and wild-type females were continuously (24 h/day) exposed to mercury vapor (Hg0) at 0.055 mg/m3 (range: 0.043-0.073 mg/m3), which was similar to the current threshold limit value (TLV), for 29 weeks. The effects on behavior, such as locomotor activity in the open field (OPF), learning ability in the passive avoidance response (PA) and spatial learning ability in the Morris water maze (MM) were examined immediately and 12 weeks after the cessation of exposure. Immediately after the exposure had ceased, total locomotor activity in OPF was decreased in the both strain of mice, although the MT-null mice appeared to show more distinct effect. In the PA test, the exposed animals of both strains showed learning impairment as compared to un-exposed mice. Twelve weeks after the cessation of exposure, the locomotor activity in OPF was elevated in the exposed mice of both strains, while the learning ability in the PA test appeared normal in both strains. Spatial learning ability was not affected at all. Immediately after the exposure had ceased, the brain mercury concentration of the exposed wild-type mice was 1.75 microg/g, twofold of that in the MT-null mice. In 12 weeks, brain mercury levels decreased to approximately 1/20 of those in immediately after the exposure in both of the strains. These results for the first time indicated that long-term, low-level exposure to Hg0 could exert neurobehavioral effects, which were not reversible even after a long exposure-free period. Whereas the effects on learning ability were presumably transient, the effects on spontaneous behavior as evaluated in OPF were persistent. Finally, the MT-null mice seemed more susceptible to Hg0-induced neurotoxicity than the wild-type mice, confirming our previous results.

Animals↗
PubMed2003

A heparin derived oligosaccharide normalizes the fear response of old Brown Norway rats.

Old animals exhibit impaired spatial learning and an exaggerated response to stress. It was predicted that the heparin derived oligosaccharide (HDO), C3, would reverse these age-related deficits. Young (4-5 months) and old (19-20 months) Brown Norway male rats ingested C3 (25 mg/kg per day, p.o.) or vehicle (drinking water) daily for 42-44 days. Two weeks after the initiation of drug treatment, the rats were examined using a series of behavioral tests. The old control rats evidenced: (1) increased neophobia and reduced exploratory behavior in a novel open field (OF); and (2) exaggerated freezing during the acquisition and retention of a conditioned response (CR) to a Pavlovian light-shock pairing ("foreground" conditioning). C3 treatment attenuated or reversed this age-related impairment of emotional behavior. Analysis of spatial learning using the Morris water maze (MWM), and of CR formation to the place in which the foreground conditioning was conducted ("background" conditioning) during context dependent fear conditioning (CDFC) did not reveal major age or drug effects on memory processes. It is hypothesized that C3 repairs damage to the extracellular matrix (ECM) that occurs during the aging process and thereby normalizes age-related exacerbated fear behaviors without affecting mnestic processes.

Aging↗
PubMed2006

Hippocampal synaptic plasticity and water maze learning in cocaine self-administered rats.

Previously, we have shown that long-term potentiation (LTP) in hippocampus of Lewis rats was significantly modulated by cocaine self-administration. Using a single train of high-frequency stimulation of 100 Hz for 1s (HFS), we found an enhancement of LTP after cocaine self-administration that was maintained even during the extinction of this behavior. However, the effects of cocaine self-administration on a hippocampal-dependent spatial learning task were unknown. Therefore, in the present study our first objective was to analyze if cocaine self-administration might affect the performance in a hippocampus-dependent task, such as the Morris water maze test. Male adult Lewis (LEW) rats self-administered cocaine (1 mg/kg/injection) or saline (0.9% NaCl) for 3 weeks. Three hours after finishing the last self-administration session, animals were submitted to Morris water maze training for 3 consecutives days. A memory test was carried out 24 h after the last training session. No significant differences were found in escape latencies and time spent in the quadrant where the platform was located during training. Given that we did not find any cocaine effect on this spatial learning task, our second objective was to estimate indirectly if brain cocaine levels have failed to modulate LTP in animals that were performing the water maze trials. To this end, we tested if cocaine application to hippocampal slices of naïve subjects was able to evoke LTP. The results indicated that cocaine produced an enhanced LTP in these hippocampal slices. Taking together, the results of the present study suggest that hippocampal LTP-like processes generated after cocaine self-administration are not related to spatial learning hippocampal-dependent tasks, such as the water maze test.

Animals↗
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↗
PubMed1997

Effect of ischemic cerebral volume changes on behavior.

Ischemia causes long-term effects on brain volume and neurologic function but the relationship between the two is poorly characterized. We studied the relationships between brain volume and three measures of rodent behavior after cerebral ischemia was induced by injecting several thousand microspheres into the internal carotid arteries of rats. Forty eight hours later, each subject was rated using a global neurologic rating scale. Several weeks later, the subjects were tested for open field activity and visual spatial learning. Post-mortem we measured the volume of the cerebral hemispheres and estimated the volume densities of cortex, white matter, hippocampus, basal ganglia, thalamus, ventricle, and visible infarction. Ischemia caused significant impairment, as measured by the global rating scale; the probability of an abnormal rating was correlated with the number of microspheres trapped in the brains. Visual spatial learning was significantly impaired by ischemia, but this deficit was independent of the count of microspheres, whether the subject was abnormal at 48 h, and whether the left or right hemisphere was embolized. Cerebral hemisphere volume was reduced from 430 mm3 to 376 mm3 (P < 0.05). The cortex was reduced from 22 to 19% of cerebrum (P < 0.05) and the white matter compartment was reduced to similar degree. The lesion volume was 6% of cerebrum, comparable to that seen with other ischemia methods. The global outcome rating was significantly related to total cerebral volume, but not to volume changes in any single compartment. On the other hand, visual spatial learning was significantly influenced by volume changes in the cortex and white matter, but not by the topography of the visible infarctions. Open field activity was not altered by infarction. Our data suggests that the total volume of brain tissue lost to infarction may partially determine global neurological rating independently of the topography of the volume loss. Integrative functions such as learning may depend more on the integrity of specific compartments and less on the total volume of intact brain. The volume of visible cystic infarction was not related to long term behavioral outcome. These results should be confirmed using another method of inducing ischemia.

Animals↗
PubMed1997

Dissociation of spatial reference memory, spatial working memory, and hippocampal mossy fiber distribution in two rat strains differing in emotionality.

Rats of the inbred strains DA/Han and BDE/Han were compared on two complex spatial learning tasks, a spatial reference memory task in a 16-unit multiple T-maze and a spatial working memory task in an eight-arm radial-maze. In addition, sizes of hippocampal mossy fiber terminal fields were measured. BDE rats showed marked superiority in multiple T-maze learning whereas DA rats outperformed BDE rats on the radial-maze task. DA rats had significantly larger intra- and infrapyramidal mossy fiber terminal fields (IIP-MF). This is consistent with findings from other studies suggesting that large IIP-MF are related to excellent spatial radial-maze learning, but it also indicates that size of IIP-MF is correlated with processing of a specific type of spatial information rather than with overall spatial abilities. BDE rats had more extended suprapyramidal mossy fiber projections (SP-MF) and a larger hilus. Rats of both strains differed in exploratory behaviour and emotionality: DA rats revealed little freezing and had a high rearing activity, whereas BDE rats showed frequent freezing and reared rarely. Results suggest that IIP-MF are involved with flexible expression of memory, updating environmental information and parallel processing whereas SP-MF might be linked to processing of familiar information. Presumably, emotional factors contribute to performance differences.

Animals↗
PubMedDate not supplied

Plasma and brain methamphetamine concentrations in neonatal rats.

D-Methamphetamine (D-MA) treatment during the neonatal period has been shown to induce acoustic startle hyperreactivity and Morris maze spatial learning deficits, but not to significantly affect Cincinnati maze sequential learning. In order to characterize the internal dose in these experiments, MA was measured in plasma and brain of neonatal rats at one of two ages, and using one of three dose schedules, two of which were selected to be representative of those used in previously published neurobehavioral studies. Plasma parameters showed few age and dose-frequency effects; however, brain concentrations showed more consistent age-dependent effects. Brain area under the concentration (AUC) values were consistently higher, regardless of dosing schedule, in offspring treated on postnatal day (P) 1 compared to those treated on P11. Previous results with the multiple-dose schedules have shown that Morris maze spatial learning deficits only occur in those exposed beginning on P11, whereas acoustic startle hyperreactivity is associated with exposure beginning on either P1 or P11. The pharmacokinetic parameters did not predict the long-term spatial learning and memory effects of neonatal MA administration, nor are they well correlated to the acoustic startle effects. The plasma concentrations obtained in rats are within the range for human MA abusers based on extrapolations from human low-dose values to those expected for heavy users.

Animals↗
PubMed2005

[Long-term effects of delayed hyperbaric oxygen therapy on hypoxic-ischemic brain injury in neonatal rats].

OBJECTIVE: To evaluate the long-term effects of delayed hyperbaric oxygen (HBO) therapy on neonatal rats with hypoxic-ischemic brain injury (HIBD). METHOD: Postnatal 7 days newborn rats (n = 52) were randomly set to three groups: control (n = 18, sham operation), HIBD (n = 17), or HBO (n = 17). Pups in the HBO group were subjected to hyperbaric oxygen treatment with 2 atmosphaera absolutus, 5 x 30 min at a 24 h intervals since 48-72 h after the HIBD model. All the animals were tested for the spatial learning and memory ability in the Morris water maze from postnatal days 37 to 41. At day-42, rats were decapitated and the brains were analyzed for morphological and histological changes, including brain shapes and weights, survival neurons, percentage of AchE positive area and NOS positive neurons in hippocampal CA1 region. RESULTS: Rats in HBO and HIBD groups displayed significant morphological and histological damages, as well as severe spatial learning and memory disability. The average escape latency of Morris water maze in HBO group [(56 +/- 23) s] and HIBD group [(56 +/- 22) s] were longer than the control [(23 +/- 16) s] (P < 0.05). The swimming time in HBO group [(30 +/- 5) s] and HIBD group [(29 +/- 6) s] were shorter than the control [(51 +/- 5) s] (P < 0.05). The swimming length in HBO group [(572 +/- 92) cm] and HIBD group [(548 +/- 92) cm] were shorter than the control [(989 +/- 101) cm] (P < 0.05). The weight of left brains in HBO group [(598 +/- 46) mg] and HIBD group [(601 +/- 59) mg] were lighter than the control [(984 +/- 18) mg] (P < 0.05). The survival neurons of hippocamal CA1 region in HBO group [(97 +/- 27)/mm] and HIBD group [(100 +/- 27)/mm] were less than the control [(183 +/- 8)/mm] (P < 0.05). The percentage of AchE-positive fibers in HBO group [(18.4 +/- 2.2)%] and HIBD group [(18.5 +/- 2.2)%] were less than the control [(27.5 +/- 2.2)%,] (P < 0.05). NOS-positive neurons in HBO group [(21 +/- 5)/mm(2)] and HIBD group [(19 +/- 4)/mm(2)] were also less than the control [(34 +/- 6)/mm(2)] (P < 0.05). CONCLUSION: Delayed HBO therapy resulted in no protection against either HIBD-induced brain morphological and histological deficits or spatial learning and memory disability.

Acetylcholinesterase↗