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PubMedDate not supplied

Anxiolytic and memory improving activity of fluoxetine.

The anxiolytic and memory improving effects of fluoxetine, a new antidepressant drug, were investigated in rats. Anxiolytic activity was examined using Crowley's "two compartment exploratory test". Memory was assayed in the response passive avoidance test (RPAT) and labyrinth test. Wistar rats were used in all experiments. They were given fluoxetine hydrochloride (5 mg/kg po) and scopolamine hydrobromide at the dose of 0.5 mg/kg, sc. It was found that the drug has a high anxiolytic activity after the first administration. Thereafter however, the anxiolytic effect gradually decreased and 28 days later it was no longer present. In memory testing experiments (RPAT and labyrinth test) fluoxetine improved the performance of memory task and up to 14 days there were no signs of tolerance development. The authors discuss the possibility of involvement of the anxiolytic and memory improving effects of fluoxetine in the antidepressant action of the drug.

Animals↗

PubMed1999

Functionally dissociating aspects of event memory: the effects of combined perirhinal and postrhinal cortex lesions on object and place memory in the rat.

Reciprocal interactions between the hippocampus and the perirhinal and parahippocampal cortices form core components of a proposed temporal lobe memory system. For this reason, the involvement of the hippocampus in event memory is thought to depend on its connections with these cortical areas. Contrary to these predictions, we found that NMDA-induced lesions of the putative rat homologs of these cortical areas (perirhinal plus postrhinal cortices) did not impair performance on two allocentric spatial tasks highly sensitive to hippocampal dysfunction. Remarkably, for one of the tasks there was evidence of a facilitation of performance. The same cortical lesions did, however, disrupt spontaneous object recognition and object discrimination reversal learning but spared initial acquisition of the discrimination. This pattern of results reveals important dissociations between different aspects of memory within the temporal lobe. Furthermore, it shows that the perirhinal-postrhinal cortex is not a necessary route for spatial information reaching the hippocampus and that object familiarity-novelty detection depends on different neural substrates than do other aspects of event memory.

Animals↗

PubMedDate not supplied

Functional deficits following neonatal dopamine depletion and isolation housing: circular water maze acquisition under pre-exposure conditions and motor activity.

Seven experiments and several behavioural tests were performed to study the effects of housing condition and experimental test conditions upon the behavioural responses and performance of adult rats neonatally treated with 6-hydroxydopamine (6-OHDA, 100 ug intracisternally, i.c.) or with vehicle. Postnatal 6-OHDA induced locomotor and total activity hyperactivity and deficits in navigational learning in a circular swim maze that were blocked by pretreatment with a dopamine (DA) reuptake inhibitor but not a noradrenaline (NA) reuptake inhibitor. Isolation-housing induced deficits in maze learning performance. Grouped housing improved the maze learning performance of 6-OHDA treated rats whereas vehicle treated rats that were isolation housed performed better following latent learning (LL) pre-exposure trials. 6-OHDA treated rats that received both Grouped housing and latent learning trials performed better on the spatial navigation task than those that received Grouped housing but no latent learning or Isolation housing and latent learning. Analysis of habituation quotients indicated marked deficits by 6-OHDA-treated rats suggesting inability to acquire this simple, nonassociative form of learning. Methylphenidate increased all three parameters of motor activity: locomotion, rearing and total activity, in both Isolation-housed and Group-housed rats from 60- to 90- or 120-min post-injection. NDO 008 induced variable and parameter-dependent effects: locomotion was elevated initially in both Isolated and Grouped rats by the compound and then reduced in the Isolated rats only whereas total activity was only elevated initially in the Isolated rats and unaffected in the Grouped rats. Rearing behaviour was reduced markedly, directly post-injection, in the Isolation-housed rats. DA, DOPAC and HVA concentrations in the striatum, nucleus accumbens, olfactory tubercle and midbrain were reduced but most markedly in the striatum. 5-Hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) concentrations were elevated in the striatum, nucleus accumbens (not 5-HIAA) and olfactory tubercle.

Journal Article↗

PubMed2001

Effects of ectopias and their cortical location on several measures of learning in BXSB mice.

About half of BXSB/MpJ-Yaa mice have ectopias, which are misplaced clusters of neurons located in layer I of cortex. This study replicated several previous findings showing that there are learning differences between mice with ectopias and those without. In addition, we had sufficient numbers of ectopic mice to investigate if ectopics learned differently depending on the cortical location of the ectopia(s). Mice with at least one ectopia located in prefrontal cortex were initially impaired in learning the Morris maze, as well as relearning the Lashley maze when it was inverted, but learned better in the radial-arm maze when compared to ectopic mice with ectopias located in nonprefrontal regions of cortex. Mice with at least one ectopia in motor cortex learned the Lashley maze better than mice with ectopias located outside motor cortex. In sum, the cortical location of the ectopia(s) affected learning performance in certain tasks within the ectopic group, but regardless of the cortical location of the ectopia(s), ectopics still learned differently than nonectopics in several tasks.

Animals↗

PubMed1996

Evidence for a paradoxical sleep window for place learning in the Morris water maze.

Sprague-Dawley rats were given 4 consecutive days of training in the hidden platform version of the Morris water maze. They were then given paradoxical sleep deprivation (PSD) for 12 h either immediately after each training session or after a 12-h delay. The former group showed impaired learning on the second day of training compared to the 12-h-delayed PSD group or a nondeprived control group. In a second experiment, three groups of rats were trained as before and then given PSD for a 4-h interval beginning either immediately after, 4 h after, or 8 h after the end of each training session. Only rats exposed to PSD during the period beginning 4 h after the end of training each day showed an acquisition deficit. In a third experiment, rats were trained in a visible platform version of the water maze and exposed to PSD for a 12-h period either beginning immediately after the last training trial each day or after a 12-h rest delay. Neither of these groups was impaired on the task compared to a non-PSD control group. These results suggest that there is a PS window for place, but not cue, learning in the Morris water maze.

Animals↗

PubMed2002

Conceptual, spatial, and cue learning in the Morris water maze in fast or slow kindling rats: attention deficit comorbidity.

Rat lines selectively bred for differences in amygdala excitability, manifested by "fast" or "slow" kindling epileptogenesis, display several comorbid features related to anxiety and learning. To assess the nature of the learning deficits in fast kindling rats, performance was evaluated in several variants of a Morris water-maze test. Regardless of whether the location of the platform was fixed or varied over days (matching-to-place task), the fast rats displayed inferior performance, suggesting both working and reference memory impairments. Furthermore, when the position of the platform was altered after the response was acquired, fast rats were more persistent in emitting the previously acquired response. The poor performance of fast rats was also evident in both cued and uncued tasks, indicating that their disturbed learning was not simply a reflection of a spatial deficit. Moreover, fast rats could be easily distracted by irrelevant cues, suggesting that these animals suffered from an attentional disturbance. Interestingly, when rats received several training trials with the platform elevated, permitting them to develop the concept of facile escape, the performance of fast rats improved greatly. The performance disturbance in fast rats may reflect difficulties in forming a conceptual framework under conditions involving some degree of ambiguity, as well as greater distractibility by irrelevant cues. These various attributes of the fast rats may serve as a potentially useful animal model of disorders characterized by an attention deficit.

Amygdala↗

PubMed1991

Differential involvement of anterior and posterior cingulate cortices in spatial discriminative learning in a T-maze in mice.

The contribution of the anterior and posterior cingulate cortical areas to spatial learning and memory was examined in mice using a behavioral paradigm based on a spatial discrimination task in a T-maze. Multiple injections of small amounts of ibotenic acid were used to produce fiber-sparing lesions of either the anterior (ACC) or the posterior (PCC) cingulate area. Mice with ACC lesions, though learning the initial acquisition and first reversal of the discrimination at about the normal rate, were impaired during the subsequent four reversal sessions. In contrast to control mice, they failed to improve their performance from the first to the last session. Nevertheless, when later required to repeatedly learn the same discrimination over several days (repetitive testing), animals with ACC lesions no longer exhibited any learning deficit. The converse pattern of results was found in mice with PCC lesions. These animals performed much more poorly than control animals during the acquisition and first reversal of the discrimination, but displayed remarkable improvement over the subsequent four reversal sessions, gradually overcoming their initial impairment. However, when later submitted to repetitive testing, these animals again showed a substantial learning deficit. Neither ACC nor PCC cingulate lesions significantly affected the animals' retention capacities as measured by single test-trials over a 24-h interval. Yet, mice with PCC lesions were retarded in reversal learning after a long intersession interval (10 days), indicating that PCC, but not ACC, lesions did interfere with some long-term retention processes. These results imply that the ACC, as a part of the medial frontal cortex, may play a crucial role in temporally ordering a series of spatial responses, whereas the PCC seems to contribute to the formation and retention of each individual spatial response, probably by transmitting information from limbic structures such as the anterior thalamus and hippocampal formation to posterior neocortical association areas.

Adaptation, Psychological↗

PubMed2003

Lobeline-induced learning improvement of rats in the radial-arm maze.

Lobeline is a nicotinic ligand with some nicotine-like effects, but with some atypical effects as well, including actions as a nicotinic antagonist. Lobeline, like nicotine, has been found to significantly improve memory function as well as provide anxiolytic-like effects in the elevated plus maze. Lobeline effects on learning remain to be fully characterized. Nicotine has been found to improve learning of shock avoidance tasks. Other nicotinic agonists also have been shown to improve learning performance. However, this effect is limited. In some tasks, nicotine has been found to cause deficits. In the current study, effects of lobeline and nicotine injections were assessed in a repeated acquisition procedure in the radial-arm maze for 3 weeks of drug administration. Lobeline (0.3 and 0.9 mg/kg) improved learning on the radial-arm maze. Neither nicotine dose (0.1 and 0.3 mg/kg) improved learning. This nicotine dose range was previously found to improve post-acquisition working memory performance in the radial-arm maze. The atypical effects of lobeline may underlie its greater efficacy than nicotine for improving repeated acquisition. The effect of lobeline improving learning may be useful in the development of novel treatments for learning deficits.

Animals↗

PubMed1996

Stereoselective effects of (R)- and (S)-zacopride on cognitive performance in a spatial navigation task in rats.

In the present studies we investigated the actions of (R)- and (S)-zacopride, potent 5-HT3 receptor antagonists with 5-HT4 receptor agonists properties, on performance in a spatial learning and memory task in rats, the Morris water maze. A significant cognitive/performance deficit, as indicated by the increased escape latency across several trials, was produced by systemic administration of the muscarinic receptor antagonist atropine (30 mg/kg, IP). (R)-zacopride (0.001-1 microgram/kg, but not 10 or 100 micrograms/kg) significantly reduced escape latency in atropine-treated animals. (S)-Zacopride was inactive over the entire dose range examined (0.001-100 micrograms/kg, i.p.). Moreover, pretreatment with (S)-zacopride (1 or 100 micrograms/kg) did not alter the procognitive effects of (R)-zacopride (1 microgram/kg). These data demonstrate that the cognition enhancing properties of zacopride in this model of cholinergic hypofunction are exclusive to its (R)-enantiomer and imply that this action is unrelated to 5-HT, receptor antagonism or 5-HT4 receptor agonism. The possibility that the procognitive effects of (R)-zacopride may be related to actions at the novel "(R)-zacopride site" is discussed.

Animals↗

PubMed2006

Phencyclidine affects memory in a nitric oxide-dependent manner: working and reference memory.

Phencyclidine (PCP), a non-competitive NMDA receptor antagonist, was used to model schizophrenia-like cognitive dysfunctions of learning and memory in rats using the Morris water maze model for spatial memory. A protocol introduced by Baldi and co-workers was used to distinguish working memory from reference memory. Male Sprague-Dawley rats were administered PCP (2.0 mg/kg) before the first swimming trial on each of five spatial memory acquisition days, either alone or after pre-treatment with the nitric oxide synthase inhibitor, L-NAME (10 mg/kg). Probe tests for memory were conducted before and after each acquisition session. The results showed that PCP disrupted the acquisition of both working and reference memory. Pre-treatment with L-NAME reversed both these effects of PCP. L-NAME treatment by itself did not significantly alter either acquisition or retention of spatial memory.

Analysis of Variance↗

PubMed2005

Dual effects of bryostatin-1 on spatial memory and depression.

Dementia and depression are clinical symptoms commonly associated in patients. Emerging evidence suggests that the two diseases share many profiles in their development and underlying neural/molecular mechanisms. Thus, interest is raised in developing new classes of antidepressant agents with activity of cognitive enhancement. Here, we show that bryostatin-1, a protein kinase C substrate activator, at bilateral intracerebroventricular doses of 0.64 or 2 pmol/site, significantly enhanced learning and memory of rats in a spatial water maze task. When applied at the doses at which it exhibits memory-enhancing activity, bryostatin-1 showed a significant antidepressant activity, as determined in an open space swim test. Both effects were not observed when a smaller dose was administered and were largely eliminated by co-administration of 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), a protein kinase C inhibitor. These results support the hypothesis that memory processing and mood regulation share common neural mechanisms. Restoring impaired mood regulation with antidepressant agents that also exhibit memory-enhancing activity may represent one of the new strategies in the fight against depression associated with memory impairments.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2004

Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function.

Voluntary exercise leads to an upregulation of brain-derived neurotrophic factor (BDNF) and associated proteins involved in synaptic function. Activity-induced enhancement of neuroplasticity may be considered for the treatment of traumatic brain injury (TBI). Given that during the first postinjury week the brain is undergoing dynamic restorative processes and energetic changes that may influence the outcome of exercise, we evaluated the effects of acute and delayed exercise following experimental TBI. Male Sprague-Dawley rats underwent either sham or lateral fluid-percussion injury (FPI) and were housed with or without access to a running wheel (RW) from postinjury days 0-6 (acute) or 14-20 (delayed). FPI alone resulted in significantly elevated levels of hippocampal phosphorylated synapsin I and phosphorylated cyclic AMP response element-binding-protein (CREB) at postinjury day 7, of which phosphorylated CREB remained elevated at postinjury day 21. Sham and delayed FPI-RW rats showed increased levels of BDNF, following exercise. Exercise also increased phosphorylated synapsin I and CREB in sham rats. In contrast to shams, the acutely exercised FPI rats failed to show activity-dependent BDNF upregulation and had significant decreases of phosphorylated synapsin I and total CREB. Additional rats were cognitively assessed (learning acquisition and memory) by utilizing the Morris water maze after acute or delayed RW exposure. Shams and delayed FPI-RW animals benefited from exercise, as indicated by a significant decrease in the number of trials to criterion (ability to locate the platform in 7 s or less for four consecutive trials), compared with the delayed FPI-sedentary rats. In contrast, cognitive performance in the acute FPI-RW rats was significantly impaired compared with all the other groups. These results suggest that voluntary exercise can endogenously upregulate BDNF and enhance recovery when it is delayed after TBI. However, when exercise is administered to soon after TBI, the molecular response to exercise is disrupted and recovery may be delayed.

Animals↗

PubMed2004

Effect of food deprivation during early development on cognition and neurogenesis in the rat.

Food deprivation has been recognized as having pronounced beneficial effects in adult animals, increasing longevity, reducing seizure susceptibility, and enhancing resistance to neurotoxins. It is not known whether food deprivation in developing animals is neuroprotective or harmful. To evaluate the effects of food deprivation on brain development, we evaluated visual-spatial learning and memory and neurogenesis in the dentate gyrus of the hippocampus in food-deprived (FD) and well-fed (WF) rats. To induce food deprivation, pups were removed from their dams for 12 hours per day from Postnatal Day (P) 2 to P19. FD and WF rat pups were then subjected to status epilepticus (SE) induced by lithium-pilocarpine at P20. After SE, neurogenesis was measured, while in another group of P38 rats, learning and memory were evaluated using the Morris water maze. Food deprivation was found to reduce neurogenesis when assessed after the period of food deprivation. Although SE reduced neurogenesis in the WF animals, it had little effect additional to food deprivation on neurogenesis in the FD rats. Compared with the WF group, FD rats had a mild impairment in memory in the water maze testing after SE. Our study demonstrates that food deprivation during the neonatal period in rats is associated with a decrease in neurogenesis and mild impairment of visual-spatial memory. Although SE decreased neurogenesis in the WF group, in FD animals, SE did not reduce neurogenesis more than what was seen with food deprivation alone. Our results suggest that although food deprivation during early development reduces dentate gyrus neurogenesis, the reduced neurogenesis is not a major factor in cognitive impairment after SE in FD rats.

Age Factors↗

PubMed2003

Hippocampal serotonergic damage induced by MDMA (ecstasy): effects on spatial learning.

3,4-Methylenedioxymethamphetamine (MDMA) use has been associated with a decline in various aspects of mnemonic function in humans. We therefore postulated that MDMA-induced damage of serotonergic nerve terminals would alter hippocampal processing. Seven days following treatment with MDMA (2 x 20 mg/kg sc, given 12 h apart), rat spatial learning and memory were tested utilizing the Morris water maze (MWM). No statistical differences were found in MWM platform acquisition latency or pathlength between controls and MDMA-treated animals. Probe trials revealed significantly higher proximity score averages and significantly reduced preference for the target quadrant in the MDMA-treated animals. MDMA treatment resulted in significant reduction (34%) in hippocampal serotonin (5-HT) levels 14 days after initial treatment. The findings of this study demonstrate that hippocampal serotonergic lesions induced by MDMA may be ostensibly linked to a reference memory deficit in rats tested with the MWM.

Animals↗

PubMed1999

Working memory deficits induced by single but not repeated exposures to domoic acid.

Single injections of domoic acid, given either intraperitoneally to mice or directly into the hippocampal formation of rats, have been shown to impair learning on the place version of the Morris water maze task and the eight arm radial maze task. The present study was designed to test whether both single and repeated exposures of intraperitoneally administered domoic acid (1.0 or 2.0 mg/kg) impair spatial working memory in mice on a delayed matching-to-sample task. DBA strain mice were given a series of four injections over a 7-day period consisting of either saline or one of two doses of domoic acid. During the 18 days of testing, each subject was given one trial per day consisting of one information run, followed by three test runs. On non-alternation days (days in which the correct response was the same as the preceding day) the saline injected group significantly outperformed the single injection 2.0 mg/kg domoic acid group. This indicates that domoic acid-treated animals were incapable of forming a memory that persisted for 24 h and hence were less able to utilize the prior day's experience. However, the repeated exposure groups did not perform as poorly on non-alternation days than the single exposure groups, indicating that domoic acid may affect multiple mechanisms involved in memory consolidation.

Animals↗

PubMedDate not supplied

Prenatal cocaine and/or nicotine exposure in rats: preliminary findings on long-term cognitive outcome and genital development at birth.

Prenatal cocaine or nicotine exposure is associated with a variety of teratogenic effects. The current study was conducted to determine their effects alone and in combination on cognitive function and sexual differentiation. Pregnant Long-Evans rats (N = 19) were exposed to either cocaine (15 mg/kg/dose b.i.d. SC on GD 8-20); nicotine (4 mg/kg/day continuous SC infusion on GD 4-20); both nicotine + cocaine; or vehicle only. Birth weight and anogenital distance (AGD) were measured in all pups at birth. Learning and memory were tested in the Morris water maze (MWM) during prepubertal and pubertal ages in five daily consecutive sessions and a sixth session 1 week later and in the radial-arm maze (RAM) during adulthood. In the RAM, a drug challenge of the beta-noradrenergic antagonist propranolol (10-20 mg/kg) was given after acquisition training. Maternal weight gain was reduced 13-42% and offspring birth weight was reduced by 7-12% in all three exposure groups compared to controls. Cocaine decreased the AGD of males (2.68 mm) compared to 2.88 mm in noncocaine-exposed male pups (p < 0.025). A sex-selective cocaine effect was also seen after adjustment of AGD measurements for body weight. With this measure cocaine-treated females showed significantly (p < 0.05) greater AGD than those not exposed to cocaine. In the MWM, there were two types of trials: cued reference memory trials and uncued spatial working memory trials. On cued reference memory trials significant cocaine-induced latency deficits were seen on only the first session. On spatial working memory trials cocaine-induced latency deficits were seen throughout daily training on sessions 1-5, but not the retention session 6, 1 week later. During RAM acquisition, there were no significant differences in choice accuracy between exposure groups. Following propranolol challenge, deficits in choice accuracy were demonstrated in rats prenatally exposed to cocaine or nicotine. These rats did not show any response to propranolol, whereas the controls slightly improved their choice accuracy. The results of this study indicated that prenatal cocaine exposure altered long-term cognitive function under basal conditions in the MWM and drug challenge in the RAM, birth weight, and genital development. Cocaine-induced cognitive deficits were predominately in working memory rather than reference memory or long-term retention. Prenatal nicotine exposure was only observed to alter birth weight and cognitive function in response to propranolol challenge in the RAM.

Abnormalities, Drug-Induced↗

PubMed2005

Downregulation of endocannabinoid signaling in the hippocampus following chronic unpredictable stress.

Deficits in cognitive functioning and flexibility are seen following both chronic stress and modulation of endogenous cannabinoid (eCB) signaling. Here, we investigated whether alterations in eCB signaling might contribute to the cognitive impairments induced by chronic stress. Chronic stress impaired reversal learning and induced perseveratory behavior in the Morris water maze without significant effect on task acquisition. These cognitive impairments were reversed by exogenous cannabinoid administration, suggesting deficient eCB signaling underlies these phenomena. In line with this hypothesis, chronic stress downregulated CB1 receptor expression and significantly reduced the content of the endocannabinoid 2-arachidonylglycerol within the hippocampus. CB1 receptor density and 2-arachidonylglycerol content were unaffected in the limbic forebrain. These data suggest that stress-induced downregulation of hippocampal eCB signaling contributes to problems in behavioral flexibility and could play a role in the development of perseveratory and ruminatory behaviors in stress-related neuropsychiatric disorders.

Animals↗

PubMed1998

Adaptation of the fluid percussion injury model to the mouse.

Fluid percussion injury (FPI) is a well-characterized experimental model of traumatic brain injury (TBI) in the rat. Many pathophysiologic consequences and mechanisms of recovery after TBI rely on neurochemical pathways that can be examined in genetically altered mice. Therefore, FPI applied to mice may be a useful experimental tool to investigate TBI at the molecular level. In the present study, we establish FPI as a viable model of TBI in the mouse by characterizing acute neurological, histopathological, and behavioral changes. Right-sided parasagittal FPI or sham treatment was administered in male C57BL/6 mice. Acute neurological evaluation revealed righting reflexes in the injured animals (p < 0.001). Deficits in spatial learning and memory were observed in the Morris water maze (MWM) 5 and 6 days after injury. A novel MWM data analysis protocol is described. The injured group (n = 18) demonstrated impaired performance in the MWM during acquisition (p < 0.05) and probe trials (p < 0.025) compared to sham animals (n = 16). At 7 days postinjury, glial fibrillary acidic protein immunohistochemistry revealed intense cortical, callosal, and hippocampal gliosis. The modified Gallyas silver degeneration stain consistently labeled cell bodies and terminals throughout the ipsilateral cortex, axons in the gray matter-white matter interface above the corpus callosum and within the corpus callosum bilaterally, and terminals and fibers in the thalamus bilaterally. Additionally, the mouse FPI model described is immediately employable in labs already using the FPI rat model with no modifications to a pre-existing FPI apparatus.

Animals↗