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PubMed1993

Magnesium and ketamine attenuate cognitive dysfunction following experimental brain injury.

We evaluated the therapeutic effects of two noncompetitive antagonists of the N-methyl-D-aspartate (NMDA) receptor, MgCl2 and ketamine, both individually and together, on cognitive dysfunction observed following parasagittal fluid-percussion (FP) brain injury in the rat. Using a modified Morris water maze technique, we found significant attenuation of post-traumatic memory dysfunction in animals treated with either MgCl2 (125 mumol) or ketamine (4 mg/kg) (P < 0.005). Combined MgCl2 and ketamine treatment also preserved memory function (P < 0.005), with no apparent additive effect.

Amnesia, Retrograde↗
PubMed1994

(R,S)-alpha-methyl-4-carboxyphenylglycine (MCPG) blocks spatial learning in rats and long-term potentiation in the dentate gyrus in vivo.

Recently, it was demonstrated by the use of the competitive and selective antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine (MCPG) that metabotropic glutamate receptor (mGluR) activation is required to induce long-term potentiation (LTP) in the hippocampus. Accordingly, we investigated whether MCPG also inhibits spatial learning. Rats were trained on a spatial alternation task in a Y-maze with footshock reinforcement, and MCPG (0.0208 mg) was injected intracerebroventricularly prior to training and/or retention test. Animals injected pre-training are clearly impaired in retention, whereas preretention application was without effect. A state dependency could be excluded. Additionally, MCPG at the same concentration completely blocks a potentiation at perforant path/dentate gyrus synapses in vivo. These results strongly implicate a role of mGluRs in spatial learning and LTP.

Animals↗
PubMed1995

Real-time detection of mitochondrial inhibition at frog motor nerve terminals using increases in the spatial variance in probability of transmitter release.

The effects of Hg2+, methyl mercury, and flufenamic acid, all of which inhibit mitochondria, were examined at frog motor nerve terminals. Unbiased estimates of m (no. of transmitter quanta released), n (no. of functional release sites), p (probability of release), and vars p (spatial variance in p) were obtained using K(+)-induced asynchronous neurosecretion (m, n and p not having the same definitions as with nerve-evoked release). Transient but significant increases in m, n, p and vars p were found with all three agents. These findings indicate that mitochondrial inhibition and release of sequestered Ca2+ can be detected as a real-time increase in vars p. The results also suggest that changes in vars p might be used to differentiate between cellular (membrane) and subcellular (organellar) actions of drugs at the nerve terminal.

Animals↗
PubMed1985

Learning and memory deficits after lesions of the nucleus basalis magnocellularis: reversal by physostigmine.

The role of the cholinergic nucleus basalis magnocellularis in spatial learning and memory was studied in the rat. Animals received bilateral injections of ibotenic acid (5 micrograms/microliters) into the region of the nucleus basalis magnocellularis. Six weeks postoperatively they were deprived of food and trained for 5 weeks in a 16-arm radial maze in which 9 of the arms were baited with food. The nucleus basalis magnocellularis-lesioned animals showed significant deficits in the acquisition of the task. Further analysis of the data indicated that this was due primarily to a deficit in reference (long-term) as opposed to working (short-term) memory. After the 5-week training period the nucleus basalis magnocellularis-lesioned animals received intraperitoneal injections of physostigmine sulphate (0.5 mg/kg) 30 min before each daily trial for 1 week. This treatment resulted in a significant improvement in the performance of the spatial memory task on all three measures. The ibotenate lesions reduced the activity of choline acetyltransferase by about 40% in the anterior cortex and by 15% in the posterior cortex. Hippocampal choline acetyltransferase activity was not affected, indicating that the septohippocampal cholinergic projection was spared by the lesions. The activity of glutamate decarboxylase was not affected in any of these regions. These results suggest that the cholinergic projections of the nucleus basalis magnocellularis play an important role in the acquisition of a spatial memory task.

Animals↗
PubMed1990

Hippocampal mossy fibers and radial-maze learning in the mouse: a correlation with spatial working memory but not with non-spatial reference memory.

One hundred and eight male mice from nine different inbred strains were tested for two aspects of learning in an eight-arm radial maze. In the first experimental arrangement of the maze, measuring spatial working memory, clear strain differences were found on the fifth day of training. Furthermore, this type of learning showed a high positive correlation with the size of the intra- and infrapyramidal hippocampal mossy fiber terminal field as revealed with Timm's staining. In the second experiment, in which non-spatial reference memory was tested, significant strain differences were found for the learning variables, but there were no significant covariations with the sizes of the intra- and infrapyramidal mossy fiber terminal fields. These results, combined with previous data, suggest that heritable variations of the hippocampal intra- and infrapyramidal mossy fiber projection influence processes determining spatial learning capabilities in mice.

Animals↗
PubMed1991

Effects of cholinergic-rich neural grafts on radial maze performance of rats after excitotoxic lesions of the forebrain cholinergic projection system--I. Amelioration of cognitive deficits by transplants into cortex and hippocampus but not into basal forebrain.

After ibotenate (10.0 mg/ml) lesions to the nucleus basalis and medial septal regions, at the source of the cortical and hippocampal branches of the forebrain cholinergic projection system, rats displayed long-lasting stable impairment in reference and working memory in both spatial (place) and associative (cue) radial maze tasks. Cell suspension transplants of cholinergic-rich fetal basal forebrain tissue dissected at embryonic day 15 substantially improved all aspects of radial maze performance to a comparable degree whether sited in cortex, hippocampus, or both regions of the host brain. No additive effects were obtained with grafts in both terminal regions, but total graft volume, assessed stereologically, showed a significant negative correlation with error scores. Rats with behaviourally effective grafts, like controls, were disrupted in the place task when tested in dim light which obscured extra-maze spatial cues. Lesioned rats were not affected by change in lighting. Grafts of cholinergic-poor fetal hippocampal tissue did not improve radial maze performance; neither did grafts of cholinergic-rich tissue placed within the host basal forebrain lesion sites. In rats with cholinergic-rich terminal grafts, cortical and hippocampal choline acetyltransferase activity was restored to control level, commensurate with site of transplant, whereas it was significantly reduced in lesioned animals and those with functionally ineffective grafts. The indiscriminate error pattern and insensitivity to changes in lighting shown by lesioned rats suggested that lesioning primarily disrupted attention rather than short- or long-term spatial or associative memory processes. Since rats with cholinergic-rich grafts showed both reduced errors and recovery of stimulus control, the data indicated that grafts affected information processing, rather than changes in motor or motivational processes. Changes in choline acetyltransferase activity and the behavioural efficacy of cholinergic-rich grafts are consistent with the involvement of acetylcholine in the behavioural deficits and recovery displayed by lesioned and grafted groups, but do not rule out contributions from other factors. The equipotency of grafts within each terminal region suggests also that there may be a considerable degree of functional cooperation between the two branches of the forebrain cholinergic projection system. Functional recovery may involve local, nonspecific synaptic or paracrine mechanisms within the target regions, since grafts were efficacious only when placed in the terminal areas, but not when sited homotopically in the basal forebrain, indicating that they did not achieve any functionally significant structural repair to the host brain at that site.

Acetylcholine↗
PubMed1991

Effects of cholinergic-rich neural grafts on radial maze performance of rats after excitotoxic lesions of the forebrain cholinergic projection system--II. Cholinergic drugs as probes to investigate lesion-induced deficits and transplant-induced functional recovery.

The effects of two doses of muscarinic (arecoline and scopolamine) and nicotinic (nicotine and mecamylamine) cholinergic receptor agonists and antagonists on the radial maze errors of rats, performing poorly after ibotenate lesions to the nucleus basalis and medial septal brain regions, were assessed before and after transplantation of cholinergic-rich and -poor fetal grafts, using tasks which measured short- (working) and long-term (reference) spatial and associative memory. Lesioned rats showed improvement with the agonists, and impairment with the antagonists, at low doses which did not affect the performance of controls; these effects were more marked for working than reference memory, especially in the spatial task. The peripherally acting antagonists N-methylscopolamine and hexamethonium did not affect the performance of control or lesioned rats. Effects of the cholinergic probes were re-examined 16 weeks after grafting, in groups with cholinergic-rich grafts to cortex and/or hippocampus which showed functional recovery, and groups with cholinergic-rich grafts to basal forebrain, or cholinergic-poor grafts to basal forebrain, cortex, and hippocampus, which showed no improvement. All lesioned rats, regardless of site, type, or efficacy of transplant, continued to show marked impairment with the antagonists. Poorly performing grafted animals also showed improvement with the agonists. In rats with behaviourally effective cholinergic-rich grafts, arecoline had no effect, but nicotine substantially increased working and reference memory errors, particularly spatial working memory errors. Rats with grafts in both cortex and hippocampus showed the largest increases in errors after nicotine. These results show that lesioned rats were more sensitive to the bi-directional effects of cholinergic receptor ligands than controls, consistent with a role for acetylcholine in the lesion-induced deficits. The predominant effect of drugs on working memory may also be consistent with disruption of acquisition rather than of storage or retrieval processes in memory, and may be related to impairment of attention. The results further show that, despite behavioural recovery, supersensitive responses to cholinergic drugs were not normalized in rats with cholinergic-rich grafts, and that an additive interaction between graft and host may have occurred in response to nicotine.

Acetylcholine↗
PubMed1993

Effects of acidic fibroblast growth factor on cholinergic neurons of nucleus basalis magnocellularis and in a spatial memory task following cortical devascularization.

The ability of acidic fibroblast growth factor to elicit a trophic response in the nervous system of the rat was tested in vitro and in vivo. Treatment of cultured septal cells with acidic fibroblast growth factor resulted in an elongation of glial processes as assessed by immunostaining for glial fibrillary acidic protein. Increased choline acetyltransferase was also observed. The responses to acidic fibroblast growth factor in vivo were studied in rats trained in a spatial memory task, using the Morris water maze. Randomly selected animals were subjected to unilateral cortical devascularization. This lesion results in partial unilateral infarction of the neocortex, and in retrograde degeneration of the nucleus basalis magnocellularis. Animals were tested post-lesion for memory retention and were then killed for morphological studies. Intracerebroventricular administration of acidic fibroblast growth factor (0.6 microgram/h for seven days starting at surgery) prevented the lesion-induced impairment in this test, and reduced the nucleus basalis magnocellularis cholinergic degeneration, as assessed by morphometric choline acetyltransferase-like immunoreactivity and radioenzymatic assay for choline acetyltransferase activity. The preservation of the phenotype of injured cholinergic neurons of the nucleus basalis magnocellularis by acidic fibroblast growth factor was indicated by the maintenance of the cross-sectional area of cell bodies and mean length of neuritic processes one month after surgery. The effect of acidic fibroblast growth factor in non-cholinergic cells remains to be investigated. It is suggested that acidic fibroblast growth factor may alleviate the lesion-induced deficit in the memory retention task by preventing disruption of functional connections between nucleus basalis magnocellularis and intact cortical areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Spatial working memory over long retention intervals: dependence on sustained cholinergic activation in the septohippocampal or nucleus basalis magnocellularis-cortical pathways?

Previous direct neurochemical studies of the temporal dynamics of cholinergic activation in the septohippocampal and nucleus basalis magnocellularis-cortical pathways at various stages during repeated testing of mice with selective spatial reference or working memory protocols [Durkin and Toumane (1992), Behav. Brain Res. 50, 43-52] showed that the post-test durations of cholinergic activation in each pathway varied as a function of the type of memory tested and the level of task mastery. Since (i) the hippocampal formation is considered to constitute a critical component of a temporary memory buffer, and (ii) working memory items are not thought to be submitted to consolidation and permanent storage, we postulated that the duration of testing-induced cholinergic activation in the septohippocampal pathway may govern the maintenance of the working memory trace over the retention interval. In order to test directly this hypothesis C57 B1/6 mice were extensively trained (one trial/day, 25-30 days) on an identical selective working memory task to attain high levels of retention (> 80% correct), but using either 5 min (Group 1), or 60 min (Group 2) retention intervals. At various times (30 s-75 min) following the initial acquisition phase of the test, cholinergic activity in the hippocampus and frontal cortex was quantified using measures of high-affinity choline uptake. Whereas cholinergic activation was observed in both pathways at 30 s post-acquisition and throughout the 5 min retention interval in Group 1, the situation in Group 2 is different, activation of the septohippocampal pathway being maintained for only 15 min, while activation in the nucleus basalis magnocellularis-cortical pathway is maintained for the totality of the 1 h retention interval. The nucleus basalis magnocellularis-cortical cholinergic pathway, in addition to its role in long-term reference memory storage processes may, thus, via an intervention in the temporal encoding of information, also subsume a complementary intermediate-term buffer storage role in working memory situations requiring retention intervals in excess of 15 min in mice. This secondary, "backup", function of the nucleus basalis magnocellularis-cortical pathway would thus liberate the septohippocampal complex from its primary active role in the temporary maintenance and/or accessibility of the working memory trace in these particular cases requiring long retention intervals.

Acetylcholine↗
PubMed1996

Contrasting effects of fetal CA1 and CA3 hippocampal grafts on deficits in spatial learning and working memory induced by global cerebral ischaemia in rats.

Functional effects of fetal hippocampal field grafts were assessed in rats with spatial learning and memory impairments following global cerebral ischaemia. Experiment 1 examined effects of grafts dissected from fields CA1 and CA3 at embryonic day 19 and from the dentate gyrus at postnatal day 1. Cell suspensions (15,000 cells/site) were implanted bilaterally at two points above the dorsal CA1 area two weeks after four-vessel occlusion (electrocoagulation of the vertebral arteries followed the 24 h later by occlusion of the carotid arteries for 15 min). Histological examination showed that CA1 neuronal loss (60-70%) was equivalent in all ischaemic groups and that 80% of CA1 and 60% of CA3 grafts survived and were sited appropriately in the alveus or corpus callosum above the area of ischaemic CA1 damage in the host, but there was no survival of dentate grafts. Results from rats with poor pyramidal cell graft survival were excluded, but those from rats with non-surviving dentate grafts were retained as an additional control group. Acquisition in the water maze was examined nine and 25 weeks after transplantation, and spatial working memory was assessed in three-door runway and water maze matching-to-position tasks 19 and 28 weeks after grafting, respectively. For water maze acquisition rats were trained with two trails/day and a 10 min inter-trial interval for 10-12 days to locate a submerged platform. Ischaemic rats with CA1 grafts learned the platform position as rapidly as non-ischaemic controls, searched appropriately in the training quadrant and were accurate in heading towards the platform, but were initially impaired on recall of the precise platform position on probe trials with the platform removed. Performance of ischaemic controls and groups with CA3 and non-surviving dentate graft groups was significantly impaired relative to controls and to the CA1 grafted group. The CA1 grafted group was also as successful as controls in matching-to-position in the water maze and substantially superior to the other ischaemic groups, assessed using three trials/day, with a 30-s inter-trial interval and a different platform position on each day. In a more complex matching-to-position task in the three-door runway, the performance of the CA1 grafted group was significantly impaired relative to controls, although superior to that of the other ischaemic control and graft groups. Functional recovery with CA1, but not CA3, grafts in ischaemic rats was replicated in a second experiment which assessed water maze acquisition and working memory at 10 and 14 weeks after transplantation, in rats with 90% graft survival. These results indicate that long-lasting, task-dependent improvements can be seen in ischaemic rats with CA1 fetal grafts in both aversively and appetitively motivated spatial learning tasks. The findings suggest that functional recovery requires homotypic replacement of CA1 cells damaged by ischaemia, rather than provision of structurally similar glutamate-releasing CA3 pyramidal cells.

Animals↗
PubMed1990

Estrogen-related variations in human spatial and articulatory-motor skills.

A group of normally cycling women completed a battery of cognitive and motor tests during menses and during the late follicular phase of the menstrual cycle. Enhanced performance on tests of articulatory and fine motor skills was observed during the late follicular phase, while performance on tests of spatial ability was poorer at that time, compared with performance during menses. Variations in estradiol (E2) levels may be at least partially responsible for these effects.

Adult↗
PubMed1987

Large and small medial frontal cortex lesions and spatial performance of the rat.

Rats with sham operations, or small or large medial frontal cortex lesions were compared for the acquisition of a position habit and for learning a series of 4 position habit reversals. No differences were found during acquisition of the position habit. On the reversals, the rats with the larger lesions were markedly impaired, while less severe deficits or control-like performance characterized the rats with the smaller ablations. Analyses of the error scores showed that the rats with the larger lesions made more perseverative errors than the other groups and performed more sporadically even after breaking a previous position habit. These results confirm the hypothesis that a strong relationship exists between medial frontal cortex lesion features (depth and length) and performance. The differences found in acquisition vs. reversal learning, and the nature of the errors observed, also suggest that this part of the brain functions as more than simply a spatial analyzer.

Animals↗
PubMedDate not supplied

Dissociating performance and learning deficits on spatial navigation tasks in rats subjected to cholinergic muscarinic blockade.

The spatial navigation abilities of rats, subject to muscarinic blockade with atropine sulfate (50 mg/kg), were examined with the object of dissociating putative performance and learning deficits. A number of aspects of performance were not disrupted by the drug treatments, including development of position responses, cue responses, nonspatial discriminations, and the retention of place responses. Acquisition of place navigation was disrupted in a variety of tasks including: dry-land tasks in which rats searched for a hole from which to escape or searched for buried food and swimming pool tasks in which rats searched for a hidden platform on which to escape from the water. Task acquisition as well as motor performance was changed by the drug treatments in each task. Priming animals with experience on a subset of task variables did not significantly improve subsequent place performance. Priming animals with all motoric and spatial demands of a task, except the use of a specific set of distal cues aided performance, whereas priming animals with the use of a specific set distal cues but not motor experience produced little improvement in performance. The results indicate that impairments in the use of motoric skills contribute significantly to the deficits produced by cholinergic muscarinic blockade in spatial navigation tasks.

Animals↗
PubMed1995

Posttreatment with EPC-K1, an inhibitor of lipid peroxidation and of phospholipase A2 activity, reduces functional deficits after global ischemia in rats.

In this study the effect of an inhibitor of lipid peroxidation and of phospholipase A2 activity, EPC-K1, on spatial learning deficit and neuronal damage following transient cerebral ischemia was evaluated. Global ischemia was induced by four-vessel occlusion (4VO) for 20 min in rats. EPC-K1 (10 mg/kg IP) was administered either a) 15 min before induction of ischemia, b) immediately after, or c) 30 min after onset of reperfusion. One week after surgery spatial learning was tested in the Morris water maze. EPC-K1 reduced the deficit in spatial learning when given immediately or 30 min after the onset of reperfusion but not when applied 15 min before ischemia. Neuronal damage in the CA1 sector of the hippocampus produced by 4VO was slightly, but not significantly attenuated by posttreatment. The present data demonstrate that posttreatment with EPC-K1 exerts a protective effect on deficits in spatial learning induced by 4VO. These results support the hypothesis that lipid peroxidation and activation of phospholipase A2 contribute to functional alterations of the brain during reperfusion following forebrain ischemia.

Animals↗
PubMed1994

Spatial working memory score of humans in a large radial maze, similar to published score of rats, implies capacity close to the magical number 7 +/- 22.

To compare the working memory (WM) capacity of humans to rats, we tested humans with a 17-arm radial maze and, in a follow up experiment, with a 13-arm radial maze. Both mazes were 15.2 meters in diameter, painted on a grassy field. In one version of the 13-arm experiment, we required a concurrent nonsense vocalization to impede subjects' use of language to remember locations. Subjects were instructed to choose arms of the radial maze unsystematically--as rats generally appear to do--and to visit the end of each arm only once. In additional procedures, we tested working memory capacity in a verbal task that is more analogous to the radial maze than is the typical ordered recall test. Subjects were asked to try to recite a sequence of 17 numbers (i.e., 18 through 34) or letters (A through Q) in unsystematic order, with no repeats. In another experiment subjects recited 13 numbers (14-26) or letters (A-M). In all tests, subjects were allowed only as many responses as there were distinct items (17 or 13, respectively). Average correct-response (nonrepeat) scores were 14.4 for the 17-arm maze and 14.1 for both of the verbal 17-item tests; these scores are close to the reported score for rats in a 17-arm radial maze. Average scores were between 10.8 and 11.4 in all of the 13-item maze and recitation tasks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Learning in monkeys exposed perinatally to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

TCDD is an extremely toxic chemical pollutant which bioaccumulates in maternal adipose tissue, and is transferred to the developing organism during gestation and lactation. Long-term cognitive deficits have been reported following perinatal exposure to polychlorinated biphenyls, which are structurally and toxicologically similar to TCDD. In the current study, monkeys exposed to TCDD perinatally were later tested in two cognitive paradigms, discrimination-reversal learning (RL) and delayed spatial alternation (DSA). RL detected effects; whereas DSA, as analyzed, did not. RL consisted of a series of simple spatial reversals, followed by spatial reversals with color and shape as irrelevant cues, then by color reversals and finally by shape reversals. TCDD-exposed monkeys exhibited retarded learning of the shape reversals. The deficit was most pronounced on the first reversal following overtraining. There were no group differences on the spatial or color reversals. However, the number of trials the TCDD-exposed monkeys individually took to learn the spatial reversals was positively correlated with TCDD concentration in body fat. Conversely, the number of trials they took to learn the color reversals was negatively correlated with TCDD in body fat.

Animals↗
PubMedDate not supplied

Effects of postnatal aluminum exposure on choline acetyltransferase activity and learning abilities in the rat.

Young rats were treated by gastric intubation with aluminum lactate (0, 100, and 200 mg Al/kg/day) from postnatal days 5 to 14 to determine the treatment's influence on brain choline acetyltransferase activity and learning abilities. The results indicated that aluminum concentrations in the cerebral areas increased in parallel to plasma aluminum at the dose of 200 mg. In the same case, choline acetyltransferase activity was reduced. At postnatal days 50 and 100, the treated rats did not show alterations in their learning abilities in the 2 tests which are based on different motivations (avoidance of an aversive light or alimentary motivation) and different ways of achievement (pressing on a lever or running in a maze). A low reduction in the general activity, particularly in the radial maze test, was only observed in rats treated with 200 mg Al/kg/day.

Animals↗
PubMed1993

Crack cocaine use and high-risk behaviors among sexually active black adolescents.

The recent spread of crack cocaine use among inner-city teenagers has been accompanied by dramatic increases in juvenile delinquency and sexually transmitted diseases (STDs) among teenagers. This study examined the prevalence of five factors which promote STDs, including human immunodeficiency virus (HIV), among a sample of sexually active black adolescent crack users and non-users from the San Francisco Bay Area. Significant differences were observed between these groups with respect to history of engaging in sexual intercourse under the influence of drugs or alcohol, exchanging sexual favors for drugs or money, condom use in the most recent sexual encounter, and having five or more sexual partners in the last year. Approximately 63% of all respondents reported engaging in at least one of these risk behaviors. In multiple logistic regression analysis, reporting one or more of these STD/HIV risk behaviors was significantly associated with crack use and having one or more relatives who used drugs. Intervention efforts need to address both individual and environmental risk factors in order to reduce teens' risk for STDs, including HIV.

Adolescent↗