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PubMed1996

Effects of some psychotropic agents on cognitive functions in rats.

The effects of some psychotropic agents were evaluated on cognitive function in rats. Acute administration of antipsychotic agents chlorpromazine, haloperidol or pimozide-all inhibited the active avoidance response as elicited by pole climbing test-the least effect being seen with pimozide. The antianxiety benzodiazepines, lorazepam and alprazolam, also attenuated active avoidance learning with the latter showing lesser effects. Maze task performance was differentially affected by these psychotropic drugs with maze traversing time being increased significantly after all drug treatment, except alprazolam.

Animals↗

PubMed1997

Manipulation of behavioral disorders in autoimmune mice via prolactin.

Autoimmune mice perform poorly in two-way active avoidance tasks, and the extent of this performance deficit appears to be related to the extent of autoimmunity following developmental manipulations. In the current study, the pituitary hormone prolactin, which has immune-enhancing effects, was used to manipulate this behavioral disorder in adulthood. Prolatinergic manipulation may be achieved by the use of dopaminergic drugs. In two experiments, autoimmune NZB X NZW F1 (BW) mice received either pimozide (PIM; a D2 antagonist) or bromocriptine (CB154; a dopamine agonist) in their drinking water. Control subjects received plain water. Following treatment, subjects were tested in an activity monitor, and active avoidance learning. Circulating PRL levels, as measured by RIA, were significantly increased by PIM and significantly decreased by CB154. Neither drug affected circulating levels of autoantibodies to DNA or cardiolipin, a phospholipid. In Experiment 1, in which mice were tested at 12 weeks of age, after 6 weeks of drug treatment, PIM treated animals of both sexes showed significantly more failures to escape the shock in avoidance conditioning, while CB154 did not have significant effects. In Experiment 2, in which mice were tested at 16 weeks of age, after 12 weeks of drug treatment, CB154 treated females (males were not tested) showed significantly fewer failures to escape, while PIM did not have significant effects. The effects of PRL on behavior, and its relation to immune system function, are discussed.

Animals↗

PubMed2001

Hyperactivity, neuromotor defects, and impaired learning and memory in a mouse model for metachromatic leukodystrophy.

Deficiency of arylsulfatase A (ASA) causes the autosomal recessive lipidosis, metachromatic leukodystrophy (MLD). Performance on tests of activity, motor ability and learning/memory was assessed in ASA-deficient mice and normal controls at 3, 6 and 12 months-of-age. ASA-deficient mice showed consistently increased cage activity in all age groups, whereas open field activity was increased only in the 3-month-old group. Motor coordination and equilibrium, as tested in the rotarod test, was impaired in 12-month-old ASA-deficient mice. Passive avoidance learning was tested in the step-through box. Performance on this test was impaired in the 12-month-old group only. Spatial learning and memory abilities were tested in the Morris water maze. Six-month-old ASA-deficient mice displayed slightly impaired hidden-platform acquisition performance. Three-month-old animals, on the other hand, did not show any acquisition or retention defect on this task, notwithstanding significantly reduced swimming velocity. Acquisition training, both in the hidden- and visible-platform conditions of the Morris water maze, and retention performance during the probe trials were impaired in 12-month-old ASA-deficient mice. The hyperactivity, motor incoordination and slowing, and the age-related learning/memory defects, reported here in ASA-deficient mice, may relate to the decline of neuromotor and cognitive functions in MLD patients, and could be used as correlative or outcome measures in the study of MLD pathophysiology and treatment.

Age Factors↗

PubMed2006

Effects of neonatal dexamethasone treatment on hippocampal synaptic function.

OBJECTIVE: Synthetic glucocorticoid dexamethasone (DEX) is frequently used as a therapeutic agent to lessen the morbidity of chronic lung disease in premature infants. Surprisingly, little is known about the long-term neurodevelopmental outcomes of this therapy. METHODS: Using a schedule of tapering doses of DEX similar to that used in premature infants, we examined the consequences of neonatal DEX treatment on hippocampal synaptic plasticity of infants and associative memory later in their lives. RESULTS: Neonatal DEX treatment changed the direction of synaptic plasticity, favoring low-frequency, stimulation-induced, long-term depression and opposing the induction of long-term potentiation by high-frequency stimulation in adolescent (5-week-old) rats, but these alterations disappeared in young adult (8-week-old) rats. The effects of DEX on long-term depression and long-term potentiation were found to correlate with an increase in the autophosphorylation of Ca(2+)/calmodulin-dependent protein kinase II and a decrease in the protein phosphatase 1 activity. Neonatal DEX treatment also disrupted memory retention in 5-week-old (but not 8-week-old) rats subjected to passive avoidance learning tasks. INTERPRETATION: These results suggest that neonatal DEX treatment alters hippocampal synaptic plasticity and contextual fear memory formation in later life, but these impairments apparently are not permanent.

Animals↗

PubMed2005

Facilitation of serotonergic activity and amnesia in rats caused by intravenous anesthetics.

BACKGROUND: Midazolam and propofol often provoke retrograde amnesia after recovery from anesthesia in humans. Because an increase in central serotonergic activity impairs learning and memory, the authors examined the relation between changes in the serotonergic activity caused by intravenous anesthetics and memory. METHODS: Changes in extracellular concentrations of monoamines and their metabolites were investigated in rat striatum by a microdialysis procedure, and the effects of intraperitoneal injections of midazolam (5 mg/kg), propofol (60 mg/kg), and pentobarbital (15 mg/kg) were then examined. To evaluate the behavioral alteration with these agents, the authors used a step-through passive avoidance test. RESULTS: Midazolam and propofol slightly increased the extracellular concentration of 5-hydroxytryptamine in the striatum, although pentobarbital did not produce any changes. Midazolam and propofol increased the extracellular concentration of 5-hydroxyindoleacetic acid, a metabolite of 5-hydroxytryptamine, with the peak values each 138% and 138% of that in saline-injected animals, respectively. However, pentobarbital decreased the 5-hydroxyindoleacetic acid concentration to 61% of that in the saline group. Administration of midazolam or propofol immediately after the completing the passive avoidance learning reduced step-through latencies after 24 h, although pentobarbital-injected animals maintained a consistent performance. The effects of midazolam and propofol on step-through latencies were completely antagonized by intracerebroventricular administration of spiroxatrine (5 microg), a 5-hydroxytryptamine 1A antagonist, 30 min before training. CONCLUSIONS: Midazolam and propofol increased central serotonergic activity and provoked retrograde amnesia. Because amnesia was completely diminished by a 5-hydroxytryptamine antagonist, facilitation of the serotonergic system may be involved in retrograde amnesia caused by these agents.

Amnesia↗

PubMed1984

Diphenylhydantoin extension of short-term and intermediate stages of memory.

Diphenylhydantoin was shown to extend the duration of maximum availability of both short-term and intermediate memory in day-old chicks following a single trial passive avoidance learning task. Diphenylhydantoin also extended the time of susceptibility of long-term memory to inhibition by cyloheximide, suggesting that the extention of the life of intermediate memory was accompanied by a delay in long-term memory formation. Furthermore, while diphenylhydantoin counteracted amnesia induced by cycloheximide given 5 min before or immediately after learning, it had no effect on amnesia induced by cycloheximide administered 5 min or later after learning. For the latter, a second injection of diphenylhydantoin was necessary. This is consistent with the argument that the first injection of diphenylhydantoin extended the life of intermediate memory and delayed the formation of long-term memory.

Animals↗

PubMed1984

Passive-avoidance behavior of spontaneously hypertensive rats.

Spontaneously hypertensive rate (SHR) generally exhibit higher performance in avoidance tasks than Wistar-Kyoto control rats (WKY) do. The SHR are more active than the WKY after transfer to a novel environment and after electric footshocks. The present study examined the performance, behavior, and plasma corticosterone of young male SHR and WKY in a passive-avoidance task in which high levels of locomotor activity do not facilitate performance. The effects of three levels of discriminability of the safe area were studied. Passive-avoidance performance was statistically significantly lower in the SHR, but the difference was small. There was no difference between the SHR and the WKY in post-test plasma-corticosterone levels, and there was no relationship between ambulation and plasma-corticosterone levels. The behavioral differences between the SHR and the WKY varied as a function of the discriminability of the safe area. Specifically, in the low-discriminability condition, ambulation, but not rearings, was equally suppressed in the SHR as in the WKY and there was no difference in immobility. In the high-discriminability condition the SHR exhibited more ambulation, more rearing, and less immobility than the WKY. These data confirm that the SHR exhibit an increased tendency for facilitation of locomotor activity during activation compared to the WKY. Because the passive-avoidance performance of the SHR was lower than that of the WKY, these data suggest that previous reports of superior avoidance learning in the SHR reflect their elevated level of locomotor activity rather than an improved ability to acquire conditioned responses. Ability to discriminate stimuli seems to be normal in the SHR since ambulation was modified according to stimulus parameters.

Animals↗

PubMed1998

Increased immunogold labelling of neural cell adhesion molecule isoforms in synaptic active zones of the chick striatum 5-6 hours after one-trial passive avoidance training.

An area of the chick striatum, the lobus parolfactorius plays an important role in one-trial passive avoidance learning tasks. In the present study we report evidence that 5-6 h post-training, a significantly higher proportion of synaptic active zones in this area contain labelled epitopes of the neural cell adhesion molecule, with the greatest occurrence of labels at the edges of active zone profiles (in both control and trained groups). This suggests that there is a period after training when expression of the neural cell adhesion molecule in synaptic membranes almost doubles, and that events at active zone edges may play a specific role in mechanisms of synaptic adhesion. Cellular mechanisms of long-term memory formation are believed to include alterations in neural circuitry at the synaptic level. The involvement of the neural cell adhesion molecule (NCAM) in functional synaptic modifications has been demonstrated using a number of physiological models. Performance of rats in the Morris water maze, a spatial learning paradigm which requires the hippocampus, is impaired by either intraventricular injection of NCAM antibodies, or injection into the hippocampus of an enzyme which increases homophilic adhesion of the molecule, due to the removal of polysialic acid residuals from extracellular NCAM domains. In addition, intraventricular injections of anti-NCAM antibodies 6-8 h post-training were shown to impair memory for a one-trial passive avoidance task in the rat. An avoidance training model in the one-day-old chick indicates a similar time window, 5-6 h post-training during which memory for the task can be impaired by intraventricular injection of NCAM antibodies. In the hyperstriatum ventrale, a chick forebrain area involved in the passive avoidance task. subtle changes in the distribution pattern, but not density of NCAM molecules in synaptic membranes were revealed 5-6 h post-training. However, on the basis of studies of synaptic morphometry, a region of striatum, the lobus parolfactorius (LPO), appears to play a more important role in longer term memory storage for the task.

Animals↗

PubMed1989

Interrelationship of brain edema, motor deficits, and memory impairment in rats exposed to focal ischemia.

We investigated the relations of brain edema, ion shifts, motor performance, and memory impairment using a focal ischemia model in rats. Cortical infarction was produced by ligation of the middle cerebral artery and the ipsilateral common carotid artery combined with temporary occlusion of the contralateral common carotid artery for 1 hour. Water content and sodium, potassium, and calcium concentrations were measured until Day 14 after the ischemic insult. Significant edema formation was observed; it peaked on Day 3 (p less than 0.001) and then declined. The tissue sodium concentration changed in a manner similar to that of water content, but the tissue potassium concentration changed in an opposite fashion. Massive accumulation of calcium was detected as early as Day 1 after ischemia (almost four times the normal level). The increased calcium concentration was sustained even up to Day 14. Motor performance examinations performed on Day 3, including inclined plane, balance beam, and prehensile tests, demonstrated significantly reduced (p less than 0.001) motor ability that did recover even by Day 7. Passive avoidance learning was carried out on Day 2, followed by a memory retention test on Day 3. Significant memory dysfunction was observed in ischemic compared with sham-operated rats (p less than 0.001). A high correlation coefficient (r = 0.91, p less than 0.01, n = 13) was obtained between water content and calcium concentration on Day 3. Both the total motor score and the degree of disturbance of the passive avoidance reaction also correlated well with water content.

Animals↗

PubMed1989

Effects of a new thyrotropin-releasing hormone analogue administered in rats 1 week after middle cerebral artery occlusion.

We observed the effects of a new thyrotropin-releasing hormone analogue, YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]-L-histidyl-L-prolinamide dihydrate) on behavioral changes in 26 rats subjected to middle cerebral artery occlusion. The administration of 0.1 mg/kg i.p. YM-14673 was started 1 week after occlusion and was repeated daily for 2 weeks. YM-14673 significantly accelerated the recovery of neurologic deficits and ameliorated the disturbance of passive avoidance learning. Thus, YM-14673 improved behavioral response in a model of chronic focal cerebral ischemia. The availability of a chronic middle cerebral artery occlusion model for the evaluation of drugs is also discussed.

Animals↗

PubMed1998

Motor and learning dysfunction during postnatal development in mice defective in dopamine neuronal transmission.

Mice lacking expression of tyrosine hydroxylase (TH), the first and rate-limiting enzyme of the catecholamine biosynthetic pathway, in dopaminergic neuronal cell types were generated by a transgenic rescue approach to clarify the role of dopamine signaling during postnatal development. Introduction of the TH transgene directed by the dopamine beta-hydroxylase gene promoter into TH knockout mice restored noradrenaline and adrenaline synthesis, preventing perinatal lethality and cardiac dysfunction in the knockout mice. Lack of TH expression in the cells that normally express the dopaminergic phenotype resulted in a marked reduction of dopamine accumulation in the tissues, which led to multiple behavioral abnormalities at the juvenile stage. These abnormalities were characterized by a reduction in spontaneous locomotor activity, blockade of methamphetamine-induced hyperactivity, cataleptic behavior, and defects in active avoidance learning. In contrast, development of the pituitary gland as well as production and secretion of the pituitary peptide hormones dependent on hypothalamic dopaminergic control were normally maintained, despite defective dopamine synthesis. These results demonstrate that dopamine neurotransmission is essential for controlling spontaneous and voluntary movement and associative learning during postnatal development through the nigrostriatal and mesocorticolimbic pathways.

Animals↗

PubMed2004

Physiological and behavioural responses to duodenal pain in freely moving rats.

Luminal distention of the intestine can be aversive in humans and laboratory animals, and hypersensitivity to distention is found in functional gastrointestinal disorders. Current animal models either require anaesthesia or acute balloon intubation or use implanted balloons of irritant materials, for which the aversive quality of distention and physiological responses have not been well characterised. We report here that silicone balloon catheters implanted in the duodenum via the stomach have long patency without obvious tissue damage. Balloon inflation in freely moving rats caused passive avoidance learning and classic 'pain' postures, as well as graded cardiovascular responses which can be recorded telemetrically. The method should make long-lasting studies of pharmacological and environmental effects on visceral sensitivity more feasible.

Abdominal Pain↗

PubMed1988

Synthesis and cognition activating properties of some mono- and bicyclic lactam derivatives.

Upon reductive cyclization cyano esters 2, 3, and 9 yielded piperidones and perhydropyrrolo[3,4-c]pyridine lactams, generally as a mixture of diasteromeric cis-trans forms. X-ray crystallographic analyses were carried out on bicyclic dilactam derivatives 6 and 10, and a cis configuration at the ring junction was determined in both cases. A series of neuropsychopharmacological tests performed on the title compounds indicated that they are generally nontoxic even at high doses (up to 1000 mg/kg ip). The cognition activating properties of lactams 4, 5, 6, and 10 were evaluated in enhancing retention for passive avoidance learning in rats without and after electroconvulsive shock (ECS); compounds 5 and 10 were found to be more potent than piracetam in the amnesia-reversal testing.

Amnesia↗

PubMed1996

Administration of lanthanum chloride following a reminder induces a transient loss of memory retrieval in day-old chicks.

Lanthanum chloride (5.0 mM) administered immediately after a visual reminder presented to day-old chickens between 7.5 min and 48 h following a single trial passive avoidance learning task produced an immediate but transient loss of memory on retention test, an effect not observed in the absence of a reminder. The duration of the transient deficit was relatively stable with lanthanum chloride consistently inducing a loss of memory that was evident 5 min after the reminder, with recovery by 10-15 min. The results suggest that, for a period of at least up to 48 h after passive avoidance training, the activation of memory retrieval by a reminder stimulus may lead to processes which are sensitive to inhibition by the calcium channel antagonist lanthanum chloride. These results extend previously reported findings implicating the involvement of glutamate-sensitive channels in a transient memory process that is also activated as a result of a reminder stimulus, but that is no longer present 48 h after training. The glutamate-sensitive mechanism appears to be a secondary mechanism activated following memory retrieval and to be dependent on the level of memory consolidation that the memory for the original experience has undergone. The results presented here suggest that lanthanum chloride, a calcium channel antagonist, inhibits memory retrieval in the day-old chick. This effect implicates calcium channel mediated processes in immediate memory recall. Further, the results suggest the lanthanum inhibits a primary mechanism, that precedes that glutamate-sensitive mechanism identified previously and that both are dependent on the activation of memory retrieval by a reminder.

Animals↗

PubMedDate not supplied

Brain MAP-2 phosphorylation is decreased following prenatal alcohol exposure in rats.

The effects of prenatal alcohol treatment on the development and in vitro phosphorylation of specific neuronal phosphoproteins isolated from the frontal cortex and hippocampus of rat brains were studied. In vitro phosphorylation of microtubule-associated protein-2 (MAP-2) was decreased in the frontal cortex but not the hippocampus of animals exposed prenatally to alcohol. Phosphorylation of additional phosphoproteins, including tau proteins, Synapsin I, and GAP-43, was not affected by prenatal alcohol exposure. Littermates of animals used for the phosphorylation assays showed impaired passive avoidance learning. These data demonstrate that the previously reported structural changes in the development of the cerebral cortex following prenatal alcohol exposure and behavioral deficits are accompanied by changes in the phosphorylation of the important cytoskeletal protein MAP-2.

Animals↗

PubMed1986

Retrograde memory enhancement by diazepam: its relation to anterograde amnesia, and some clinical implications.

The effect of diazepam on retention of an inhibitory avoidance task was investigated in mice. In Experiment 1, animals were trained in this task, and tested for retention 24 h later. The mice received, 20 min after training, an IP injection of either diazepam (2 mg/kg) or saline; half of the mice in each treatment group were exposed, 40 min after avoidance training (and 20 min after the injections) to a Y maze. Exposure to the Y maze disrupted retention of the avoidance task in the saline-treated animals, and enhanced it in the diazepam-treated mice. Retention of habituation to the Y maze was impaired in the diazepam group. The effect can be explained by an interaction of the drug with the Y maze, by which exposure to the Y maze became facilitatory, instead of deleterious, to retention of the avoidance task. This may or may not be related to anterograde amnesia for the Y maze; and may be related to effects of diazepam seen in clinical practice. In Experiment 2, diazepam was given prior to, instead of after, inhibitory avoidance training; it caused anterograde amnesia for this task, which was not reversed by pre-test diazepam, and was therefore not due to state dependency. In conclusion, the effect of diazepam on inhibitory avoidance learning depends on the time at which the drug is given. A pretraining injection causes amnesia, whereas a post-training injection, while ineffective per se, may facilitate retention of the task when it is followed by exposure to a habituation procedure.

Amnesia↗

PubMed1978

Effects of ethanol on pregnant rats and their offspring.

Pregnant rats were intubated with either 1.0 or 2.0 g/kg of ethanol daily throughout gestation. Pair-fed vehicle-treated, and nontreated rats fed ad libitum, served as control groups for ethanol-treated animals. Ethanol treatment reduced food and water consumption and attenuated the gain in body weight of pregnant animals relative to nontreated animals fed ad libitum. Litter size, litter weight, and the mean weight per pup were reduced in both the ethanol-treated and pair-fed control groups. There was no evidence of gross malformations in any of the off-spring. Since the reduction in litter size and litter weights did not differ significantly between ethanol-treated and pair-fed controls, the effects of treatment with ethanol appeared to be related to a reduction in maternal intake of calories rather than to the direct effect of ethanol on the developing fetus. There were no significant differences between any of the groups of offspring on one-way shock avoidance learning, water maze escape learning, spontaneous alternation, or brightness discrimination learning in tests beginning at 75 days of age. Thus, at the doses of alcohol used in this study, there was no evidence of behavioral teratogenesis comparable to that reported for higher doses in animals or in man characterized by the fetal alcohol syndrome.

Animals↗

PubMed1997

Intra-septal infusions of glucose potentiate inhibitory avoidance deficits when co-infused with the GABA agonist muscimol.

This experiment examined the effects of co-infusions of glucose with the gamma-aminobutyric acid (GABA) agonist muscimol into the medial septum on memory for inhibitory avoidance learning. Co-infusions of muscimol (3 nmol) and glucose (33 nmol) impaired memory, but neither drug did so when administered alone. Thus, although glucose typically reverses memory deficits, these results indicate that glucose potentiates the memory-impairing effects of a GABA agonist.

Animals↗