Relation of cranial electroshock to convulsive and maze behavior in the white rat.
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Animals↗
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Neural representation of navigational relevance is rapidly induced and long lasting.
Successful navigation is facilitated by the presence of landmarks. Previous functional magnetic resonance imaging (fMRI) evidence indicated that the human parahippocampal gyrus automatically distinguishes between landmarks placed at navigationally relevant (decision points) and irrelevant locations (nondecision points). This storage of navigational relevance can provide a neural mechanism underlying successful navigation. However, an efficient wayfinding mechanism requires that important spatial information is learned quickly and maintained over time. The present study investigates whether the representation of navigational relevance is modulated by time and practice. Participants learned 2 film sequences through virtual mazes containing objects at decision and at nondecision points. One maze was shown one time, and the other maze was shown 3 times. Twenty-four hours after study, event-related fMRI data were acquired during recognition of the objects. The results showed that activity in the parahippocampal gyrus was increased for objects previously placed at decision points as compared with objects placed at nondecision points. The decision point effect was not modulated by the number of exposures to the mazes and independent of explicit memory functions. These findings suggest a persistent representation of navigationally relevant information, which is stable after only one exposure to an environment. These rapidly induced and long-lasting changes in object representation provide a basis for successful wayfinding.
Adolescent↗
Profound ataxia in complexin I knockout mice masks a complex phenotype that includes exploratory and habituation deficits.
Complexins are presynaptic proteins that bind to the SNARE complex where they modulate neurotransmitter release. A number of studies report changes in complexins in psychiatric (schizophrenia and depression) and neurodegenerative disorders (Huntington's disease, Wernicke's encephalopathy and Parkinson's disease). Here, we characterize the behavioural phenotype of Cplx1 knockout (Cplx1-/-) mice. Cplx1-/- mice develop a strong ataxia in the absence of cerebellar degeneration. Although originally reported to die within 2-4 months after birth, when reared using an enhanced feeding regime, these mice survive normally (i.e. >2 years). Cplx1-/- mice show pronounced deficits in motor coordination and locomotion including abnormal gait, inability to run or swim, impaired rotarod performance, reduced neuromuscular strength, dystonia and resting tremor. Although the abnormal motor phenotype dominates their overt symptoms, Cplx1-/- mice also show other behavioural deficits, particularly in complex behaviours. They have deficits in grooming and rearing behaviour and show reduced exploration in several different paradigms. They also show deficits in tasks reflecting emotional reactivity. They fail to habituate to confinement and show a 'panic' response when exposed to water. The abnormalities seen in the behaviour of Cplx1-/- mice reflect those predicted from the distribution of complexin I in the brain. Our data show that complexin I is essential not only for normal motor function in mice, but also for normal performance of other complex behaviours. These results support the idea that altered expression of complexins in disease states may contribute to the symptomatology of disorders in which they are dysregulated.
Adaptor Proteins, Vesicular Transport↗
Essential fatty acid preparation (SR-3) rehabilitates learning deficits induced by AF64A and 5,7-DHT.
The purpose of this study was to examine the possible effects of a novel mixture of fatty acids, SR-3 (a specific ratio between alpha-linolenic and linoleic acids) on learning deficits induced by cholinergic (AF64A) and serotonergic (5,7-DHT) neurotoxins in rats. I.c.v. AF64A and 4th ventricle administration of 5,7-DHT induce severe learning deficit using the Morris Water Tank. Three weeks of treatment with SR-3 rehabilitated the learning capacity of rats. However, learning deficits induced by a lesion in area postrema was not rehabilitated by SR-3. The mode of action of SR-3 is unknown. We propose that this combination of free fatty acids modulates the composition of neuronal membrane lipids and allows better neuronal communication.
Animals↗
Impaired learning and motor behavior in heterozygous Pafah1b1 (Lis1) mutant mice.
Heterozygous mutation or deletion of Pafab1b1 (LIS1) in humans is associated with syndromes with type 1 lissencephaly, a severe brain developmental disorder resulting from abnormal neuronal migration. We have created Lis1 heterozygous mutant mice by gene targeting. Heterozygous mutant mice are viable and fertile, but display global organizational brain defects as a result of impaired neuronal migration. To assess the functional impact of the mutation, Lis1 heterozygous mice and their wild-type littermates were evaluated on a wide variety of behavioral tests. Lis1 mutant mice displayed abnormal hindpaw clutching responses and were impaired on a rotarod test. Lis1 heterozygous mice were also impaired in the spatial learning version of the Morris water task. Impaired motor behavior and spatial learning and memory in Lis1 mutant mice indicates that impaired neuronal migration can have functional effects on complex behavioral responses. The behavioral findings also support the use of the Lis1 mutant mice as a model from human type 1 lissencephaly.
1-Alkyl-2-acetylglycerophosphocholine Esterase↗
A test of transitive inferences in free-flying honeybees: unsuccessful performance due to memory constraints.
We asked whether honeybees, Apis mellifera, could solve a transitive inference problem. Individual free-flying bees were conditioned with four overlapping premise pairs of five visual patterns in a multiple discrimination task (A+ vs. B-, B+ vs. C-, C+ vs. D-, D+ vs. E-, where + and - indicate sucrose reward or absence of it, respectively). They were then tested with the nonadjacent pairs A vs. E and B vs. D. Preference of B to D is consistent with the use of the implicit hierarchy A > B > C > D > E. Equal choice of B and D supports choice based on the associative strength of the stimuli. The bees' choice was determined by their memory constraints: experience with the last premise pair (D+ vs. E-) predominated. In the tests, bees preferred A to E and chose equally B and D. An analysis of the performance in terms of a reward/penalty ratio showed that B had a higher associative strength than D. Thus, bees do not establish transitive inferences but, rather, guide their choices by the joint action of a recency effect and the associative strength of the stimuli. The former supports choice of D, whereas the latter supports choice of B, thus determining equal choice of B and D in the tests.
Animals↗
A double dissociation of dorsal and ventral hippocampal function on a learning and memory task mediated by the dorso-lateral striatum.
The objectives of this research were to further delineate the neural circuits subserving proposed memory-based behavioural subsystems in the hippocampal formation. These studies were guided by anatomical evidence showing a topographical organization of the hippocampal formation. Briefly, perpendicular to the medial/lateral entorhinal cortex division there is a second system of parallel circuits that separates the dorsal and ventral hippocampus. Recent work from this laboratory has provided evidence that the hippocampus incidentally encodes a context-specific inhibitory association during acquisition of a visual discrimination task. One question that emerges from this dataset is whether the dorsal or ventral hippocampus makes a unique contribution to this newly described function. Rats with neurotoxic lesions of the dorsal or ventral hippocampus were assessed on the acquisition of the visual discrimination task. Following asymptotic performance they were given reversal training in either the same or a different context from the original training. The results showed that the context-specific inhibition effect is mediated by a circuit that includes the ventral but not the dorsal hippocampus. Results from a control procedure showed that rats with either dorso-lateral striatum damage or dorsal hippocampal lesions were impaired on a tactile/spatial discrimination. Taken together, the results represent a double dissociation of learning and memory function between the ventral and dorsal hippocampus. The formation of an incidental inhibitory association was dependent on ventral but not dorsal hippocampal circuitry, and the opposite dependence was found for the spatial component of a tactile/spatial discrimination.
Animals↗
Platelet-activating factor receptor-deficient mice are protected from experimental sleep apnea-induced learning deficits.
Intermittent hypoxia (IH) during sleep, a hallmark of sleep apnea, is associated with neurobehavioral impairments, regional neurodegeneration and increased oxidative stress and inflammation in rodents. Platelet-activating factor (PAF) is an important mediator of both normal neural plasticity and brain injury. We report that mice deficient in the cell surface receptor for PAF (PAFR-/-), a bioactive mediator of oxidative stress and inflammation, are protected from the spatial reference learning deficits associated with IH. Furthermore, PAFR-/- exhibit attenuated elevations in inflammatory signaling (cyclo-oxygenase-2 and inducible nitric oxide synthase activities), degradation of the ubiquitin-proteasome pathway and apoptosis observed in wild-type littermates (PAFR+/+) exposed to IH. Collectively, these findings indicate that inflammatory signaling and neurobehavioral impairments induced by IH are mediated through PAF receptors.
Animals↗
A phenotypic and molecular characterization of the fmr1-tm1Cgr fragile X mouse.
Fragile X Syndrome is the most common form of inherited mental retardation. It is also known for having a substantial behavioral morbidity, including autistic features. In humans, Fragile X Syndrome is almost always caused by inactivation of the X-linked FMR1 gene. A single knockout mouse model, fmr1-tm1Cgr, exists. In this report we further characterize the cognitive and behavioral phenotype of the fmr1-tm1Cgr Fragile X mouse through the use of F1 hybrid mice derived from two inbred strains (FVB/NJ and C57BL/6J). Use of F1 hybrids allows focus on the effects of the fmr1-tm1Cgr allele with reduced influence from recessive alleles present in the parental inbred strains. We find that the cognitive phenotype of fmr1-tm1Cgr mice, including measures of working memory and learning set formation that are known to be seriously impacted in humans with Fragile X Syndrome, are essentially normal. Further testing of inbred strains supports this conclusion. Thus, any fmr1-tm1Cgr cognitive deficit is surprisingly mild or absent. There is, however, clear support presented for a robust audiogenic seizure phenotype in all strains tested, as well as increased entries into the center of an open field. Finally, a molecular examination of the fmr1-tm1Cgr mouse shows that, contrary to common belief, it is not a molecular null. Implications of this finding for interpretation of the phenotype are discussed.
Animals↗
Resolution of stroke deficits following contralateral grafts of conditionally immortal neuroepithelial stem cells.
BACKGROUND AND PURPOSE: Grafts of MHP36 cells have previously been shown to reduce dysfunction after global ischemia in rats. To test their efficacy after focal ischemia, MHP36 cells were grafted 2 to 3 weeks after transient intraluminal middle cerebral artery occlusion (tMCAO) in rats. METHODS: MHP36 cells were implanted into the hemisphere contralateral to the lesion, with 8 deposits of 3 microL of cell suspension (25 000 cells per microliter). Sham grafted rats received equivalent volumes of vehicle. Three groups, sham-operated controls (n=11), MCAO+sham grafts (n=10), and MCAO+MHP36 grafts (n=11), were compared in 3 behavioral tests. RESULTS: In the bilateral asymmetry test, MCAO+MHP36 grafted rats exhibited neglect before grafting but subsequently showed no significant dysfunction, whereas MCAO+sham grafted rats showed stable sensorimotor deficits over 18 weeks relative to controls. MCAO+sham grafted rats demonstrated spontaneous motor asymmetry and increased rotational bias after injection of dopamine agonists. MCAO+MHP36 and control groups exhibited no bias in either spontaneous or drug-induced rotation. In contrast to motor recovery, MCAO+MHP36 grafted rats showed no improvement relative to MCAO+sham grafted rats in spatial learning and memory in the water maze. MCAO produced large striatal and cortical cavitations in both occluded groups. Lesion volume was significantly reduced (P<0.05) in the MCAO+MHP36 grafted group. The majority of MHP36 cells were identified within the intact grafted hemisphere. However, MHP36 cells were also seen in the cortex, striatum, and corpus callosum of the lesioned hemisphere. CONCLUSIONS: MHP36 cells may improve functional outcome after MCAO by assisting spontaneous reorganization in both the damaged and intact hemispheres.
Amphetamine↗
Toward optimal classifier system performance in non-Markov environments.
Wilson's (1994) bit-register memory scheme was incorporated into the XCS classifier system and investigated in a series of non-Markov environments. Two extensions to the scheme were important in obtaining near-optimal performance in the harder environments. The first was an exploration strategy in which exploration of external actions was probabilistic as in Markov environments, but internal "actions" (register settings) were selected deterministically. The second was use of a register having more bit-positions than were strictly necessary to resolve environmental aliasing. The origins and effects of the two extensions are discussed.
Algorithms↗
Limited impairment of learning performances in mice treated with cysteamine.
Cysteamine has been reported to disturb learning performance in rats. Our study was made to determine if this is also true in mice. Adult male ddY mice were subjected to a battery of learning tests following our standard experimental protocols. Cysteamine injected 30 min prior to the learning trial dose-dependently increased the number of errors in the testing trial of step-down test, and its effect was statistically significant at a dose of 200 mg/kg. In the lever press test, 200 mg/kg injection of cysteamine also suppressed the conditioned avoidance rate. However, no significant changes were observed in other tests. These results suggest that the learning disorder induced by cysteamine in mice is restricted to a specific type of behavioral performance. In conclusion, the mechanism by which cysteamine generates learning deficiency in mice may differ from that in rats.
Animals↗
Effects of post-training lesions in the hippocampus and the parietal cortex on idiothetic information processing in the rat.
Dead reckoning can be defined as the ability to navigate using idiothetic information based on self-movement cues without using allothetic information such as environmental cues. In the present study, we investigated the effects of hippocampal and parietal cortex lesions on homing behavior using dead reckoning in rats. Experimentally naive Wistar rats were trained with a homing task in which rats were required to take a food pellet from a cup in the arena and to return home with the pellet. After training, rats were divided into a control (CONT) group (n = 16), hippocampal lesioned (HIPP) group (n = 16), and parietal cortex lesioned (PARC) group (n = 16), and rats in the lesioned groups underwent surgery. After surgery, Test 1 (with four cups) and Test 2 (with one cup but the outgoing path was diverted by a barrier) were conducted. The HIPP group showed severe impairment in homing, but the performance of the PARC group did not differ from that of the CONT group. HIPP rats either approached wrong doors or ate the pellet in the arena. Circular statistics showed that homing directions of CONT and PARC rats showed concentration towards home, whereas those of HIPP rats did not. Our results exhibiting HIPP rats' failure in homing agree with many previous studies, but the results obtained from PARC rats were different from previous studies. These results indicate that the intact hippocampus is important for dead reckoning, but the role of the parietal cortex in dead reckoning is still not clear.
Animals↗
Attenuation of ischemia-induced cellular and behavioral deficits by X chromosome-linked inhibitor of apoptosis protein overexpression in the rat hippocampus.
Transient forebrain ischemia produced by four-vessel occlusion (4-VO) triggers the delayed death of CA1 neurons in the hippocampus, resulting in behavioral deficits of spatial learning performance. We demonstrate that CA1 neuronal loss induced by 4-VO (12 min) is preceded by a selective and marked elevation of catalytically active caspase-3 in these neurons, indicative of apoptosis. Virally mediated overexpression of the anti-apoptotic gene X chromosome-linked inhibitor of apoptosis protein (XIAP) prevented both the production of catalytically active caspase-3 and degeneration of CA1 neurons after transient forebrain ischemia. CA1 neurons protected in this manner appeared to function normally, as assessed by immunohistochemical detection of the neuronal activity marker nerve growth factor inducible-A and by spatial learning performance in the Morris water maze. These findings indicate that caspase-3 activation is a key event in ischemic neuronal death and that blockade of this event by XIAP overexpression permits CA1 neurons to survive and operate properly after an ischemic insult.
Animals↗
Blocking in the spatial domain with arrays of discrete landmarks.
A characteristic feature of associative conditioning is that learning a predictive relationship between two events can block later learning about an added event. It is not yet well established whether blocking occurs in the spatial domain or the circumstances in which it does. We now report, using rats trained to search for hidden food near landmarks in an open field arena, that blocking can occur in spatial learning. The animals noticed the added landmark at the start of the blocking phase and explored it, but either failed to incorporate it into their spatial map or developed a representation in which only some landmarks actually control behavior. Additionally, performance at asymptote was controlled by the shape of the landmark array rather than the individual landmarks comprising it, indicating that blocking in the spatial domain may represent a failure to alter the encoded geometry of a learned array.
Animals↗
Role of voltage-dependent calcium channel long-term potentiation (LTP) and NMDA LTP in spatial memory.
This experiment explores the role of two forms of long-term potentiation (LTP) in behavioral memory. NMDA and/or voltage-dependent calcium channels (VDCCs) were antagonized pharmacologically at levels that block nmdaLTP and vdccLTP, respectively, in rats learning an eight-arm radial maze task. Animals were trained twice a day for 11 d under the systemic influence of MK-801, verapamil, both drugs, or saline. During acquisition, the mixed drug group displayed significantly more working memory errors and reference memory errors than all other groups. The mixed drug group was markedly impaired on the first daily trial but improved dramatically on their second daily trial. After a 7 d delay, saline and MK-801 animals maintained their predelay level of performance. The performance of the verapamil groups declined significantly over the delay. These results demonstrate that: (1) vdccLTP is necessary for the retention of information over a 7 d period, (2) the blockade of both forms of LTP prevents the retention of information over a 21 hr period, and (3) blockade of both forms of LTP does not prevent the storing of information over a short period of time (3 hr).
Animals↗
3,4-methylenedioxymethamphetamine (ecstasy)-induced learning and memory impairments depend on the age of exposure during early development.
Use of 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) has increased dramatically in recent years, yet little is known about its effects on the developing brain. Neonatal rats were administered MDMA on days 1-10 or 11-20 (analogous to early and late human third trimester brain development). MDMA exposure had no effect on survival but did affect body weight gain during treatment. After treatment, body weight largely recovered to 90-95% of controls. MDMA exposure on days 11-20 resulted in dose-related impairments of sequential learning and spatial learning and memory, whereas neonatal rats exposed on days 1-10 showed almost no effects. At neither stage of exposure did MDMA-treated offspring show effects on swimming ability or cued learning. Brain region-specific dopamine, serotonin, and norepinephrine changes were small and were not correlated to learning changes. These findings suggest that MDMA may pose a previously unrecognized risk to the developing brain by inducing long-term deleterious effects on learning and memory.
3,4-Methylenedioxyamphetamine↗
[The expression levels of GIRK1 and IRK1 in memory deficit rats].
AIM: To study the expression level of GIRK1 and IRK1 in cerebral cortex after aggregated beta-amyloid peptide25-35 injection into the rat cerebral ventricle for different times. METHODS: To test the spatial learning and memory in Morris water maze. To observe GIRK1 and IRK1 expression levels by RT-PCR. RESULTS: In Morris water maze task, the latencies of beta-amyloid peptide treated rats were longer than those of the sham rars in the 4, 5, 8, 10 training periods ("student" t-test, P < 0.05). The expression levels of GIRK1 in beta-amyloid peptide injection day 1 and day 3 groups are decreased significantly compared with sham group (Tukey's test, P < 0.05) and there is no difference between beta-amyloid peptide injection day 17 group and sham group. IRK1 expression levels are no difference among the four groups. CONCLUSION: Injection of aggregated beta-amyloid peptide25-35 into rat cerebral ventricles can induce memory and potassium channel expression changes. Beta-amyloid peptide induced inhibition of GIRK1 expression may have some relations with brain dysfunction.
Amyloid beta-Peptides↗