Brightness Discrimination Task Research Articles

The effects of ibotenic acid lesions of the basal forebrain on visual discrimination performance in rats

Rats were trained to stable performance in a conditional brightness discrimination task and then received infusions of ibotenic acid or vehicle into the basal forebrain. Following 2 weeks of recovery, animals were retested in the original discrimination. Lesioned rats tended to performed badly on the first day of testing as measured by all parameters (percent correct responding, latency to respond, and missed trials) but thereafter, most rats recovered quickly to prelesion levels. In keeping with previous reports, an approximately 30% reduction in choline acetyltransferase activity was observed in the lesioned animals. Four rats showed no recovery over a period of several months; however, an analysis of the choline acetyltransferase in several brain regions revealed no obvious differences to those animals in which performance recovered. Postlesion testing with the putative nootropic β-carboline ZK 93426 showed no major differences to the effects observed in control animals. Scopolamine had similar negative effects in both groups tested. These data indicate that deficits induced by lesions of the basal forebrain do not correlate with reductions in cholinergic activity.

Recovery of brightness discrimination in adult rats despite progressive loss of retrogradely labelled retinal ganglion cells after controlled optic nerve crush.

Restoration of brightness discrimination was studied in adult rats after controlled crush of the optic nerve in order to further characterize a recently introduced experimental brain injury model. Mild, moderate or severe crush of the optic nerve produced partial or complete loss of the ability to perform a brightness discrimination task. Two to three weeks following mild injury we observed nearly complete spontaneous behavioural recovery whereas recovery was more limited after moderate and totally absent after severe crush. Horseradish peroxidase (HRP) injected into the superior colliculus was transported retrogradely across the lesion site and accumulated in retinal ganglion cells (RGCs). Two days following mild, moderate or severe crush, 28, 23 and 8% respectively of RGCs were found to be labelled with HRP, indicating that they are still connected with their target and are therefore presumably intact. RGC loss affected all areas of the retina homogeneously. At postoperative day 14, the number of morphologically 'intact' RGCs declined even further to 11% in the mild injury group, despite our observation of recovery of vision to near-normal levels. The mechanism whereby such impressive neuronal plasticity is achieved despite the rather small number of intact RGCs is still unknown. However, further studies of the crush model using additional behavioural, morphological and electrophysiological techniques may allow us to determine more clearly the biological basis of recovery of function after central nervous system injury.

Methanesulfonyl fluoride (MSF) blocks scopolamine-induced amnesia in rats

—Cholinesterase inhibitors, such as physostigmine and tetrahydroaminoacridine, have been found to alleviate some of the memory deficits characteristic of senile dementia of the Alzheimer's type (SDAT). Many toxic side effects, however, have been associated with the use of these compounds. Recently, a cholinesterase inhibitor, methanesulfonyl fluoride (MSF), was discovered to have low toxicity, central nervous system (CNS) selectivity, and a long therapeutic duration. The purpose of this research was to determine if MSF (1.5 mg/kg) would be effective in reducing or blocking amnesia induced by various doses of scopolamine (0.2, 0.6, and 2.0 mg/kg). One hundred and twenty two female Sprague-Dawley albino rats were trained and retention tested in a Y- maze brightness discrimination task. MSF was highly effective in reducing scopolamine-induced amnesia.

Memory dysfunction following disruption of glutamergic systems in the temporal region of the rat: effects of agonistic amino acids

It has previously been shown that disruptions of fiber connections between the temporal cortex (TC) and the lateral entorhinal cortex (LEC) in rats result in severely impaired retention of a simultaneous brightness discrimination task. This memory impairment is accompanied by reduced high affinity d-aspartate uptake in both TC and LEC. The purpose of this study was to investigate whether systemic administration of glutamergic agonists might ameliorate the mnemonic dysfunction seen to follow TC/LEC transections. The results from Experiment 1 show that agonists acting selectively at the NMDA receptors (NMDA and glycine) or the quisqualate receptors (AMPA) produced complete amelioration of the memory deficit. Injection of kainic acid only produced a slight improvement of memory. The results from Experiment 2 show that the positive effects of agonists are probably not attributable to drenergic mechanisms, because blockade of sympathetic terminal release did not prevent mitigating effect of glycine. The results are discussed in terms of possible central nervous mechanisms interfered with by the various agonists.

GM1 ganglioside treatment reduces visual deficits after graded crush of the rat optic nerve

Despite numerous reports of beneficial effects of GM1 ganglioside treatment following brain lesions in animals, the underlying neurobiological mechanism of ganglioside-induced functional restoration is still unclear. In order to obtain a better insight into this question, we have made use of a newly developed animal model of brain injury that would potentially permit us to determine the causal relationships(s) among behavioral and neuroanatomical/neurochemical parameters of restoration of function. Following graded crush of the adult rat optic nerve, we have treated the rats with intraperitoncally injected gangliosides and studied the functional outcome with electrophysiological and behavioral parameters. The electrophysiological recprding of the compound action potential (CAP) from excised rat optic nerve revealed a significant loss of CAP throughout the first 2 weeks after the injury. However, when rats were treated daily for 7 days with GM1-gangliosides, the CAP measured 10 days after the crush was significantly larger compared to operated controls without treatment. Thus, GM1 appeared to be capable of delaying or partially preventing retinal ganglion cells or their axons from secondary degeneration. Loss of visual function was also evident on the behavioral level of analysis: when rats with unilateral optic nerve crush were evaluated in a visual orienting paradigm, the rats revealed deficits in their ability to orient towards small, moving visual stimuli. However, within about 2 weeks, the animals recovered spontaneously to near normal performance. Daily treatment with GM1-gangliosides was found to significantly improve outcome, largely due to a reduction of the immediate post-lesion deficit. In a second behavioral experiment we also created graded crush in rats bilaterally and evaluated the animals visual capacities in a two-choice brightness discrimination task. In this park, an initial loss of function was followed by recovery within about 2 weeks, but GM1 treatment was without beneficial effects in this paradigm. It is concluded that GM1 improves outcome after graded crush of the adult rat optic nerve, although it appears that improved function needs to be documented with sufficiently sensitive behavioral assays.

Retroactive memory of a visual discrimination task in the rat: role of temporal-entorhinal cortices and their connections

It has previously been shown that the temporal and entorhinal cortices may be critically involved in memory. In Experiment 1, rats with either damage to the temporal cortex (TC), lateral entorhinal cortex (LEC), or the medial entorhinal cortex (MEC) were tested for retention of a preoperatively acquired simultaneous brightness discrimination task. TC and LEC lesions impaired retention, whereas MEC lesions were without mnemonic effect. In Experiment 2, rats with either disruptions of the anterior neural connections of TC (TC/Ant), posterior connections of TC (TC/Post), or conjoint disruptions (Ant/Post) were tested for retention of the visual discrimination task. TC/Ant and Post/Ant lesions resulted in relatively mild, but significant memory impairment, whereas a profound effect was seen after TC/Post lesions. The results are discussed in terms of a very important role for LEC and its connections with TC in mnemonic function.

Flumazenil (Ro 15‐1788) enhances learning in both negatively and positively reinforced tasks

AbstractFlumazenil (Ro 15‐1788) is classically described as a benzodiazepine‐receptor (BZ‐R) antagonist, devoid of any intrinsic effect and thus used to selectively block the effects of others BZ‐R ligands. The present report provides evidence that flumazenil enhances learning in a multiple‐trial brightness discrimination task in mice, whether the reinforcement is negative (electric foot‐shock) or positive (food reward). However, in contrast to the negative reinforcement, we obtained a significant effect with the positive reinforcement only after a delay of a few days. The type of reinforcement might be involved in this delay necessary to observe enhanced learning. These results are discussed.

Similar effects of a beta-carboline and of flumazenil in negatively and positively reinforced learning tasks in mice

Methyl beta-carboline-3-carboxylate (beta-CCM) and flumazenil (Ro15-1788) are known to be respectively an inverse agonist and an antagonist of the central benzodiazepine-receptor. Surprisingly, these two drugs have shown a similar enhancing effect in a negatively reinforced multiple-trial brightness discrimination task in mice. Thus, to evaluate the role of anxiety in this task, the action of these two drugs were compared in the same learning task with a positive or a negative reinforcement. Mice were trained for sessions of ten trials per day for six consecutive days. The sessions during the first three days took place after administration of beta-CCM (0.3 mg/kg), flumazenil (15 mg/kg) or vehicles of these drugs. A negative reinforcement (electric foot-shock) was used in a first experiment, and a positive one (food reward) in a second experiment. Results showed that, whatever the reinforcement, the two drugs enhance learning in a brightness discrimination task. The hypothesis is that flumazenil could have an inverse agonist profile in learning tasks. The equation remains as to whether the flumazenil enhancing learning process results from increased arousal and/or anxiogenic factors, or from a negative modulatory influence of endogenous diazepam-like ligands for benzodiazepine receptors.

Effects of intraventricularly applied gangliosides and N-acetylneuraminic acid on acquisition and retention performance of a brightness discrimination task in rats

The effects of intraventricularly applied gangliosides (about 90 to 120 nmoles/10 μl) and N-acetylneuraminic acid (800 nmoles/10 μl) on acquisition and retention of a brightness discrimination task were studied in rats. Single injections of GT 1b and N-acetylneuraminic acid improved the retention performance. GM 1 showed an enhancing effect on both acquisition and retention, while GD 1a and GD 1b exerted no influence on the behavioral parameters tested. The findings presented show how memory may be improved by exogenous application of substances commonly occurring in the mammalian body.

Idebenone improves learning and memory impairment induced by cholinergic or serotonergic dysfunction in rats

The effects of idebenone, a cerebral metabolic enhancer, on learning and memory impairment in two rat models with central cholinergic or serotonergic dysfunction were investigated using positively reinforced learning tasks. A delayed alternation task using a T maze was employed to test the effect of idebenone on short-term memory impairment induced by a cholinergic antagonist, scopolamine. A correct response, defined as a turn toward the arm opposite to that in the forced run, was rewarded with food pellets. Scopolamine (0.2 and 0.5 mg/kg, i.p.) significantly decreased the correct responses to the chance level in the 60-s-delayed alternation task. The scopolamine (0.2 mg/kg, i.p.)-induced impairment of short-term memory was improved by idebenone (3–30 mg/kg, i.p.) or an acetylcholinesterase inhibitor, physostigmine (0.1 and 0.2 mg/kg, i.p.), administered simultaneously. The central serotonergic dysfunction model was produced by giving rats a diet deficient in tryptophan, a precursor of serotonin. The rats fed on a tryptophan-deficient diet (TDD) showed a slower learning process in the operant brightness discrimination task (mult VI15 EXT) than did rats fed on a normal diet. Idebenone (60 mg/kg/day) admixed with the TDD decreased the number of lever-pressing responses emitted during the extinction periods. The percentage of correct responses was significantly higher in the idebenonetreated group than in the control TDD group. These results suggest that idebenone may improve both the impairment of short-term memory induced by a decreased cholinergic activity and the retardation of discrimination learning induced by central serotonergic dysfunction.

The temporal-hippocampal region and retention: the role of temporo-entorhinal connections in rats.

Results from previous studies suggest that the entorhinal cortex may be involved in mnemonic processes. The present study was carried out to investigate whether disruption of fibre connections between the temporal cortex and lateral entorhinal area may impair retention of a pre-operatively acquired simultaneous brightness discrimination task. The lesion resulted in a severe impairment in retaining the discrimination task (Experiment 1). The retention deficit could not be traced into the hippocampal formation by making perforant path lesions or hippocampal lesions (Experiment 2). The results indicate that the lateral entorhinal cortex is more crucial for reference memory than the hippocampal formation.

The contribution of the rewarded and the non-rewarded stimulus in visual discrimination learning in mice

The relative contribution of the rewarded and non-rewarded stimulus in the learning of a visual discrimination task in various species is unclear. A number of different parameters have been suggested as influencing the importance of the one over the other, among them the type of reinforcement. Our results show that with both positive reinforcement (using water as reward after a correct choice, and no reinforcement after an incorrect choice) and negative reinforcement (electroshock punishment after an incorrect choice) mice use the position of the incorrect stimulus as a cue for the discrimination. Mice trained by positive reinforcement without the added negative reinforcement of blocking the door on which the incorrect stimulus is projected, do not learn a brightness discrimination task. This suggested that the added negative reinforcement of the closed door had a strong influence on the learning behaviour in our experiments.

Impairment of glycoprotein fucosylation in rat hippocampus and the consequences on memory formation

The intraventricular injection of 2-deoxy-D-galactose led to a dose-and-time-dependent decrease in the fucosylation of hippocampal glycoproteins in rats whereas the incorporation of 3H-N-acetyl-glucosamine was not influenced. This effect is not related to an interference with fucose activating or transferring enzymes but can be abolished by an application of D-galactose. Thus, it seems likely that also in brain tissue a deoxy-galactose induced decrease in the fucosylation is due to a hindering of a glycosidic linkage of fucose to the deoxy-sugar incorporated into glycoprotein chains. As a consequence of an intrahippocampal injection of the deoxy-sugar the retention performance of the animals in a foot-shock motivated brightness discrimination task was considerably impaired. But deoxy-galactose is effective only when administered before and immediately after training whereas either a pre- or a post-training injection did not influence the retention performance of the rats. Thus, an effective metabolic inhibition of the glycoprotein completion by the deoxy-sugar starting at the time of training seems to be crucial to interfere with such morphofunctional alterations in the neuronal network underlying the formation of a memory trace.

Discrimination learning and reversal following electrolytic lesions of the median raphe nucleus

The current study examined the effects of electrolytic median raphe lesions on the performance of several T-maze discrimination tasks. Raphe lesions were found to impair the reversal, but not the acquisition, of a learned position habit, but to be without effect on either the acquisition or reversal of simultaneous brightness discrimination task. Rats with raphe damage were severely impaired in the acquisition of either a successive brightness discrimination task or of a delayed spatial alternation task. These results are similar to those which have been reported after limbic damage, and support the view that the paramedian midbrain tegmentum may play an important role in the functioning of limbic structures.

Effect of posterior cortical lesion on two versions of the brightness-discrimination task

The brightness-discrimination performancę of normal and posterior decorticate rats was measured in two test situations designed to provide different spatial task characteristics. A Y-maze and an open field with otherwise matched stimulus properties provided tests with many or few spatial characteristics, respectively. In contrast to predictions from visuospatial integrative interpretations of lesion consequences, the present results indicated no attenuation of the typical operative impairment when the reduced spatial-cue tasks were employed. Furthermore, this outcome was common to both simple acquisition/retention (Experiment 1) and successive discrimination reversal (Experiment 2) versions of the tasks. Interpretations of the relative contribution of memory or visuospatial integrative deficits to the measured behavioral consequences are discussed.

Vasopressin and vasotocin facilitate reversal of a brightness discrimination

Male albino rats received vasopressin, vasotocin, pressinoic acid or placebo and were tested on an aversively motivated brightness discrimination task. Treatment with both vasopressin and vasotocin had no effect on acquisition but facilitated the reversal of the discrimination. Pressinoic acid had an inconsistent effect. The results are interpreted to show that the C terminal of the peptides vasopressin and vasotocin influence potency of these peptides. Furthermore, the results are interpreted as showing that both vasotocin and vasopressin influence selective attention during aversively motivated tasks.

Effect of apomorphine on retention of a brightness discrimination in dopamine supersensitive rats

Apomorphine is known to improve the retention performance of a brightness discrimination task after post-training intrahippocampal application to rats. The present study shows that the retention performance of dopamine supersensitive rats was improved by a low dose of apomorphine which was still ineffective in control animals. Dopamine supersensitivity by itself had no effect on acquisition and retention parameters of brightness discrimination. The result further supports the assumption that dopamine receptors in rat hippocampus can modulate the formation of memory.

Perinatal linoleate deprivation impairs learning and memory in adult rats

Rats receiving polyunsaturated fatty acid (PUFA) deficient diets during the perinatal period showed in adult age undisturbed acquisition of a footshock motivated brightness discrimination task, but a significant impairment of retention. The same effects on retention were obtained in rats receiving the PUFA deficient diet in adulthood, when the behavioral parameters were investigated at the end of the dietary treatment.

Apomorphine and glycoprotein synthesis during consolidation

The dopamine agonist, apomorphine, was injected intrahippocampally immediately after acquisition of a brightness discrimination task, which was motivated by footshock in rats. This led to an increase in the incorporation of L-fucose into total proteins which were measured in the hippocampus 7–9 hours later. In behavioral experiments, the same application improved the retention of a learned task. A possible linkage between increased glycoprotein synthesis and improvement of the retention of a new learned behavior due to the action of apomorphine is discussed.

Recovery of visual pattern discrimination by rats without visual cortex when trained by fading procedure

The effects of two training and two surgical procedures on the recovery of a visual pattern discrimination were compared in rats with visual cortex damage (areas 17,18, and 18a). Normal control subjects and rats with serial or simultaneous visual cortex lesions were first trained on a brightness (black vs. white) discrimination task and then on a pattern (horizontal vs. vertical stripes) discrimination task by either classical or fading procedures. The rats’ performance in the preoperative, interoperative, and postoperative stages of training were compared. Rats with serial lesions showed postoperative savings in the brightness task and relearned the pattern discrimination task when trained by either the fading or the classical method. Serially lesioned subjects presented fewer errors to criterion when trained by the fading procedure than when trained by the classical procedure. Rats with simultaneous lesions showed no savings on the brightness discrimination task and all of the subjects in this group relearned the pattern discrimination task when trained by the fading procedure. Simultaneously lesioned subjects trained to a maximum of 750 trials using the classical method did not relearn the pattern discrimination task, except for one subject. Interaction between the surgical and training variables is discussed.