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PubMed1977

Spatial memory.

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Action Potentials↗
PubMed2006

Inhibition of fatty-acid amide hydrolase accelerates acquisition and extinction rates in a spatial memory task.

Recent reports have demonstrated that disruption of CB(1) receptor signaling impairs extinction of learned responses in conditioned fear and Morris water maze paradigms. Here, we test the hypothesis that elevating brain levels of the endogenous cannabinoid anandamide through either genetic deletion or pharmacological inhibition of its primary catabolic enzyme fatty-acid amide hydrolase (FAAH) will potentiate extinction in a fixed platform water maze task. FAAH (-/-) mice and mice treated with the FAAH inhibitor OL-135, did not display any memory impairment or motor disruption, but did exhibit a significant increase in the rate of extinction. Unexpectedly, FAAH-compromised mice also exhibited a significant increase in acquisition rate. The CB(1) receptor antagonist SR141716 (rimonabant) when given alone had no effects on acquisition, but disrupted extinction. Additionally, SR141716 blocked the effects of OL-135 on both acquisition and extinction. Collectively, these results indicate that endogenous anandamide plays a facilitatory role in extinction through a CB(1) receptor mechanism of action. In contrast, the primary psychoactive constituent of marijuana, Delta(9)-tetrahydrocannabinol, failed to affect extinction rates, suggesting that FAAH is a more effective target than a direct acting CB(1) receptor agonist in facilitating extinction. More generally, these findings suggest that FAAH inhibition represents a promising pharmacological approach to treat psychopathologies hallmarked by an inability to extinguish maladaptive behaviors, such as post-traumatic stress syndrome and obsessive-compulsive disorder.

Amidohydrolases↗
PubMed1996

Long-term functional recovery from age-induced spatial memory impairments by nerve growth factor gene transfer to the rat basal forebrain.

Nerve growth factor (NGF) stimulates functional recovery from cognitive impairments associated with aging, either when administered as a purified protein or by means of gene transfer to the basal forebrain. Because gene transfer procedures need to be tested in long-term experimental paradigms to assess their in vivo efficiency, we have used ex vivo experimental gene therapy to provide local delivery of NGF to the aged rat brain over a period of 2.5 months by transplanting immortalized central nervous system-derived neural stem cells genetically engineered to secrete NGF. By grafting them at two independent locations in the basal forebrain, medial septum and nucleus basalis magnocellularis, we show that functional recovery as assessed in the Morris water maze can be achieved by neurotrophic stimulation of any of these cholinergic cell groups. Moreover, the cholinergic neurons in the grafted regions showed a hypertrophic response resulting in a reversal of the age-associated atrophy seen in the learning-impaired aged control rats. Long-term expression of the transgene lead to an increased NGF tissue content (as determined by NGF-ELISA) in the transplanted regions up to at least 10 weeks after grafting. We conclude that the gene transfer procedure used here is efficient to provide the brain with a long-lasting local supply of exogenous NGF, induces long-term functional recovery of cognitive functions, and that independent trophic stimulation of the medial septum or nucleus basalis magnocellularis has similar consequences at the behavioral level.

Aging↗
PubMed1999

One-year study of spatial memory performance, brain morphology, and cholinergic markers after moderate controlled cortical impact in rats.

Persistent cognitive deficits are one of the most important sequelae of head injury in humans. In an effort to model some of the structural and neuropharmacological changes that occur in chronic postinjury brains, we examined the longitudinal effects of moderate vertical controlled cortical impact (CCI) on place learning and memory using the Morris water maze (MWM) test, morphology, and vesicular acetylcholine (ACh) transporter (VAChT) and muscarinic receptor subtype 2 (M2) immunohistochemistry. Vertical CCI (left parietal cortex, 4 m/sec, 2.5 mm; n = 10) or craniotomy (sham) was produced in male Sprague-Dawley rats (n = 10). Place learning was tested at 2 weeks, 4 weeks, 3 months, 6 months, and 12 months postinjury with the escape platform in a different maze quadrant for each time point. At each interval, rats received 5 days of water maze acquisition (latency to find hidden platform), a probe trial to measure place memory, and 2 days of visible platform trials to control for nonspecific deficits. At 3 weeks, half the animals were sacrificed for histology. At these injury parameters, CCI produced no significant differences in place learning between injured and sham rats at 2 weeks, 4 weeks, or 6 months after injury. However, at 3 and 12 months, the injured rats took significantly longer to find the hidden platform than the sham rats. Probe trial performance differed only at 12 months postinjury between injured (25.73+/-2.1%, standard error of the mean) and sham rats (44.09+/-7.0%, p < 0.05). The maze deficits at 1 year were not due to a worsening of performance, but may have resulted from a reduced ability of injured rats to benefit from previous water maze experience. Hemispheric loss of 30.4+/-5.5 mm3 was seen at 3 weeks after injury (versus respective sham). However, hemispheric loss almost doubled by 1 year after injury (51.5+/-8.5 mm3, p < 0.05 versus all other groups). Progressive tissue loss was also reflected by a three- to fourfold increase in ipsilateral ventricular volume between 3 weeks and 1 year after injury. At 1 year after injury, immunostaining for VAChT was dramatically increased in all sectors of the hippocampus and cortex after injury. Muscarinic receptor subtype 2 (M2) immunoreactivity was dramatically decreased in the ipsilateral hippocampus. This suggests a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission. Moderate CCI in rats produces subtle MWM performance deficits accompanied by persistent alteration in M2 and VAChT immunohistochemistry and progressive tissue atrophy. The inability of injured rats to benefit from repeated exposures to the MWM may represent a deficit in procedural memory that is independent of changes in hippocampal cholinergic systems.

Analysis of Variance↗
PubMed1986

Adult age differences in spatial memory: effects of distinctiveness and repeated experience.

Young (mean age = 25.0) and elderly (mean age = 65.0) women's memory for buildings in a large model town was assessed. Participants viewed and constructed the town on two trials. Building distinctiveness was manipulated by showing differentiated buildings with unique physical and functional properties (e.g., school, gas station), or nondifferentiated buildings that were not functionally distinct and only somewhat physically distinct (e.g., red cube-like structure with curved roof, yellow cube-like structure with flat roof). Building distinctiveness was further manipulated by verbally labeling or not labeling each building type. On Trial 1 young adults were more accurate than elderly adults only on the differentiated buildings; on Trial 2 this age difference was evident on differentiated and nondifferentiated buildings. Verbal labeling did not significantly affect construction accuracy. It was concluded that age differences occurred because elderly adults have more difficulty utilizing encoding strategies than young adults.

Adult↗
PubMed1994

Impaired spatial memory in aged rats is associated with alterations in inositol phospholipid metabolism.

WE have investigated changes in inositol phospholipid turnover and membrane arachidonic acid concentration in the dentate gyrus and frontal cortex of animals aged 3-6 months, 14 months or 22 months which were trained in the Morris water maze. Ageing was associated with poorer performances in the behavioural test, characterized by increased variability in retention and acquisition amongst individuals, a decrease in membrane arachidonic acid concentration and increased unstimulated inositol phospholipid metabolism in synaptosomes prepared from frontal cortex and dentate gyrus. Arachidonic acid stimulated inositol phospholipid metabolism in synaptosomes, but in the older groups, stimulation was associated with good performance in the Morris water maze. In slices prepared from frontal cortex, responsiveness of inositol phospholipid metabolism to glutamate was also age- and performance-dependent. The findings highlight a correlation between age, inositol phospholipid metabolism and performance in the Morris water maze.

Aging↗
PubMed1997

Perinatal choline supplementation increases the threshold for chunking in spatial memory.

Chunking and perinatal choline supplementation each provide rats with alternative memory processing advantages. Evidence from radial-arm maze performance of adult (2- to 5-month-old) rats indicates that chunking of multiple food types (sunflower seeds, Noyes pellets and rice puffs) emerges for stable, differentiable baiting patterns as a function of the memory load (6, 12, 18 or 24 maze arms). The number of maze arms appeared to determine both the level of task difficulty at which rats began to implement a chunking strategy as well as when they were unable to successfully implement such a strategy due to the excess memorial demands of the task. In comparison to control rats, rats treated perinatally with choline supplementation displayed a horizontal rightward shift of the response function that related level of clustering of like-food types to the number of maze arms. These results indicate a higher threshold for implementing a chunking strategy in rats treated perinatally with choline supplementation, possibly due to a choline-induced increase in memory capacity.

Animals↗
PubMedDate not supplied

A cell-permeable phospholipase Cgamma1-binding peptide transduces neurons and impairs long-term spatial memory.

Growth factor-mediated signaling has emerged as an essential component of memory formation. In this study, we used a phospholipase C gamma 1 (PLCgamma1) binding, cell-penetrating peptide to sequester PLCgamma1 away from its target, the phosphotyrosine residues within the activated growth factor receptor. Peptides appear to transduce neurons but not astrocytes or oligodendrocytes. The presence of the peptides in the hippocampus during training in the Morris water maze significantly impaired long-term memory, but not memory acquisition. These results, along with previous studies on extracellular signal-regulated kinase (ERK) and phosphoinositide-3 kinase (PI3K), implicate all three key growth factor receptor-activated intracellular signaling pathways in memory storage.

Animals↗
PubMedDate not supplied

Tests of a dynamic systems account of the A-not-B error: the influence of prior experience on the spatial memory abilities of two-year-olds.

Recently, Smith, Thelen, and colleagues proposed a dynamic systems account of the Piagetian "A-not-B" error in which infants' errors result from general processes that make goal-directed actions to remembered locations. Based on this account, the A-not-B error should be a general phenomenon, observable in different tasks and at different points in development. Smith, Thelen, et al.'s proposal was tested using an A-not-B version of a sandbox task. During three training trials and three "A" trials, 2-year-olds watched as a toy was buried in a sandbox at Location A. Following a 10-s delay, children searched for the object. Across five experiments, children's (total N = 92) performance on the A trials was accurate. After the A trials, children watched as a toy was hidden at Location B, 8 to 10 inches from Location A. In all experiments, children's searches after a 10-s delay were significantly biased in the direction of Location A. Furthermore, this bias toward Location A decreased with repeated trials to Location B, as well as when children completed fewer trials to Location A. Together, these data suggest that A-not-B-type errors are pervasive across tasks and development.

Child Development↗
PubMed1994

Does neuronal damage of CA1 relate to spatial memory performance of rats subjected to transient forebrain ischemia?

The effect of ischemia-induced hippocampal neuronal damage on acquisition and performance in the Morris water maze task was investigated in male Wistar rats, subjected to 8 min of transient forebrain ischemia, induced by the 4-vessel occlusion (4-VO) method. After a morphological scoring of the neuronal damage within the CA1, CA2, and CA3 subfields of the anterior-dorsal part of hippocampus we found that rats with a total neuronal cell loss of the anterior-dorsal CA1 region showed memory performance impairments in the acquisition trials, in a probe trial, and in a reversal experiment. However, rats with only partial damage to the CA1 region did not exhibit significant impairments during the acquisition trials of the water maze test or in the probe trial and the reversal experiment. In conclusion, these results suggest that it is possible to relate the histological damage score of CA1 in the anterior-dorsal hippocampus to impaired memory performance in the present water maze setup.

Animals↗