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PubMed2006

Low dose citalopram reverses memory impairment and electroconvulsive shock-induced immobilization.

Citalopram, a selective serotonin reuptake inhibitor (SSRI), is one of the most widely used antidepressants. Recently, citalopram has been reported to improve working memory in patients with depression, and psychotic symptoms and behavioral disturbances in patients with dementia. However, the possibility of using citalopram in the treatment of cognitive disorders has not received much attention. The present study investigated the effects of citalopram on scopolamine- and Delta9-tetrahydrocannabinol (THC)-induced impairment of spatial memory using an eight-arm radial maze and electroconvulsive shock (ECS)-induced immobilization (a behavioral model for the disturbance of consciousness). Low dose citalopram reversed both scopolamine- and THC-induced impairment of spatial memory, suppressed ECS-induced immobilization reversed the THC-induced decrease of acetylcholine (ACh) release in the dorsal hippocampus in vivo microdialysis, and enhanced tremors induced by oxotremorine, a muscarinic M1 receptor agonist. Taken together these findings suggest that low dose citalopram is useful for the treatment of memory deficits and consciousness disturbance.

Animals↗
PubMed2004

The mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) potentiates PCP-induced cognitive deficits in rats.

RATIONALE: Recent studies have shown that metabotropic glutamate receptor 5 (mGluR5) can modulate N-methyl-D-aspartate (NMDA) receptor function in vivo. For example, the mGluR5 antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP) can potentiate PCP (phencyclidine)-evoked hyperactivity and PCP-induced disruptions in pre-pulse inhibition (PPI) in rats. OBJECTIVE: To extend these previous behavioral findings and determine whether the mGluR5 antagonist MPEP can modulate the disruptions in learning and memory induced by PCP in rats. METHODS: The effects of MPEP, alone and in combination with PCP, were evaluated in rats trained to perform a repeated acquisition procedure (learning) or a delayed non-matching to position (DNMTP) radial maze task (spatial memory). RESULTS: In the repeated acquisition task, MPEP (0-10 mg/kg, IP) dose-dependently decreased response rates but had no effect on response accuracy. In contrast, PCP (0.625-1.25 mg/kg, SC) reduced response rate and response accuracy in a dose-dependent manner. Although MPEP (10 mg/kg, IP) had no effect when administered alone, the mGluR5 antagonist potentiated the disruptions in learning induced by a low dose of PCP (0.625 mg/kg, SC). In the DNMTP maze task, MPEP (0-10 mg/kg, IP) had no effect on spatial memory, whereas PCP (1.25-2.5 mg/kg, SC) produced a dose-dependent disruption. MPEP (10 mg/kg, IP) potentiated the impairments in memory induced by PCP (1.25 mg/kg, SC). CONCLUSION: The mGluR5 antagonist, MPEP, potentiated the disruptions in learning and memory induced by PCP. These behavioral data extend previous behavioral findings and further suggest that mGluR5 can modulate NMDA receptor function in vivo.

Animals↗
PubMed1989

Effects of amygdaloid and amygdaloid-hippocampal lesions on object recognition and spatial working memory in rats.

Neurotoxic lesions of the amygdala did not affect the postoperative acquisition of a nonspatial test of object recognition (delayed nonmatching to sample) even when retention delays were increased from 0 s to 20 or 60 s, or when test stimuli were deliberately repeated within a session. Although these amygdaloid lesions did not alter forced-choice spatial alternation, they slightly increased neophobic responses to novel foods and environments. In contrast, combined amygdalohippocampal (A + H) lesions impaired performance on the object recognition task when the retention intervals were increased beyond 0 s and when test stimuli were repeated within a session. The A + H rats were also severely impaired on the spatial alternation task, and they showed reduced neophobia. Comparisons with a previous study show that damage to the amygdala or hippocampus does not affect object recognition, whereas A + H damage produces clear deficits.

Amygdala↗
PubMed2000

Caspase activity plays an essential role in long-term memory.

Activation of intracellular second messenger cascades has been linked to learning and memory in various organisms. Identification of down-stream targets of these second messengers that play a role in learning and memory is an active area of research. Recently, it has been reported that increases in intracellular calcium can activate a cysteine-dependent aspartate-directed protease (caspase) cascade in mice. Using an antibody that selectively recognizes activated caspase-3, we detected the presence of this enzyme in hippocampal neurons. Inhibition of caspase activity in the hippocampus blocked long-term, but not short-term, spatial memory. These results suggest that a caspase-mediated cellular event(s) in hippocampal neurons is critical for long-term spatial memory storage.

Amino Acid Chloromethyl Ketones↗
PubMed2004

Age differences in neural correlates of route encoding and route recognition.

Spatial memory deficits are core features of aging-related changes in cognitive abilities. The neural correlates of these deficits are largely unknown. In the present study, we investigated the neural underpinnings of age-related differences in spatial memory by functional MRI using a navigational memory task with route encoding and route recognition conditions. We investigated 20 healthy young (18-29 years old) and 20 healthy old adults (53-78 years old) in a random effects analysis. Old subjects showed slightly poorer performance than young subjects. Compared to the control condition, route encoding and route recognition showed activation of the dorsal and ventral visual processing streams and the frontal eye fields in both groups of subjects. Compared to old adults, young subjects showed during route encoding stronger activations in the dorsal and the ventral visual processing stream (supramarginal gyrus and posterior fusiform/parahippocampal areas). In addition, young subjects showed weaker anterior parahippocampal activity during route recognition compared to the old group. In contrast, old compared to young subjects showed less suppressed activity in the left perisylvian region and the anterior cingulate cortex during route encoding. Our findings suggest that age-related navigational memory deficits might be caused by less effective route encoding based on reduced posterior fusiform/parahippocampal and parietal functionality combined with diminished inhibition of perisylvian and anterior cingulate cortices correlated with less effective suppression of task-irrelevant information. In contrast, age differences in neural correlates of route recognition seem to be rather subtle. Old subjects might show a diminished familiarity signal during route recognition in the anterior parahippocampal region.

Adolescent↗
PubMed2000

Effects of batroxobin on spatial learning and memory disorder of rats with temporal ischemia and the expression of HSP32 and HSP70.

The effect of Batroxobin on spatial memory disorder of left temporal ischemic rats and the expression of HSP32 and HSP70 were investigated with Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats in searching a goal were significantly longer than those of the sham-operated rats and at the same time HSP32 and HSP70 expression of left temporal ischemic region in rats was significantly increased as compared with the sham-operated rats. However, the mean reaction time and distance of the Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of HSP32 and HSP70 immune reactive cells of Batroxobin-treated rats was also less than that of the ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats; and the down-regulation of the expression of HSP32 and HSP70 is probably related to the attenuation of ischemic injury.

Animals↗
PubMed1984

Intellectual and memory impairment in moderate and heavy drinkers.

Heavy drinkers (more than 2 liters of wine per day), without clinical evidence of brain dysfunction, moderate drinkers (1 liter of wine per day) and control subjects (no more than 250 cc of wine per day) were given the Progressive Matrices test and two learning tests, one tapping verbal memory and the other spatial memory. Heavy drinkers' performance was significantly worse than that of the other groups on the Progressive Matrices test and the spatial learning test. With a more lenient method of analysis, the difference between heavy drinkers and controls on the verbal learning test and that between moderate drinkers and controls on the Progressive Matrices test were also significant. When the influence of intelligence on memory performance was partialled out by covarying memory scores for Progressive Matrices scores, all differences on the verbal learning test disappeared whereas the spatial learning test still discriminated heavy drinkers from mild drinkers and controls. The bearing of these findings on the continuum of impairment hypothesis and the right hemisphere vulnerability hypothesis is discussed.

Adult↗
PubMed2006

NT-3 facilitates hippocampal plasticity and learning and memory by regulating neurogenesis.

In the adult brain, the expression of NT-3 is largely confined to the hippocampal dentate gyrus (DG), an area exhibiting significant neurogenesis. Using a conditional mutant line in which the NT-3 gene is deleted in the brain, we investigated the role of NT-3 in adult neurogenesis, hippocampal plasticity, and memory. Bromodeoxyuridine (BrdU)-labeling experiments demonstrated that differentiation, rather than proliferation, of the neuronal precursor cells (NPCs) was significantly impaired in DG lacking NT-3. Triple labeling for BrdU, the neuronal marker NeuN, and the glial marker GFAP indicated that NT-3 affects the number of newly differentiated neurons, but not glia, in DG. Field recordings revealed a selective impairment in long-term potentiation (LTP) in the lateral, but not medial perforant path-granule neuron synapses. In parallel, the NT-3 mutant mice exhibited deficits in spatial memory tasks. In addition to identifying a novel role for NT-3 in adult NPC differentiation in vivo, our study provides a potential link between neurogenesis, dentate LTP, and spatial memory.

Animals↗
PubMed2000

Effect of batroxobin on expression of c-Jun in left temporal ischemic rats with spatial learning and memory disorder.

The effect of Batroxobin on expression of c-Jun in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats, and at the same time c-Jun expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of c-Jun immune reactive cells of Batroxobin-treated rats was also less than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder in temporal ischemic rats, and the down-regulation of the expression of c-Jun is probably related to the neuroprotective mechanism.

Animals↗
PubMed2001

Genetic predisposition and the development of posttraumatic stress disorder in an animal model.

BACKGROUND: Exposure to extremely stressful events can lead to Posttraumatic stress disorder (PTSD). Due to the complexity of PTSD, animal models have been designed and advanced to address the role of psychosocial stressors in the etiology; however, the apparent role of genetics in susceptibility to PTSD-like behaviors in animals remains unexplored. METHODS: An animal model of congenital learned helpless (cLH) behavior has been used to study the effects of genetic disposition as a risk factor for the development of PTSD-like behaviors. Animals were monitored for changes in pain tolerance, spatial memory and hypothalamic-pituitary-adrenal functioning after re-exposure to intermittent stress in the presence and absence of situational cues. RESULTS: Exposure to stress resulted in an increase in pain tolerance in the cLH animals. In the spatial memory test 80% of the cLH animals manifested a decrease in performance after exposure to stress. These animals also had a blunted poststress corticosterone response. CONCLUSIONS: The genetic learned helpless animal model exhibited physiologic symptoms of analgesia, cognitive deficits and hyporesponsivity of the hypothalamic-pituitary-adrenal axis similar to those observed in human subjects with PTSD. It is proposed that the cLH model may be a valuable tool for exploring the role of genetic predisposition in the etiology of PTSD.

Animals↗
PubMedDate not supplied

Phonological and visuo-spatial working memory alterations in dyslexic children.

BACKGROUND: Working memory allows the retention of a limited amount of information for a brief period of time and the manipulation of that information. This study was undertaken to compare possible differences in working memory between dyslexic and control children. METHODS: To test the executive central process that controls attention, subjects were requested to assemble a 100-piece puzzle. To test the phonological loop, subjects were requested to repeat orally a 10-item list with the following characteristics: digits spanning two numbers; phonologically similar words, and unfamiliar pseudowords. The visuo-spatial sketchpad was tested by means of assembling a 25-piece puzzle. RESULTS: Forty dyslexic and and forty control children were studied. Dyslexic children recall a lesser number of similar words in the phonological loop and spend a longer time in puzzle assembly in the visuo-spatial sketchpad. No statistical difference in the central executive process was found. CONCLUSIONS: Present results suggest the importance of visuo-spatial and phonological loop alterations in dyslexic children that may result in difficulties with similar words and spatial information.

Child↗
PubMed1994

Increased anticholinergic sensitivity following closed skull impact and controlled cortical impact traumatic brain injury in the rat.

Evidence suggests that prolonged memory deficits in several neurodegenerative diseases are attributable to deficits in central cholinergic neurotransmission. In traumatic brain injury (TBI), such cholinergic deficits also may contribute to prolonged memory disturbances. This study determined whether moderate magnitudes of TBI produced by controlled cortical impact and mild magnitudes of experimental TBI produced by a new closed head impact technique in rats would produce an enhanced vulnerability to the memory disruptive effects of scopolamine, a muscarinic cholinergic receptor antagonist. Water maze performance was used to determine changes in cholinergic hippocampal function following TBI. In the first experiment, rats received a moderate level of TBI by means of a controlled cortical impact. A Morris water maze task assessed spatial memory function on days 30-34 postinjury. During the 5 day assessment period, statistical analyses showed a group main effect for swim latency. Subsequent post hoc analyses indicated that injured rats had significantly longer latencies on days 30 and 31 (p < 0.05, injury vs sham controls). By days 32-35, injured rats showed no statistically significant deficits in spatial memory performance. On day 35, scopolamine (1 mg/kg, IP) was injected into injured rats and sham-injured rats 15 min prior to being retested in the maze. Results showed that although the scopolamine had no effects on the performance of the sham-injured rats, the same dose significantly (p < 0.05) increased the latency to find the hidden platform in the injured group. In the second experiment, rats received a mild concussive closed head impact. Water maze performance was assessed on days 8-12 postinjury. No significant water maze performance deficits were observed. On day 13, injured and uninjured rats were pharmacologically challenged with scopolamine (1 mg/kg) and retested. Similar to the first experiment, injured rats manifested a significantly greater (p < 0.05) sensitivity to scopolamine than sham controls. The results from both experiments suggest that concussive and more severe levels of TBI can produce an enhanced vulnerability to disruption of cholinergically mediated memory function, even when memory function appears normal in the absence of secondary challenges. These data demonstrate that covert deficits can persist after the recovery of normal function. These deficits may be attributable to a decrease in the ability of cholinergic neurons to function properly. These data also provide important insights into features of receptor-coupled disturbances that could contribute to the maintenance of enduring cognitive deficits following TBI.

Acetylcholine↗
PubMed2000

Pregnenolone sulfate increases hippocampal acetylcholine release and spatial recognition.

The pregnenolone sulfate is a neurosteroid with promnesic properties. Recently, a correlation between endogenous levels of pregnenolone sulfate in the hippocampus and performance in a spatial memory task has been reported in aged rats. Cholinergic transmission is known to modulate memory processes and to be altered with age. In the present experiment we investigated the effect of increasing doses of pregnenolone sulfate on hippocampal acetylcholine release. Our results show that intracerebroventricular administrations of this neurosteroid induced a dose-dependent increase in acetylcholine release. Administration of 12 and 48 nmol of pregnenolone sulfate induced a short lasting (20 min) enhancement of acetylcholine output with a maximum around 120% over baseline and the administration of 96 and 192 nmol doses induced a long-lasting (80 min) increase that peaked around 300% over baseline. In a second experiment we have observed that the 12 nmol dose enhanced spatial memory performance, whereas the 192 nmol dose was inefficient. These results are consistent with previous work suggesting that, a modest increase in acetylcholine release facilitates memory processes, while elevation beyond an optimal level is ineffective. Nevertheless, neurosteroids may be of value for reinforcing depressed cholinergic transmission in certain age-related memory disorders.

Acetylcholine↗
PubMed1997

Influence of dietary restriction on ionotropic glutamate receptors during aging in C57B1 mice.

The present study was designed to determine whether the memory sparing effects of dietary restriction during aging could be through an effect on ionotropic glutamate receptors. Quantitative autoradiography was performed on 3, 10, and 26 month old mice to examine the density changes of NMDA, AMPA and kainate binding sites in aging animals. Spatial memory performance was also tested in these mice with the use of the Morris water maze. The 10 and 26 month olds were either ad libitum-fed or diet-restricted (60% of ad libitum-fed calories). Ad libitum-fed, 26 month old mice had significant decreases in NMDA-displaceable [3H]glutamate in all ten cortical, two out of seven hippocampal, and two out of four subcortical regions, as compared to 3 month olds. Diet-restricted, 26 month old mice only differed significantly from young in three cortical and two subcortical regions. The aged ad libitum-fed mice exhibited significantly poorer performance in the spatial memory task than all other groups. The diet-restricted 26 month olds only performed significantly worse than 3 month olds and diet-restricted 10 month olds. These results suggest that some of the memory sparing effects of dietary restriction on aged animals may be due to an influence on NMDA receptors.

Aging↗
PubMed1998

Matching patterns of activity in primate prefrontal area 8a and parietal area 7ip neurons during a spatial working memory task.

Single-unit recording studies of posterior parietal neurons have indicated a similarity of neuronal activation to that observed in the dorsolateral prefrontal cortex in relation to performance of delayed saccade tasks. A key issue addressed in the present study is whether the different classes of neuronal activity observed in these tasks are encountered more frequently in one or the other area or otherwise exhibit region-specific properties. The present study is the first to directly compare these patterns of neuronal activity by alternately recording from parietal area 7ip and prefrontal area 8a, under the identical behavioral conditions, within the same hemisphere of two monkeys performing an oculomotor delayed response task. The firing rate of 222 posterior parietal and 235 prefrontal neurons significantly changed during the cue, delay, and/or saccade periods of the task. Neuronal responses in the two areas could be distinguished only by subtle differences in their incidence and timing. Thus neurons responding to the cue appeared earliest and were more frequent among the task-related neurons within parietal cortex, whereas neurons exhibiting delay-period activity accounted for a larger proportion of task-related neurons in prefrontal cortex. Otherwise, the task-related neuronal activities were remarkably similar. Cue period activity in prefrontal and parietal cortex exhibited comparable spatial tuning and temporal duration characteristics, taking the form of phasic, tonic, or combined phasic/tonic excitation in both cortical populations. Neurons in both cortical areas exhibited sustained activity during the delay period with nearly identical spatial tuning. The various patterns of delay-period activity-tonic, increasing or decreasing, alone or in combination with greater activation during cue and/or saccade periods-likewise were distributed to both cortical areas. Finally, similarities in the two populations extended to the proportion and spatial tuning of presaccadic and postsaccadic neuronal activity occurring in relation to the memory-guided saccade. The present findings support and extend evidence for a faithful duplication of receptive field properties and virtually every other dimension of task-related activity observed when parietal and prefrontal cortex are recruited to a common task. This striking similarity attests to the principal that information shared by a prefrontal region and a sensory association area with which it is connected is domain specific and not subject to hierarchical elaboration, as is evident at earlier stages of visuospatial processing.

Animals↗
PubMed1996

Reduction of postischemic brain damage and memory deficits following treatment with the selective adenosine A1 receptor agonist.

Agonists of adenosine A1 receptors have been frequently proposed as candidates for clinical development in treatment of cerebral ischemia and stroke. Numerous experimental studies have shown that pre- and postischemic administration of these drugs results in a very significant reduction of postischemic brain damage. However, only a few studies determined the impact of cerebral ischemia and drug treatment on postischemic recovery of spatial memory. The present paper demonstrates that preischemic i.p. administration of adenosine amine congener (ADAC) at 100 micrograms/kg in gerbils results in a significant (P < 0.05) reduction of postischemic mortality and hippocampal, cortical and striatal morbidity. Postischemic Morris' water maze tests show that preischemic treatment with ADAC also leads to a very significant (P < 0.001) reduction of postischemic spatial memory loss. Our results indicate feasibility of further consideration of adenosine A1 receptor agonists as a clinically applicable acute treatment of brain ischemia. Recent development of neuroprotective adenosine A1 receptor agonists that are free of cardiovascular side effects supports such development.

Adenosine↗
PubMed1991

Physical activity effects on hippocampal and parietal cortical cholinergic function and spatial learning in F344 rats.

In the present investigation, the effects of physical activity on hippocampal cholinergic function, parietal cortical cholinergic function, and spatial memory were examined in F344 rats. Single bouts of physical activity elevated hippocampal and cortical high affinity choline uptake, whereas chronic physical activity significantly reduced only hippocampal high affinity choline uptake (HACU) and elevated muscarinic (QNB) receptor density. Three weeks prior to the end of the 14-week chronic treadmill running protocol, a group of chronic-run rats and their non-run controls were tested on a stringent version of Whishaw's place learning-set task. Chronic-run rats exhibited enhanced performance on the spatial task by significantly reduced second trial latencies and elevated first and second trial proximity ratio scores. Chronic-run spatial memory tested rats also showed enhanced hippocampal HACU and muscarinic receptor binding. These data indicate that chronic physical activity improves spatial learning performance. This improvement may be due, in part, to a chronic running-induced enhancement of hippocampal cholinergic functioning.

Animals↗
PubMed1999

Brain dysfunction associated with an induction of nitric oxide synthase following an intracerebral injection of lipopolysaccharide in rats.

We investigated the pathophysiological role of nitric oxide synthesized by inducible nitric oxide synthase in the brain, by injecting lipopolysaccharide directly into the rat cerebral cortex/hippocampus. The levels of nitric oxide metabolites, nitrite and nitrate, began to increase in a dose-dependent manner with a 3-h lag, and reached approximately seven-fold the basal levels 8 h after the direct injection of lipopolysaccharide (5 microg). The lipopolysaccharide-induced increase in nitrite and nitrate levels was inhibited by treatment with the specific inducible nitric oxide synthase inhibitor aminoguanidine. The protein synthesis inhibitor cycloheximide delayed the onset of the increase in nitric oxide metabolite levels, and reduced the peak levels. Lipopolysaccharide increased Ca2+-independent, but not Ca2+-dependent, nitric oxide synthase activity in the brain. Intense nicotinamide adenine dinucleotide phosphate-diaphorase activity was observed in round cells in the vicinity of the site of injection of lipopolysaccharide 8 h after the injection. Neuronal death was observed seven days after the injection of lipopolysaccharide. Spatial memory, as assessed by performance in a water maze task and spontaneous alternation behavior in a Y-maze, was significantly impaired in rats which had had previous bilateral injections of lipopolysaccharide into the hippocampus. The lipopolysaccharide-induced neuronal death and spatial memory impairments were prevented by aminoguanidine. These results suggest that direct injection of lipopolysaccharide into the brain causes an induction of inducible nitric oxide synthase in vivo. Furthermore, it is suggested that nitric oxide produced by inducible nitric oxide synthase is responsible for the lipopolysaccharide-induced brain dysfunction.

Analysis of Variance↗