Spatial Learning Ability Of Rats Research Articles

Effects of rTMS on working memory abilities and time-varying spectrum coherence of LFPS and spikes in rats

PurposeThe purpose of this study was to evaluate the effects of repetitive transcranial magnetic stimulation (rTMS) at different frequencies on working memory (WM) and neuroelectric activity in rats.Design/methodology/approachThree rTMS protocols involving different frequencies were applied to rats, and 16-channel local field potentials (LFPs) and spikes were recorded from the prefrontal cortex (PFC) of rats in each group during the WM task. First, the behavior of rats during the T-maze task was analyzed, and then, the firing rate of spikes and the energy of the θ-band and γ-band in LFPs when rats performed the WM tasks were calculated. Finally, the spectral coherence between LFPs and spikes was analyzed by wavelet transform.FindingsThe results showed that rats in the stimulation groups needed fewer days than those in the control group to reach the task correction standard during the WM experiment (p < 0.05). High-frequency rTMS increases the firing rate of spikes and the degree of synchronization of LFPs-spikes in the θ-band and γ-band in the WM process.Originality/valueThis study showed that high-frequency rTMS can improve the spatial learning ability of rats, which might be due to the increased neuronal excitability of the PFC and the enhancement of co-coding between different modes of neural signals. This study is helpful for understanding the neuroregulatory mechanism of rTMS and will provide a reference for the selection of a suitable frequency for TMS treatment.

Effects of green tea catechins on spatial learning abilities of wistar rats

Introduction: Green tea has drawn much attention because of the increase in the number of studies describing its potential health benefits which are attributed to Epigallocatechin-3-gallate (EGCG). Recent studies have also shown that in addition to antioxidant effects, green tea catechins modulates cell cycle signaling, generates non amylodogenic APP, enhances activity in dorsolateral prefrontal cortex etc. Materials and Method: The study was done in 18 male albino Wistar rats and divided in three groups of six. The spatial learning ability of rats were assessed by their behavior in 8 arm radial maze. Results: Statistical analysis was done using SPSS version 22 and data analyzed using Independence sample T test, Paired T test and ANOVA. The maze study showed an improvement in spatial learning ability of rats after green tea consumption in group1 and 2 as the time taken by the animal to complete the maze was found to be decreased. Conclusion: Administration of green tea catechins improves the spatial learning abilities of rats with an improved performance in radial maze tasks. The neuroprotective effect of green tea catechins may be due to their antioxidant property and hence can be used an effective tool in delaying cognitive impairment in elderly. Keywords: Green tea, EGCG, Radial maze, Cognition

Involvement of NMDAR/PSD-95/nNOS–NO–cGMP pathway in embryonic exposure to BPA induced learning and memory dysfunction of rats

Bisphenol A (BPA), can lead to learning and memory impairment, but the underlying mechanism is poorly understood. Researchers have indicated that the N-methyl-D-aspartate receptor (NMDAR)/postsynaptic density protein 95 (PSD-95)/neuronal nitric oxide synthase (nNOS)-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway greatly contributes to learning and memory process. Pregnant rats were exposed to 0, 0.05, 0.5, 5 and 50 mg/kg/day BPA via oral gavage from gestational day (GD) 5 to GD 19. Morris water maze, transmission electron microscope, western blot, real time PCR, biochemical analysis and ELISA were used to analyze the changes in behavior, synaptic ultrastructure, protein and gene expression of NMDAR, PSD-95, nNOS, together with nNOS activity, NO (Nitrate reductase method) and cGMP levels of the rat pups at different growth stages. Results of this research displayed that exposure to 0.5 mg/kg/day BPA could damage the spatial learning ability of rats at postnatal day (PND) 56. However, spatial memory ability could be affected by exposure to BPA at doses up to 5 mg/kg/day. Moreover, the thickness of the postsynaptic density decreased after exposure to BPA at doses of 5 and 50 mg/kg/day. Levels of NR1, NR2A, PSD-95 protein and mRNA were downregulated to some extent after exposure to BPA, whereas the expression of NR2B increased at GD 20 but decreased at PND 21 and 56. Contrarily, the nNOS expression along with the enzyme activity were promoted after exposure to BPA. Meanwhile, the NO and cGMP levels were suppressed at GD 20 but promoted at PND 21 and 56. In conclusion, these results demonstrated that NMDAR/PSD-95/nNOS–NO–cGMP pathway could be affected by embryonic exposure to BPA, which may involve in the spatial learning and memory dysfunction of rats in later life.

Effects of PYRIN-containing Apaf1-like protein 1 on isoflurane-induced postoperative cognitive dysfunction in aged rats.

Postoperative cognitive dysfunction (POCD) is a prevalent neurocognitive disorder following surgery and anesthesia, particularly in elderly patients. Isoflurane is a widely used anesthetic agent, which is associated with the development of POCD; however, the precise mechanisms remain unclear. In the present study, aged rats were exposed to 2% isoflurane to establish a POCD model. The expression of PYRIN-containing Apaf1-like protein 1 (PYPAF1) was knocked down using a lentivirus containing specific short hairpin RNA. Subsequently, the spatial learning ability of rats was assessed using the Morris water maze. In addition, mRNA and protein expression levels were detected using reverse transcription-quantitative PCR and western blot analysis, respectively. Immunofluorescence double staining was also used to determine the expression of PYPAF1 and Iba-1 in the hippocampus. Neural apoptosis was observed using TUNEL-NeuN double staining. The results revealed that isoflurane exposure impaired the spatial learning ability of rats, while PYPAF1 knockdown alleviated cognitive impairment. In addition, isoflurane exposure induced activation of the PYPAF1 inflammasome, as evidenced by elevated expression of PYPAF1 and apoptosis-associated speck-like protein containing a caspase recruitment domain, while silencing of PYPAF1 partially reversed this effect. Furthermore, isoflurane exposure promoted the activation of microglia and caspase-1, and the secretion of interleukin (IL)-1β and IL-18, all of which were alleviated following PYPAF1 silencing. Moreover, isoflurane exposure induced neuronal apoptosis, elevated the levels of Bax and cleaved caspase-3, and inhibited the expression of Bcl-2; all of these effects were partially abrogated following PYPAF1 silencing. In conclusion, the results of the present study indicated that PYPAF1 silencing partially abolished isoflurane-induced cognitive impairment, neuroinflammation and neuronal apoptosis. Therefore, PYPAF1 may be a potential therapeutic target for treatment of POCD.

High-intensity treadmill running impairs cognitive behavior and hippocampal synaptic plasticity of rats via activation of inflammatory response.

Although appropriate exercise is beneficial for enhancing brain functions, high-intensity exercise (HIE)-induced cognitive dysfunction is causing more and more concerns nowadays. In the present study, we observed the effects of high-intensity treadmill running on the spatial learning of the adult Sprague Dawley male rats in Y-maze (n = 16 per group), and investigated its possible electrophysiological and molecular mechanisms by examining in vivo hippocampal long-term potentiation (LTP), central inflammatory responses, and JNK/p38/ERK signal pathway. The Y-maze active avoidance test showed that high-intensity treadmill running impaired spatial learning ability of rats, with increased error times and prolonged training time in recognizing safety condition. Associated with the cognitive dysfunction, the induction and maintenance of hippocampal LTP were also impaired by the HIE. Furthermore, accompanied by elevated levels of inflammatory factors IL-1β, TNF-α, and iNOS, overactivation of microglia and astrocytes was also found in the CA1 region of hippocampus in the excessive exercise group, indicating an inflammatory response induced by HIE. In addition, Western blot assay showed that the phosphorylation of JNK/p38/ERK proteins was enhanced in the exercise group. These results suggest that exercise stress-induced neuronal inflammatory responses in the hippocampus are associated with HIE-induced cognitive deficits, which may be involved in the upregulation of the JNK/p38/ERK pathway. © 2016 Wiley Periodicals, Inc.

Effects of Nano-MnO2 on dopaminergic neurons and the spatial learning capability of rats.

This study aimed to observe the effect of intracerebrally injected nano-MnO2 on neurobehavior and the functions of dopaminergic neurons and astrocytes. Nano-MnO2, 6-OHDA, and saline (control) were injected in the substantia nigra and the ventral tegmental area of Sprague-Dawley rat brains. The neurobehavior of rats was evaluated by Morris water maze test. Tyrosine hydroxylase (TH), inducible nitric oxide synthase (iNOS) and glial fibrillary acidic protein (GFAP) expressions in rat brain were detected by immunohistochemistry. Results showed that the escape latencies of nano-MnO2 treated rat increased significantly compared with control. The number of TH-positive cells decreased, GFAP- and iNOS-positive cells increased significantly in the lesion side of the rat brains compared with the contralateral area in nano-MnO2 group. The same tendencies were observed in nano-MnO2-injected rat brains compared with control. However, in the the positive control, 6-OHDA group, escape latencies increased, TH-positive cell number decreased significantly compared with nano-MnO2 group. The alteration of spatial learning abilities of rats induced by nano-MnO2 may be associated with dopaminergic neuronal dysfunction and astrocyte activation.

Effect of thiomersalate exposure on the behaviour and humoral immunity of premature rats

Objective To discover the influence of thiomersalate exposure on the behavior and humoral immunity of premature rats. Methods According to common thiomersalate dose of vaccine used in human, the surface conversation method was used to change the dose to 1, 2, 3, 4 times for rats(32.8, 65.6, 98.4 and 131.2 μg/kg), and the thiomersalate was separately injected to the gluteus maximus of premature rats respectively, which were delivered on the 20th day of gestation by cesarean for the injection on day 1(premature). Simultaneously, saline was injected to the control group.On day 44 to 48 after injection, the Morris water maze test was used to evaluate the spatial learning and memory abilities of rats and on the post-injection day 49, immunoglobulin content in rat blood and cerebrospinal fluid was measured. Results The spatial learning abilities of rats in 131.2 μg/kg group and the memory abilities in 65.6 μg/kg, 98.4 μg/kg and 131.2 μg/kg group were significantly weaker than those in 9 g/L saline group(all P<0.001). The immunoglobulin content in blood and cerebrospinal fluid changed in different groups exposed to thiomersalate.The levels of IgG, IgA, IgE, IgM in 98.4 μg/kg group and 131.2 μg/kg group rose significantly higher than those in 9 g/L saline group(all P<0.01). Analysis of rectilinear correlation between the immunoglobulin and learning abilities of rats revealed that IgG, IgA, IgE levels in the blood were correlated with the spatial learning abilities(r=0.36, 0.47, 0.50, all P<0.05)and the levels of IgG, IgA, IgE, IgM in blood were rectilinear correlated with the memory abilities of rats(r=-0.39, -0.43, -0.49, -0.38, all P<0.05). In rats'cerebrospinal fluid, IgG, IgA, IgE, IgM levels were rectilinear correlative with both the spatial learning and memory abilities(r=0.48, 0.59, 0.54, 0.41, all P<0.05; r=-0.39, -0.61, -0.57, -0.44, all P<0.05). Conclusion With the dose of thiomersalate increased, the learning and memory and humoral immunity are sustained damaged for premature rats. Key words: Thiomersalate; Humoral immunity; Premature rat

Low (20 cGy) Doses of 1 GeV/u56Fe-Particle Radiation Lead to a Persistent Reduction in the Spatial Learning Ability of Rats

Exposure to galactic cosmic radiation (GCR) is considered to be a potential health risk in long-term space travel, and it represents a significant risk to the central nervous system (CNS). The most harmful component of GCR is the HZE [high-mass, highly charged (Z), high-energy] particles, e.g. (56)Fe. In previous ground-based experiments, exposure to high doses of HZE-particle radiation induced pronounced deficits in hippocampus-dependent learning and memory in rodents. Recent data suggest that glutamatergic transmission in hippocampal synaptosomes is impaired after low (60 cGy) doses of 1 GeV/u (56)Fe particles, which could lead to impairment of hippocampus-dependent spatial memory. To assess the effects of mission-relevant (20-60 cGy) doses of 1 GeV/u (56)Fe particles on hippocampus-dependent spatial memory, male Wistar rats either received sham treatment or were irradiated and tested 3 months later in the Barnes maze test. Compared to the controls, rats that received 20, 40 and 60 cGy 1 GeV/u (56)Fe particles showed significant impairments in their ability to locate the escape box in the Barnes maze, which was manifested by progressively increasing escape latency times over the 3 days of testing. However, this increase was not due to a lack of motivation of the rats to escape, because the total number of head pokes (and especially incorrect head pokes) remained constant over the test period. Given that rats exposed to X rays did not exhibit spatial memory impairments until >10 Gy was delivered, the RBE for 1 GeV/u (56)Fe-particle-induced hippocampal spatial memory impairment is ∼50. These data demonstrate that mission-relevant doses of 1 GeV/u (56)Fe particles can result in severe deficits in hippocampus-dependent neurocognitive tasks, and the extreme sensitivity of these processes to 1 GeV/u (56)Fe particles must arise due to the perturbation of multiple processes in addition to killing neuronal cells.

Sleep deprivation impairs spatial learning and modifies the hippocampal theta rhythm in rats

Previous work from our laboratory suggests that paradoxical sleep deprivation (PSD) decreases persistent sodium currents and hyperpolarization-activated cation currents in CA1 pyramidal neurons, and this leads to decreases in neuron excitability. Here, we further investigate the mechanisms of rhythmic theta-range activity in the hippocampus by examining the resonance characteristics of hippocampal pyramidal neurons. Sleep deprivation (SD) interfered with the rhythmic activity of theta band in the hippocampus, which may be involved in the deficit of the spatial learning ability of rats. Additionally, SD changes the voltage dependence of resonance. The effect of SD on the ion currents may contribute to the alternation of the theta resonance of neurons and further influence the physiological function. These results suggest that changes in neuron resonance lead to changes in the generation of rhythmic theta activity, and may contribute to behavioral deficits associated with theta activity during learning and memory tasks. We suggest the resonant properties of hippocampal neurons are potential targets for preventing deleterious effects of sleep deprivation.

Ionic mechanisms of the effects of sleep deprivation on excitability in hippocampal pyramidal neurons

It has been confirmed that sleep has a key role in learning and memory. Our previous study indicated that paradoxical sleep deprivation (PSD) impairs spatial learning ability of rats, and the decrease in membrane excitability of CA1 pyramidal neurons contributes to deficits in performing a spatial learning task. To investigate the further ionic mechanisms, the persistent sodium currents ( I NaP), the hyperpolarization-activated cation current ( I h), and their roles in neuron excitability were detected. PSD decreased I NaP and suppressed spike ADP, which leads to the reduction of neuron excitability and to the increase of firing accommodation. In addition, PSD reduced the I h amplitude and the rebound excitability of CA1 pyramidal neurons. The results of the present study suggested that I h and I NaP contributed to the inhibitory effect of PSD on neuron excitability, further influencing learning and memory processing. Modulating the ion channels and increasing the membrane excitability of hippocampal neurons are possible targets for preventing the effects of paradoxical sleep deprivation.

Effects of infrasound on learning and memory and the expression of 5-hydroxy tryptamine and its receptor in hippocampi and temporal cortex of rats

目的 探讨8Hz次声对大鼠空间学习记忆行为的影响及其作用机制.方法大鼠分别暴露于8Hz,90dB、100dB或130dB次声仓中,每日2小时,之后进行Morris水迷宫训练,记录其找到隐匿站台的时间;第6天训练结束后取脑并进行免疫组织化学染色,光镜下分析其海马及颞叶皮层5-羟色胺(5-HT)及5-羟色胺受体(5-HTR)含量.结果次声组大鼠在水迷宫中逃离水难的时间均较对照组延长(P=0.010及P=0.001,P=0.000);次声组大鼠海马及颞叶皮层5-HT、5-HTR含量均较对照组减少(均P=0.000);大鼠在水迷宫中找到隐匿站台的时间与其海马及颞叶皮层5-HT、 5-HTR含量呈负相关.结论 8Hz,90dB、100dB及130dB次声可使大鼠空间学习记忆能力降低,并且随次声声压级的增加其作用愈加明显,作用机制可能与海马及颞叶皮层5-HT、5-HTR的减少有关。

Long-term effects of neonatal methamphetamine exposure in rats on spatial learning in the Barnes maze and on cliff avoidance, corticosterone release, and neurotoxicity in adulthood.

Methamphetamine (MA) is a commonly abused stimulant and because of its addictive properties, abusers may not cease use during pregnancy, thereby exposing the fetus to the drug. The consequences of such exposure remain largely unknown however data from animal models show that long-term deficits in spatial learning and memory in the Morris water maze (MWM) occur. In this study we explored the spatial learning ability of rats treated four times daily with MA (5 mg/kg/dose) during the sensitive period for induction of MWM deficits, postnatal days (P) 11-20, using a different maze. In adulthood the animals were tested in a non-swimming spatial task, the Barnes maze, using either aversive (bright light) or appetitive (food reward) motivation. Approximately 30 days after behavioral testing, the pituitary and adrenal response to forced swim was assessed and susceptibility to MA-induced neurotoxicity measured. MA-treated animals tested in the aversive, but not the appetitive, version of the Barnes maze demonstrated spatial learning deficits. An attenuated corticosterone response in MA-treated animals was observed following forced swimming, however no differences in ACTH were found. Following acute MA administration in adulthood to all animals, the neonatally MA-treated animals displayed longer latencies to fall from a cliff than neonatally saline-treated rats given the same acute MA dose. This effect supports previous data showing hypoactivity in neonatally MA-treated animals. Acute MA treatment caused comparable striatal monoamine depletions in all groups, although females treated with MA as neonates displayed increased basal levels of corticosterone three days after the acute dose. These data demonstrate that MA administration during the neonatal period impairs spatial learning in an aversive non-swimming task and alters the adrenal response to a forced swim stressor, suggesting that the adrenal output during learning may contribute to the spatial learning deficits.

Disturbed spatial learning of rats after intraventricular administration of transforming growth factor-beta 1.

Patients with subarachnoid hemorrhage (SAH) who later suffer hydrocephalus show persistently high levels of transforming growth factor-beta 1 (TGF-beta 1) in the cerebrospinal fluid after the onset of SAH. Recombinant TGF-beta 1 induces hydrocephalus in mice. This study examined the spatial learning ability of rats after intraventricular administration of TGF-beta 1. Thirteen-week-old Wistar rats were treated with 0.8 or 8.0 micrograms of human recombinant TGF-beta 1 by direct injection or via osmotic pump. Three months later, their spatial learning ability was evaluated with a Morris water maze. Ventricular size, ultrastructural features, and sodium-potassium-adenosine triphosphatase (Na+, K(+)-ATPase) activity of the subarachnoid space were examined. All three TGF-beta 1-treated groups clearly exhibited impaired spatial learning ability, but they did not exhibit ventricular dilation. Histological examination revealed subarachnoid fibrosis and deactivation of Na+, K(+)-ATPase in the arachnoid cells. These findings are similar to those of our previous experiments involving injection of TGF-beta 1 in mice. The present and previous studies suggest that subarachnoid fibrosis is an important factor in the disturbance of the spatial learning ability of rats, whereas ventricular size is less important.

Effects of binge ethanol administration on the behavioral outcome of rats after lateral fluid percussion brain injury.

This study examined the effects of 4 weeks of binge ethanol administration (BEAn) on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were intragastrically given 7.5 mL/kg of either 40% ethanol in 5% glucose solution (3 g ethanol/kg; binge ethanol group), or 5% glucose solution (vehicle group), twice on Thursday and Friday of 3 consecutive weeks. Then rats from both groups were subjected to either lateral FP brain injury of moderate severity (1.8 atm) or to sham operation. Postinjury behavioral measurements revealed that brain injury caused significant spatial learning disability in both groups. There were no significant differences in mean search latencies in the sham animals between the vehicle and binge ethanol groups. On the other hand, the mean search latency of the binge ethanol group was significantly higher than that of the vehicle group in trial blocks 2 and 4. There were no significant differences in the target visits (expressed as mean zone difference [MZD]) during the probe trial between the injured animals of binge ethanol and vehicle groups. However, there was only a minor trend towards worsened MZD score in the binge-injured animals. Histologic analysis of injured animals from both injured ethanol and vehicle groups revealed similar extents of ipsilateral cortical and observable hippocampal damage. These results suggest that 4 weeks of binge ethanol treatment followed by ethanol intoxication at the time of injury worsens some aspects of the spatial learning ability of rats. This worsening is probably caused by subtle, undetectable morphologic damage by binge ethanol administration.

Stress impairs performance in spatial water maze learning tasks

The water maze task has been developed to test spatial learning abilities in rats or mice, and is widely used. Though it has been reported before that numerous cognitive abilities are of importance for learning this task, poor performance is usually interpreted as an impairment of spatial memory formation. Previous investigations that tried to correlate long-term potentiation (LTP) of synaptic transmission with spatial learning abilities in rats reported that injection of drugs or specific gene deletions which blocked the expression of LTP correlated with learning impairments of spatial tasks in a water maze. Recent studies, however, have shown that pretraining enables these animals to learn such spatial tasks even though LTP was still found to be blocked. I investigated to what degree altered fear condition and stress perception could account for the impaired spatial learning when no pretraining is given. In a fear habituation task, unhandled rats preferred a dark over a well lit chamber more than handled animals did, but unhandled rats favoured the lit chamber more in an active avoidance task. They also performed poorly in a spatial water maze task compared with handled rats. Rats pretrained in a radial arm maze performed better in a water maze than non-pretrained rats. No difference between groups was found in a non-spatial water maze task. On the other hand, when pretrained in a water maze, rats performed only marginally better in a radial arm maze compared to non-pretrained animals. Since animals have to be handled to learn a radial arm maze, the difference in this task was not due to stress but most probably due to getting accustomed to the room dimensions prior to learning the spatial task. The results suggest that impaired learning of spatial tasks in the water maze can be due to increased stress and decreased fear conditioning without actually affecting spatial learning abilities. These results question the interpretations of the results of some previously published results of spatial water maze tasks.

Chronic Administration of Quinolinic Acid in the Rat Striatum Causes Spatial Learning Deficits in a Radial Arm Water Maze Task

Chronic intrastriatal administration of quinolinic acid (QA) in the rat produces a pattern of neurodegeneration similar to that seen in Huntington's disease (HD). Although these changes have been related to transient motor abnormalities, the effects of chronic QA administration on cognitive abilities have not been assessed. The present study investigated whether the striatal deterioration observed during chronic QA administration produces cognitive impairments in this animal model of HD by testing the effects of chronic administration of QA on spatial learning ability of rats in a radial arm water maze (RAWM) task. Rats were given bilateral implantation of a chronic dialysis probe apparatus which delivered either vehicle or QA (20 mM) into the striatum. Beginning 1 day after implantation, the rats were tested daily for 3 weeks in the RAWM. Nocturnal activity levels were also assessed at 1-, 3-, 5-, 7-, 14-, and 21-days following probe implantation. Results of behavioral testing indicated that chronic exposure to QA causes spatial learning deficits in the RAWM task with only a transient increase in activity levels. Collectively, these results suggest that chronic striatal exposure to QA mimics some aspects of the cognitive deficits observed in HD.

Spatial Learning Ability of Rats Following Differing Levels of Exposure to Alcohol During Early Postnatal Life

TOMLINSON, D., P. WILCE AND K. S. BEDI.Spatial learning ability of rats following differing levels of exposure to alcohol during early postnatal life.PHYSIOL BEHAV 63(2) 205–211, 1998.—Rats exposed to a relatively high dose (7.5 g/kg body weight) of alcohol on either the fifth or tenth postnatal day of age have been reported to have long-lasting deficits in spatial learning ability as tested on the Morris water maze task. The question arises concerning the level of alcohol required to achieve this effect. Wistar rats were exposed to either 2, 4 or 6 g/kg body weight of ethanol administered as a 10% solution. This ethanol was given over an 8-h period on the fifth postnatal day of age by means of an intragastric cannula. Gastrostomy controls received a 5% sucrose solution substituted isocalorically for the ethanol. Another set of pups raised by their mother were used as suckle controls. All surgical procedures were carried out under halothane vapour anaesthesia. After the artificial feeding regimes all pups were returned to lactating dams and weaned at 21 days of age. The spatial learning ability of these rats was tested in the Morris water maze when they were between 61–64 days of age. This task requires the rats to swim in a pool containing water made opaque and locate and climb onto a submerged platform. The time taken to accomplish this is known as the escape latency. Each rat was subjected to 24 trials over 3 days of the test period. Statistical analysis of the escape latency data revealed that the rats given 6 g/kg body weight of ethanol had significant deficits in their spatial learning ability compared with their control groups. However, there was no significant difference in spatial learning ability for the rats given either 2 or 4 g/kg body weight of ethanol compared with their respective gastrostomy or suckle control animals. We concluded that ethanol exposure greater than 4 g/kg over an 8-h period to 5-day-old rats is required for them to develop long-term deficits in spatial learning behaviour.

Spatial learning ability of rats following acute exposure to alcohol during early postnatal life

Previous research has indicated that the developing brain is vulnerable to the effects of alcohol exposure. Most of this research has used an experimental design in which animals where chronically subjected to alcohol for a lengthy period of time during gestation and/or the preweaning period. Recent evidence has indicated that the morphology of the brain and the subsequent behaviour of the animal may also be susceptible to alcohol administered for a short duration during specified periods of development. Wistar rats were exposed to 7.5 g/kg body weight of ethanol administered as a 10% solution via an intragastric cannula over an 8 h period either on the 5th (PND5) or the 10th (PND10) postnatal day of age. Gastrostomy controls received a 5% sucrose solution substituted isocalorically for the ethanol. Another set of pups raised by their mother were used as ‘suckle controls’. All surgical procedures were carried out under halothane vapour anaesthesia. After the artificial feeding regimes all pups were returned to lactating dams and weaned at 21 days of age. The spatial learning ability of these rats was tested in the Morris water maze when they were between 41–54 days of age. This task requires the rats to swim in a pool containing water made opaque and locate and climb onto a submerged platform. The time taken to accomplish this is known as the “escape latency.” Each rat was subjected to 24 trials over three days and a further trial on each of days 4 and 11 of the test period. Statistical analysis of the escape latency data revealed that both the PND5 and PND10 ethanol treated groups had significant deficits in their spatial learning ability compared with the control groups. However, there was no significant difference in the degree of impairment between the PND5 and PND10 rats. It is concluded that even short periods of alcohol exposure during brain development can cause lasting impairment of spatial learning behaviour in rats.