Y-maze Discrimination Research Articles

Functional dissociation along the rostrocaudal axis of Japanese quail hippocampus.

The mammalian hippocampus (Hp) can be functionally segregated along its septotemporal axis, with involvement of dorsal hippocampus (dHp) in spatial memory and ventral hippocampus (vHp) in stress responses and emotional behaviour. In the present study, we investigate comparable functional segregation in proposed homologues within the avian brain. Using Japanese quail (Coturnix Japonica), we report that bilateral lesions of the rostral hippocampus (rHp) produce robust deficits in a spatial Y-maze discrimination (YMD) test while sparing performance during contextual fear conditioning (CFC), comparable to results from lesions to homologous regions in mammals. In contrast, caudal hippocampus (cHp) lesions failed to produce deficits in either CFC or YMD, suggesting that, unlike mammals, both cHp and rHp of birds can support emotional behavior. These observations demonstrate functional segregation along the rostrocaudal axis of the avian Hp that is comparable in part to distinctions seen along the mammalian hippocampal septotemporal axis.

Protective Role Of Quercetin On Hippocampus Inflammatory And Oxidative Damage Induced By Monosodium Glutamate In Rats

The aim of the current study was to investigate the possible protective role of quercetin against monosodium glutamate (MSG) induced oxidative stress and inflammation on the brain hippocampus of adult male albino rats. Thirty adult male albino rats were equally divided into 5 groups; Group I (control), group II received1 ml/ kg/ day of 0.5% of Dimethyl sulfoxide (DMSO), group III received 50 mg of quercetin/ kg/ day, group IV received1.6 g/ kg/ day of MSG, group V received quercetin and after one hour, rats received MSG as previously mentioned. All treatments were given orally for 8 weeks. Then rats were anesthetized, sacrificed and specimens from the brain hippocampus were taken for biochemical and histological studies. MSG exposure showed deleterious effects on Y-maze discrimination learning and memory, significantly increased tissue malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), interleukin- 1 beta (IL-1β), tumor necrosis factor-α (TNF-α), glutamate level and acetyl cholinesterase (AChE) activity with significant depletions of catalase (CAT) activities and reduced glutathione (GSH) content. This was accompanied with alteration in the structure of the brain hippocampus. Co-administration of quercetin along with MSG ameliorated the above mentioned effects. The results of this study have shown that quercetin has protective effects against MSG-induced toxicity in rat brain hippocampus.

Effect of exercise training on long-term potentiation and NMDA receptor channels in rats with cerebral infarction

The aim of the present study was to investigate the effects of exercise training on the characteristics of long-term potentiation (LTP) and N-methyl-D aspartate (NMDA) receptor channels in the hippocampal CA3 neurons of rats with cerebral infarction. Wistar rats were randomly allocated into the model without any training and rehabilitation with exercise training. A model of cerebral infarction was established by middle cerebral artery occlusion. Using chronically embedded electrodes combined with an electrophysiological method, the population spike (PS) amplitude and latency, as well as changes in the NMDA single channel current in the hippocampal neurons were determined prior to and following Y-maze discrimination learning 60 times in the two groups. The formation of learning-dependent LTP and synaptic efficacy in the hippocampal CA3 area after exercise training in the rehabilitation group was significantly faster compared with that in the model group without any training (P<0.05). The incubation period of the PS in the CA3 area of the rats in the rehabilitation group was significantly shorter compared with that in the model group. The PS amplitude in the rehabilitation group was significantly higher compared with that in the model group. Furthermore, the opening probability of the NMDA receptor channel in the rehabilitation group was significantly higher compared with that in the model group. In conclusion, exercise training improved the opening conductance level, time and probability of NMDA receptor channels and accelerated the formation of learning-dependent LTP in the contralateral hippocampal CA3 area.

Involvement of nitric oxide in pioglitazone memory improvement in morphine-induced memory impaired mice

IntroductionPioglitazone, a PPAR‐γ agonist, which is clinically used in treating diabetic patients, has been recently reported to have crucial roles in improving cognition and memory performance. Since the mechanisms involved in the neuroprotective effect of pioglitazone are not entirely understood, the current study was designed to investigate the possible interaction of pioglitazone with morphine in memory-impaired mice and the probable role of nitric oxide (NO) in this effect. Materials and methodsAll the experiments were performed in passive avoidance and Y-maze paradigms. To induce memory impairment, mice were administered morphine (1, 3 and 10mg/kg, s.c.) immediately before the training trial. Pioglitazone (20, 40 and 80mg/kg, p.o.) was gavaged 2h prior to the training trial. Further, an NO synthase inhibitor, L-NAME (10mg/kg, i.p.), or an inducible NO synthase inhibitor, aminoguanidine (100mg/kg, i.p.) was administered 30 min before the training trial to determine the possible involvement of NO in the restorative effect of pioglitazone. Results1) Morphine dose dependently impaired the acquisition of spatial memory and passive avoidance task. 2) Treatment with pioglitazone significantly improved the memory performance in morphine-treated mice in both tests. 3) In the passive avoidance task, L-NAME, but not aminoguanidine, altered the effect of pioglitazone on morphine-induced memory impairment. 4) In Y-maze discrimination, the memory improving effect of pioglitazone was reversed by both NO synthase inhibitors, L-NAME and aminoguanidine. DiscussionOur results demonstrate that the pioglitazone improving effect on the morphine-induced impairment of memory acquisition is at least in part through the NO pathway. It is suggested that in short term spatial recognition memory, both inducible and constitutive NO synthases are involved, but in the long term fear memory, only the constitutive NO synthases indicated a prominent role in the anti‐amnestic effect of pioglitazone on morphine-induced memory impairment.

Disrupting Effect of Drug-Induced Reward on Spatial But Not Cue-Guided Learning: Implication of the Striatal Protein Kinase A/cAMP Response Element-Binding Protein Pathway

The multiple memory systems hypothesis posits that different neural circuits function in parallel and may compete for information processing and storage. For example, instrumental conditioning would depend on the striatum, whereas spatial memory may be mediated by a circuit centered on the hippocampus. However, the nature of the task itself is not sufficient to select durably one system over the other. In this study, we investigated the effects of natural and pharmacological rewards on the selection of a particular memory system during learning. We compared the effects of food- or drug-induced activation of the reward system on cue-guided versus spatial learning using a Y-maze discrimination task. Drug-induced reward severely impaired the acquisition of a spatial discrimination task but spared the cued version of the task. Immunohistochemical analysis of the phosphorylated form of the cAMP response element binding (CREB) protein and c-Fos expression induced by behavioral testing revealed that the spatial deficit was associated with a decrease of both markers within the hippocampus and the prefrontal cortex. In contrast, drug reward potentiated the cued learning-induced CREB phosphorylation within the dorsal striatum. Administration of the protein kinase A inhibitor 8-Bromo-adenosine-3',5'-cyclic monophosphorothioate Rp isomer (Rp-cAMPS) into the dorsal striatum before training completely reversed the drug-induced spatial deficit and restored CREB phosphorylation levels within the hippocampus and the prefrontal cortex. Therefore, drug-induced striatal hyperactivity may underlie the declarative memory deficit reported here. This mechanism could represent an important early step toward the development of addictive behaviors by promoting conditioning to the detriment of more flexible forms of memory.

Repair of Excitotoxic Neuronal Damage Mediated by Neural Stem Cell Lysates in Adult Mice

The present study aimed to investigate a possibility of brain repair from diseased or damaged disorders mediated by cell-free filtrate of neural stem cell (NSC) lysates (FNSCL). Mouse NSCs were isolated from the brains of embryos at 15 day postcoitum (dpc). The expression of the Nestin was examined by immunocytochemical technique. Sonication of NSCs cultured and nestin-positive was performed in a bath-type sonicator, and the cell-free filtrate was recovered from a filtrative step of the lysates. The animals in the monosodium glutamate MSG group received intragastric(ig) administration of MSG (2.0 g/kg per day) for 10 days the animals in the MSG+NSCs and MSG+FNSCL groups received intracerebroventricular transplantation of 10 ?l of NSC suspension, approximately 1.0×105 cells, or intracerebroventricular injection of 10 ?l of cell-free filtrate of lysates of approximately 1.0×105 NSCs on day 1 and day 11 after 10-d MSG exposure, respectively. The mice in control and MSG group were intracerebroventricularly administered with 10 ?l of DMEM instead of NSCs or FNSCL. On 11 day after intracerebroventricular transplantation of NSCs or intracerebroventricular injection of FNSCL, the test of Y-maze discrimination learning were performed, and then the histopathology of the animal brains was studied, to analyze MSG-induced functional and morphological changes and the effects of intracerebroventricular transplantation of NSCs or intracerebroventricular injection of FNSCL on the brain repair from MSG-induced excitotoxic injury. Both intracerebroventricular transplantation of NSCs and intracerebroventricular injection of FNSCL facilitated the brain repair following glutamate-induced excitotoxic injury in adult mice, suggesting that there are certain NSC factors inside NSCs which are effective in repairing glutamate-induced excitotoxic brain injury. Administration of FNSCL might be a cell-free-based therapeutic strategy to repair diseased or damaged central nervous system CNS tissue.

Repair of glutamate-induced excitotoxic neuronal damage mediated by intracerebroventricular transplantation of neural stem cells in adult mice

To investigate a possibility of repairing damaged brain by intracerebroventricular transplantation of neural stem cells (NSCs) in the adult mice subjected to glutamate-induced excitotoxic injury. Mouse NSCs were isolated from the brains of embryos at 15-day postcoitum (dpc). The expression of nestin, a special antigen for NSC, was detected by immunocytochemistry. Immunofluorescence staining was carried out to observe the survival and location of transplanted NSCs. The animals in the MSG + NSCs group received intracerebroventricular transplantation of NSCs (approximately 1.0 x 10(5) cells) separately on day 1 and day 10 after 10-d MSG exposure (4.0 g/kg per day). The mice in control and MSG groups received intracerebroventricular injection of Dulbecco's minimum essential medium (DMEM) instead of NSCs. On day 11 after the last NSC transplantation, the test of Y-maze discrimination learning was performed, and then the histopathology of the animal brains was studied to analyze the MSG-induced functional and morphological changes of brain and the effects of intracerebroventricular transplantation of NSCs on the brain repair. The isolated cells were Nestin-positive. The grafted NSCs in the host brain were region-specifically survived at 10-d post-transplantation. Intracerebroventricular transplantation of NSCs obviously facilitated the brain recovery from glutamate-induced behavioral disturbances and histopathological impairs in adult mice. Intracerebroventricular transplantation of NSCs may be feasible in repairing diseased or damaged brain tissue.

The effects of pregnenolone sulfate on learning and memory in aged rats

目的 探讨神经甾体硫化孕烯醇酮对老年大鼠学习和记忆能力的影响.方法利用Y-迷宫测定24月龄老年大鼠的学习和记忆功能.结果 ⑴学习能力测试:5mg/kg、10mg/kg组老年大鼠Y-迷宫辨别学习达到标准的训练次数为(25.86±2.98)次、(22.85±5.42)次,与对照组[(36.48±4.26)次]比较,差异具有显著性(P﹤0.05,P 0.05).结论神经甾体硫化孕烯醇酮剂量依赖性地改善老年大鼠的学习和记忆功能。

Cattle discriminate between individual familiar herd members in a learning experiment

We tested the ability of cattle to discriminate between socially familiar conspecifics in a Y-maze discrimination experiment. The discriminative stimuli were herd members tethered in the Y-maze side arms (stimulus heifers); approach to one of these was rewarded with food and approach to the other was unrewarded, and their positions were randomly swapped. Each of six experimental heifers was subjected to two pairs of stimulus heifers. All subjects reached the learning criterion (19 out of 20 consecutive choices to the rewarded stimulus heifer’s position in the Y-maze) with one pair of stimulus heifers. With the other pair, learning was slower and only three of the subjects reached criterion. All heifers that reached criterion chose correctly in at least five additional trials designed to control for cues emanating from the experimenter’s behaviour or from the food reward. We conclude that cattle can discriminate between individual familiar conspecifics, that they can learn discrimination tasks quickly, and that speed of learning and level of correct response can be influenced by the identity of the stimulus individuals. We also explored the experimental heifers’ behaviour during the learning process. Behaviours indicative of agitation were observed more often in the second task than in the first and also increased with time during learning tasks ( P<0.05), but were not related to whether a heifer made a correct choice. Head orientation predicted the correct direction when this was subsequently chosen ( P<0.05), whereas body orientation tended to predict the correct direction when the incorrect arm was subsequently chosen ( P=0.063).

SLV310, a molecule combining potent dopamine D 2 receptor antagonism with serotonin reuptake inhibition: In vitro and in vivo neurochemistry

The interaction between muscarinic-cholinergic and dopaminergic systems in the modulation of memory storage of Y-maze discrimination (YMD) task was examined in C57BL/6 and DBA/2 strains of mice. In C57BL/6 mice, post-training systemic (i.p.) administration of the D2-agonist quinpirole facilitated retention and the D2-antagonist (−)-sulpiride impaired retention. Opposite effects were observed in DBA/2 strain. The facilitating or impairing effects of quinpirole and (−)-sulpiride were blocked by simultaneous post-training administration of muscarinic-cholinergic agonists and antagonists. The memory enhancing effects of the cholinergic agonist oxotremorine were not blocked by simultaneous administration of sulpiride in C57BL/6 mice or quinpirole in DBA/2 mice. Furthermore, the memory impairing effects of the cholinergic antagonist atropine were not blocked by simultaneous administration of quinpirole in C57BL/6 mice or sulpiride in DBA/2 mice. These findings indicate that the effects of D2-receptor agonists and antagonists on retention of YMD task are strain-dependent and mediated through muscarinic-cholinergic mechanisms.

Noradrenergic Receptor Blockade of the NTS Attenuates the Mnemonic Effects of Epinephrine in an Appetitive Light–Dark Discrimination Learning Task

These experiments examined the contribution of noradrenergic neurons in the nucleus of the solitary tract (NTS) in mediating the memory-facilitating effects of epinephrine. In Experiment 1, saline or 0.05 or 0.1 mg/kg of epinephrine was given intraperitoneally (ip) to rats after the second day of training in a light-dark Y-maze discrimination task. On a 20-trial retention test given 2 and 7 days later, the 0.1 mg/kg epinephrine group made significantly more correct responses than controls and required fewer trials to reach criterion. In Experiment 2, phosphate-buffered saline or the noradrenergic antagonist dl-propranolol (0.3 or 1.0 μg/0.5 μl) was infused into the NTS prior to an ip injection of saline or 0.1 mg/kg of epinephrine. The memory-enhancing effects of epinephrine were attenuated by the infusion of 0.3 μg/0.5 μl of dl-propranolol into the NTS. These findings indicate an involvement of NTS noradrenergic neurons in mediating the effects of peripheral epinephrine on memory storage processes.

The effects of noradrenergic activation of the nucleus tractus solitarius on memory and in potentiating norepinephrine release in the amygdala.

Although it is known that norepinephrine (NE) modulates memory by acting on limbic areas, few studies describe how structures supplying NE to the limbic system, such as the nucleus tractus solitarius (NTS) contribute to this process. The present study examined the effects on memory of activating the NE pathway between the NTS and the amygdala (AMYG). Rats received buffer or the beta-noradrenergic agonist clenbuterol (CLN; 10, 50, or 100 ng/0.5 microl) into the NTS after footshock training in a Y-maze discrimination task. Infusion of 100 ng CLN significantly improved memory when retention was tested in the absence or presence of cues associated with the footshock. Experiment 2 used in vivo microdialysis to determine whether the mnemonic effects of CLN are mediated by influencing NE output in the AMYG. Subjects were given an intra-NTS infusion of CLN or phosphate buffered saline, footshock (0.8 mA, 1 s), and injected with epinephrine (EPI; 0.3 mg/kg ip) or saline. CLN or EPI injection produced a significant increase in NE sampled from the AMYG. These findings indicate that activation of NTS neurons that project to and release NE in the AMYG modulates memory storage processing.

Strain-dependent effects of D 2 dopaminergic and muscarinic-cholinergic agonists and antagonists on memory consolidation processes in mice

The interaction between muscarinic-cholinergic and dopaminergic systems in the modulation of memory storage of Y-maze discrimination (YMD) task was examined in C57BL/6 and DBA/2 strains of mice. In C57BL/6 mice, post-training systemic (i.p.) administration of the D 2-agonist quinpirole facilitated retention and the D 2-antagonist (−)-sulpiride impaired retention. Opposite effects were observed in DBA/2 strain. The facilitating or impairing effects of quinpirole and (−)-sulpiride were blocked by simultaneous post-training administration of muscarinic-cholinergic agonists and antagonists. The memory enhancing effects of the cholinergic agonist oxotremorine were not blocked by simultaneous administration of sulpiride in C57BL/6 mice or quinpirole in DBA/2 mice. Furthermore, the memory impairing effects of the cholinergic antagonist atropine were not blocked by simultaneous administration of quinpirole in C57BL/6 mice or sulpiride in DBA/2 mice. These findings indicate that the effects of D 2-receptor agonists and antagonists on retention of YMD task are strain-dependent and mediated through muscarinic-cholinergic mechanisms.

Effects of maternal oral administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain

Monosodium glutamate (MSG) was shown to penetrate placental barrier and to distribute to embryonic tissues using [ 3H]glutamic acid ([ 3H]Glu) as a tracer. However, the distribution is not even; the uptake of MSG in the fetal brain was twice as great as that in the maternal brain in Kunming mice. Other maternal mice were given per os MSG (2.5 mg/g or 4.0 mg/g body weight) at 17–21 days of pregnancy, and their offspring behaviors studied. The results showed that maternal oral administration of MSG at a late stage of pregnancy decreased the threshold of convulsion in the litters at 10 days of age. Y-maze discrimination learning was significantly impaired in the 60-day-old filial mice. On the other hand, no significant difference in spatial learning or tail flick latency was measured between the experimental animals and the controls. The filial mice of MSG-treated mothers could either not grasp a rope tightly, or grasped the rope tightly but could not crawl along the rope at the beginning of the training. However, such mice, after training, could grasp and crawl along the rope as well as controls. Obvious neuronal damage was not detected in the periventricular organs or the hypothalamus under a light microscope. The rate of weight gain for experimental animals was greater than for controls throughout the period from 20 to 90 days. Mating of treated males with treated females resulted in pregnancies and normal offspring, indicating that oral administration of MSG at a late stage of pregnancy did not affected the reproductive capacity of the offspring. The possible differences and relationship between MSG-induced damage to developing human and rodent brain are discussed.

Behavioral effects of persistent lymphocytic choriomeningitis virus infection in mice

Lymphocytic choriomeningitis virus (LCMV) is a nonlytic murine virus that provides a valuable model system for studying the behavioral correlates of CNS viral infection. Newborn or immunosuppressed mice infected with LCMV develop a persistent tolerant infection characterized by continuous viral production. Virus can be found in various body organs including lung, liver, kidney, and brain. In brain, neurons are the predominant CNS cells infected and the greatest number of persistently infected neurons are found in the cerebral cortex, hippocampus, other limbic structures and parts of the hypothalamus. Despite continuous infection throughout the animal's life, neurons show no structural injury or dropout. Mice from the DBA/2J strain were infected with LCMV (1000 plaque-forming units) within 18 h of birth and tested for behavioral function as adults. Plaque assays indicated persistent infection in virus-injected mice. Mice were tested for their ability to learn a Y-maze spatial discrimination to avoid the onset of a mild footshock (0.43 mA). The number of correct avoidance responses made during training was taken as a measure of acquisition performance. The virus-infected mice showed a deficit in acquisition of the Y-maze discrimination compared to that seen in vehicle-injected and noninjected controls. Following additional training to reach control levels of performance, the infected mice and the controls were injected with the cholinergic antagonist scopolamine. Scopolamine (2.0 mg/kg) disrupted the performance of the infected mice significantly more than control performance, suggesting that a cholinergic dysfunction accounted for some of the learning deficit. A separate group of virus-infected mice exhibited hypoactivity during the first exposure to a locomotor testing apparatus.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of cholinergic-dopaminergic systems in the regulation of memory storage in aversively motivated learning tasks

These experiments examined the interaction between muscarinic cholinergic and dopaminergic systems in the modulation of memory storage. Male CD1 mice (25–30 g) were trained in an inhibitory avoidance (IA) and a Y-maze discrimination (YMD) task. The first experiment examined the dose-response effects, on retention, of agonists and antagonists specific for either D 1- or D 2-receptors. Immediately posttraining mice were given i.p. injections of saline, the D 1-receptor agonists SKF 38393 (3.0, 10.0 or 30.0 mg/kg) or SKF 77434 (3.0, 10.0 or 30.0 mg/kg), the D 1-receptor antagonists SCH 23390 (0.03 (0.03, 0.1, 0.3 or 1.0 mg/kg), the D 2-receptor agonist quinpirole (0.3, 1.0 or 3.0 mg/kg) or the D 2-receptor antagonist sulpiride (3.0, 10.0, 30.0 or 100.0 mg/kg). Retention was tested 48 h later. The drugs affecting D 1-receptors did not affect retention. In contrast, in both tasks quinpirole enhanced retention and sulpiride impaired retention. In the IA task, quinpirole (3.0 mg/kg) blocked the retention impairing effects of the muscarinic cholinergic antagonist atropine (10.0 mg/kg), and sulpiride (3.0, 10.0, 30.0 or 100.0 mg/kg) significantly attenuated the memory enhancing effects of the muscarinic cholinergic agonist oxotremorine (35.0 or 70.0 μg/kg). D 1-receptor agents did not modify the effects of either atropine or oxotremorine on retention of the IA response. These findings suggest that the effects of cholinergic muscarinic agents on retention of the IA response are mediated by influences involving D 2-dopaminergic mechanisms. In the YMD task, atropine (10.0 mg/kg) blocked the memory-enhancing effects of quinpirole (3.0 mg/kg) and oxotremorine (35.0 or 70.0 μg/kg) attenuated the memory impairing effect of sulpiride (3.0, 10.0, 30.0 or 100.0 mg/kg). D 1-receptor agents did not modify the effects of either atropine or oxotremorine on retention of the YMD task. These results suggest that the effects of the D 2-dopaminergic agents on retention of the YMD are mediated by muscarinic cholinergic mechanisms. Although retention of both the IA and the YMD are modulated by interactions between D 2-dopaminergic and muscarinic cholinergic systems, the ways in which these mechanisms interact are task-dependent.

Memory-enhancing effects of post-training dipivefrin and epinephrine: Involvement of peripheral and central adrenergic receptors

These experiments examined the effects, in mice, of post-training i.p. injections of dipivefrin (DPE), a lipophilic prodrug of epinephrine, and epinephrine (EPI) on 48-h retention assessed in inhibitory avoidance and Y-maze discrimination tasks. DPE, in doses of 0.3–10 μg/kg significantly facilitated retention: the effects were approximately 10-fold more potent than those of EPI obtained with similar experimental conditions. The α-adrenergic antagonists prazosin (α 1; 3.0 mg/kg; i.p.), yohimbine (α 2; 3.0 mg/kg; i.p.) and phentolamine (α 1andα 2; 3.0 mg/kg; i.p.) did not block the enhancement of retention induced by either DPE (10.0 μg/kg; i.p.) or EPI (0.1 mg/kg; i.p.). However, the β-adrenergic antagonist propranolol (2.0 mg/kg; i.p.) attenuated the effects of both DPE and EPI. Sotalol (2.0 mg/kg; i.p.), a peripherally-acting β-adrenergic antagonist, attebuated the effects of EPI but not those DPE. These findings suggest the DPE-induced enhancement of memory involves central β- but not α-adrenergic mechanisms while EPI's effects are initiated by activation of peripheral β-adrenergic systems.

Stria terminalis lesions attenuate the effects of posttraining oxotremorine and atropine on retention

In these experiments, we examined the effects of posttraining administration of the cholinergic agonist oxotremorine and the cholinergic antagonist atropine on retention in rats with lesions of the stria terminalis (ST). Male Sprague-Dawley rats, with either sham or bilateral ST lesions, were trained in a one-trial step-through inhibitory-avoidance task and a Y-maze discrimination task. Immediately after training on each task, they received i.p. injections of saline, oxotremorine (50.0 μg/kg), or atropine (3.0 mg/kg). Retention of each task was tested 1 week following training. Lesions of the ST did not affect retention of either task in otherwise untreated animals, but blocked both the memory-enhancing effect of oxotremorine and the memory-impairing effect of atropine. These findings suggest that activation of pathways within the ST is involved in cholinergic influences on memory, and are consistent with the view that the amygdaloid complex is involved in integrating neuromodulatory influences on memory storage.

Effect of bestatin, an aminopeptidase inhibitor, on memory in inhibitory-avoidance and Y-maze discrimination tasks

Effect of bestatin, an aminopeptidase inhibitor, on memory in inhibitory-avoidance and Y-maze discrimination tasks

Memory enhancement with intra-amygdala post-training naloxone is blocked by concurrent administration of propranolol

Sprague-Dawley rats were first trained on an inhibitory avoidance task (IA) and then, two weeks later, on a Y-maze discrimination task (YMD). Bilateral intra-amygdala injections were given through implanted cannulae immediately post-training. Retention was evaluated one week following training on each task. Naloxone (0.1, 0.3 or 1.0 μg) facilitated retention performance in both tasks. The most effective doses were 0.1 μg for the IA task and 0.3 μg for the YMD task. Since naloxone (0.1 μg) did not affect retention when administered via cannulae implanted in either the caudate-putamen or cortex dorsal to the amygdala, the effects of intra-amygdala naloxone is not due to diffusion of the drug to these brain regions. Intra-amygdala injectiins of the β 1,2-adrenoceptor blocker propranolol (0.3 μg) blocked the memory enhancing effects of intra-amygdala naloxone (IA : 0.1 μg; YMD : 0.3 μg) administered concurrently immediately post-training. We interpret these findings as indicating that the enhancing effects of intra-amygdala naloxone are mediated by the activation of β-noradrenergic receptors within the amygdala. Such effects are presumably due to blocking of inhibitory effects of opioid peptides on the release of norepinephrine.