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PubMed1987

Lever pressing and active avoidance conditioning after electrolytic lesions of the entopeduncular nucleus in cats.

Several authors have shown that CN participates in the acquisition of motor conditioned responses (MCR), probably as the integrating structure. Most of CN's efferent fibers in the cat end in the entopeduncular nucleus (EPN), therefore the command for the motor pattern could be exerted through EPN, representing part of the efferent link of the neuronal circuitry involved in MCR. Thirty-two cats were trained to avoid actively an electrical stimulus when a series of flashes appeared, and to press a lever to obtain 0.5 ml of milk. After the cats reached the learning criterion for both responses, electrolytic lesions of the entopeduncular nucleus or internal capsule (IC) were made bilaterally. When the cats recovered their normal motor behavior, the conditioned sessions were resumed once a day, for 45-50 days. Both learning responses disappeared (p less than 0.01) in those animals with the largest EPN lesions. In contrast, for small EPN lesions, learned responses were absent only during the first 3 or 4 sessions, and then the level of responses increased each day. However, it never reached that of sham lesioned cats. On the other hand, IC lesioned cats showed no statistical differences with respect to sham lesioned animals. These data support the participation of EPN in the motor circuitry responsible for MCR.

Animals↗

PubMed2005

The perirhinal cortex of the rat is necessary for spatial memory retention long after but not soon after learning.

Many observations in humans and experimental animals support the view that the hippocampus is critical immediately after learning in order for long-term memory formation to take place. However, exactly when the medial temporal cortices adjacent to the hippocampus are necessary for this process to occur normally is not yet well known. Using a spatial task, we studied whether the perirhinal cortex of rats is necessary to establish representations in long-term memory. Results showed that, in a spatial task sensitive to hippocampal lesions, control and perirhinal lesioned rats can both learn at the same rate (Experiment 1). Interestingly, a differential involvement of the perirhinal cortex in memory retention was observed as time passes after learning. Thus, 24 days following the end of learning, lesioned and control rats remembered the task perfectly as measured by a retraining test. In contrast, 74 days after the learning the perirhinal animals showed a profound impairment in the retention of the spatial information (Experiment 2). Taken together, these results suggest that the perirhinal region is critical for the formation of long-term spatial memory. However, its contribution to memory formation and retention is time-dependent, it being necessary only long after learning takes place and not during the phase immediately following acquisition.

Analysis of Variance↗

PubMed2001

Cortisol differentially affects memory in young and elderly men.

Nine young and 11 elderly men participated in this placebo-controlled, double-blind, crossover study (0.5 mg/kg cortisol or intravenous placebo). Participants learned a word list before cortisol administration, and delayed recall was then tested. A 2nd word list was learned and recalled after drug administration. In addition, the Paragraph Recall Test and tests measuring working memory (Digit Span), attention (timed cancellation), and response inhibition (Stroop Color and Word Test) were administered at 2 time points after drug administration. Cortisol reduced recall from the word list learned before treatment in both groups but did not influence recall of the list learned after treatment. In contrast, Digit Span performance was decreased by cortisol in young but not elderly participants. The possibility that differential age-associated brain changes might underlie the present results is discussed.

Adult↗

PubMed2003

Lead-induced impairments in complex cognitive function: offerings from experimental studies.

Experimental studies, relying primarily on rodent and non-human primate models, have produced compelling evidence supporting effects of chronic low level lead exposure on learning, with the magnitude of those effects possibly modulated by developmental period of exposure and learning paradigm parameters. In contrast, changes in memory are not systematically demonstrated. The impact of lead exposure on attention has yet to be clearly delineated in either human or experimental studies, although impulsivity or aversion to delay appears to be a sensitive component of attention that may be targeted.

Animals↗

PubMed1999

Mechanisms of perceptual learning.

Systematic measurements of perceptual learning were performed in the presence of external or stimulus noise. In the new external noise method (Dosher, B, & Lu, Z.-L. (1997). Investigative Ophthalmology and Visual Science, 38, S687; Lu, Z.-L., & Dosher, B. (1998). Vision Research, 38, 1183-1198), increasing amounts of external noise (white Gaussian random noise) is added to the visual stimulus in order to identify mechanisms of perceptual learning. Performance improved (threshold contrast was reduced) over days of practice on a peripheral orientation discrimination task--labelling Gabor patches as tilted slightly to the right or left. Practice improvements were largely specific to the trained quadrant of the display. Performance improved at all levels of external noise. The external noise method and perceptual template model (PTM) of the observer identifies the mechanism(s) of performance improvements as due to stimulus enhancement, external noise exclusion, or internal noise suppression. The external noise method was further extended by measuring thresholds at two threshold performance levels, allowing identification of mixtures in the PTM model. Perceptual learning over 8-10 days improved the filtering or exclusion of external noise by a factor of two or more, and improved suppression of additive internal noise--equivalent to stimulus enhancement--by 50% or more. Coupled improvements in external noise exclusion and stimulus enhancement in the PTM model may reflect channel weighting. Perceptual learning may not reflect neural plasticity at the level of basic visual channels, nor cognitive adjustments of strategy, but rather plasticity at an intermediate level of weighting inputs to decision.

Discrimination, Psychological↗

PubMed2003

Conditional expression in corticothalamic efferents reveals a developmental role for nicotinic acetylcholine receptors in modulation of passive avoidance behavior.

Prenatal nicotine exposure has been linked to attention deficit hyperactivity disorder and cognitive impairment, but the sites of action for these effects of nicotine are still under investigation. High-affinity nicotinic acetylcholine receptors (nAChRs) contain the beta2 subunit and modulate passive avoidance (PA) learning in mice. Using an inducible, tetracycline-regulated transgenic system, we generated lines of mice with expression of high-affinity nicotinic receptors restored in specific neuronal populations. One line of mice shows functional beta2 subunit-containing nAChRs localized exclusively in corticothalamic efferents. Functional, presynaptic nAChRs are present in the thalamus of these mice as detected by nicotine-elicited rubidium efflux assays from synaptosomes. Knock-out mice lacking high-affinity nAChRs show elevated baseline PA learning, whereas normal baseline PA behavior is restored in mice with corticothalamic expression of these nAChRs. In contrast, nicotine can enhance PA learning in adult wild-type animals but not in corticothalamic-expressing transgenic mice. When these transgenic mice are treated with doxycycline in adulthood to switch off nAChR expression, baseline PA is maintained even after transgene expression is abolished. These data suggest that high-affinity nAChRs expressed on corticothalamic neurons during development are critical for baseline PA performance and provide a potential neuroanatomical substrate for changes induced by prenatal nicotine exposure leading to long-term behavioral and cognitive deficits.

Animals↗

PubMed1996

Neural mechanisms for visual memory and their role in attention.

Recent studies show that neuronal mechanisms for learning and memory both dynamically modulate and permanently alter the representations of visual stimuli in the adult monkey cortex. Three commonly observed neuronal effects in memory-demanding tasks are repetition suppression, enhancement, and delay activity. In repetition suppression, repeated experience with the same visual stimulus leads to both short- and long-term suppression of neuronal responses in subpopulations of visual neurons. Enhancement works in an opposite fashion, in that neuronal responses are enhanced for objects with learned behavioral relevance. Delay activity is found in tasks in which animals are required to actively hold specific information "on-line" for short periods. Repetition suppression appears to be an intrinsic property of visual cortical areas such as inferior temporal cortex and is thought to be important for perceptual learning and priming. By contrast, enhancement and delay activity may depend on feedback to temporal cortex from prefrontal cortex and are thought to be important for working memory. All of these mnemonic effects on neuronal responses bias the competitive interactions that take place between stimulus representations in the cortex when there is more than one stimulus in the visual field. As a result, memory will often determine the winner of these competitions and, thus, will determine which stimulus is attended.

Animals↗

PubMed2000

Piracetam and levetiracetam: close structural similarities but different pharmacological and clinical profiles.

Piracetam (PIR) and levetiracetam (LEV), an S-enantiomer, are pyrrolidone derivatives that share similar chemical structures but have distinct pharmacological profiles and consequently different clinical uses. Although the mode of action of neither drug has been fully elucidated, they do not interact with inhibitory or excitatory neurotransmission or alter membrane excitability. A brain-specific stereoselective binding site has been identified for which LEV and other S-enantiomers, but not PIR, have high affinity. In preclinical studies, PIR significantly improves learning and memory; in contrast, LEV has less effect but is much more active in preventing seizures. Both drugs have a high therapeutic index and are well tolerated. PIR, a nootropic drug, is used in the therapy of age-related cognitive disturbances and poststroke aphasia. Clinical experience has also shown that at high doses it is effective against cortical myoclonus. LEV is an antiepileptic drug. Clinical trials have confirmed its efficacy in partial seizures and preliminary findings suggest that it is also effective in generalized seizures and myoclonus.

Animals↗

PubMed1986

Spatial contrast sensitivity in facial recognition.

Recognition and learning of complex images may depend on spatial processing characteristics of the visual system. Prosopagnosia, an impairment of visual learning and recognition of faces, might result from impaired perception in spatial channels carrying crucial information. We studied spatial contrast sensitivity (SCS) in two subjects with stable facial recognition defects. One had relative SCS reduction for high-frequency gratings but could process high frequencies in room light. The other had normal SCS. Both had intact spatial processing relative to image size. The results suggest that impairments in visual spatial channels are not necessary for the development of prosopagnosia.

Adult↗

PubMed1997

Cognitive impairment in spontaneously hypertensive rats: role of central nicotinic receptors. Part II.

The adult spontaneously hypertensive rat (SHR) has been shown to exhibit a decrease in the expression and nicotine-stimulated function of brain nicotinic acetylcholine receptors, factors that could play a role in the impaired ability of this strain in the performance of learning and memory-related tasks. The purpose of this study was to determine whether either or both the impaired task performance and the loss of nicotinic receptors is directly related to the presence of the hypertensive state. To address this issue, two experimental approaches were taken. In the first series, 4-week-old pre-hypertensive SHR were tested in two phases of a water maze (spatial memory) task, and their performance was compared with that of two age-matched normotensive strains, Wistar Kyoto (WKY) and Wistar rats. During phase 1, SHR and WKY rats were not different in their ability to learn the task. In contrast, during phase 2 (subsequent series of trials after a 4 day inter-phase period), where rats were required to find a new platform location, SHR exhibited significantly impaired performance compared to both WKY and Wistar normotensive controls. In a single trial passive avoidance paradigm, SHR again displayed significantly reduced avoidance behavior as compared with both WKY and Wistar rats. In consecutive coronal sections the density of [3H]cytisine binding sites was decreased in pre-hypertensive SHR by up to 18% in about 40% of the brain regions examined, with the deficits particularly apparent in frontal cortex (layers 4-6), posterior subiculum, several thalamic regions, and the interpeduncular nucleus. In the second series, age-matched SHR and WKY were treated with the antihypertensive agent hydralazine administered in the drinking water beginning at 4 weeks of age. Hydralazine prevented the development of hypertension in adult SHR, but did not forestall the reduced expression of brain nicotinic receptors, nor the impairment in learning- and memory-related tasks normally observed in untreated adults with established hypertension. Moreover, the magnitude of nicotine-stimulated rubidium efflux from cortical and striatal synaptosomes in vitro was significantly reduced in samples derived from hydralazine-treated SHR as compared with those from hydralazine-treated, or untreated WKY. These results support the contention that the hypertensive state does not directly contribute to the reduced expression of nicotinic receptors in SHR. Therefore, the SHR may provide an important genetic model for the study of the role of central nicotinic receptors in cognitive and learning abnormalities.

Aging↗

PubMed1999

Effects of methamphetamine on the adjusting amount procedure, a model of impulsive behavior in rats.

RATIONALE: Moderate doses of d-amphetamine (given both acutely and chronically) have been shown to decrease impulsivity in children with attention deficit hyperactivity disorder (ADHD) and to improve attention and learning in normal adults. In contrast, chronic doses of methamphetamine (METH) in drug abusers have been associated with increased impulsivity, and impairments in learning and attention. OBJECTIVES: We report the effects of METH on an animal model of impulsive behavior. METHODS: Rats were tested using the adjusting amount (AdjAmt) procedure in which the animals choose between a delayed fixed (large) amount of water and an immediate adjusting (small) amount of water. In the acute METH study, rats were given a single dose of 0.5, 1.0, 2.0, and 4.0 mg/kg METH or saline 30 min before testing. In the chronic METH study, we determined the effects of the 4.0 mg/kg dose of METH injected chronically 1 h after behavioral testing for 14 days. Thus the rats were tested using the AdjAmt procedure 22 h after injections of METH or saline. RESULTS: After 0.5, 1.0 and 2.0 mg/kg METH, the rats valued the delayed large rewards more than after saline, indicating that the METH decreased impulsiveness. At the 4.0 mg/kg dose, the rats failed to respond. Rats treated repeatedly with the post-session large behaviorally disruptive dose of METH valued the delayed large rewards less than the saline-treated rats, indicating that this dosing regimen of METH increased impulsiveness. CONCLUSIONS: In these experiments, the rats became less impulsive after acute non-disruptive doses of pre-session METH, whereas they became more impulsive after receiving repeated post-session injections of a dose that was behaviorally disruptive when administered acutely.

Animals↗

PubMed1992

High vocal center growth and its relation to neurogenesis, neuronal replacement and song acquisition in juvenile canaries.

It is generally thought that most circuits of the adult central nervous system (CNS) are sculpted, in part at least, by selective elimination of some of the neurons present in an initial overabundant set. In this scenario, the birth of neurons precedes the period when brain functions, such as learning, first occur. In contrast to this form of brain assembly, we describe here the delayed development of the high vocal center (HVC) and one of its efferent pathways in canaries. The retrograde tracer Fluoro-Gold (FG) was injected into one of HVC's two efferent targets, the nucleus robustus archistriatalis (RA), to define the boundaries of HVC. The HVC grows markedly between 1 and 4 months, invading neighboring territories of the caudal telencephalon. During this same period, 0.43%-0.64% of the HVC neurons present at 1 year of age are labeled per day of [3H]-thymidine injection. [3H]-Thymidine labeling is a marker of cell birth, and during the first 4 months HVC neuron number increases, probably accounting for part of the HVC growth observed. Thereafter, the number of HVC neurons remains constant, but neuronal birth persists. We infer from this that neuronal replacement starts as early as 4 months after hatching and perhaps before then. About half of the neurons born after posthatching day 10 grow an axon to RA to form the main efferent pathway exiting from HVC. HVC growth, neurogenesis, axogenesis, and the observed replacement of neurons happen during the period of juvenile vocal learning. However, the recruitment of neurons that are still present at 1 year shows no particular inflections corresponding to the various stages in song learning, and continues at essentially the same rate after the more stereotyped adult song has been acquired. We suggest that a combination of neurogenesis and neuronal replacement provides unique advantages for learning.

Animals↗

PubMed1975

Evoked potential correlates of early conditioning in the rat ontogeny.

In rats aged 2-8 weeks cortical EP to CS (20 flash - tone combinations, 0,9/sec, reinforced since the 10th application by electric shocks to the hind leg) were studied within different kinds of behavioral responses during avoidance learning and extinguishing. In contrast to our results in freely moving rats no developmental trend was found in this kind of avoidance (lifting of the hind leg). Average EP within reinforced trials (with escape or no reactions) differed in isolated application of CS from those when both CS and US were acting together. In younger animals the EP to CS combined with US were characterized by an evident late negative wave which shifted later (5-6 weeks toward the early negative complex. The EP changes in the auditory cortex were more pronounced, whereas visual EP with CS-US combination were rather decreased. In the youngest animals (2 weeks) the auditory EP within trials with avoidance were characterized by a distinct short latency deflection of the first positive wave, whereas in EP to extinguished CS the second deflection of the first positive wave prevailed. Also in these phenomena, the typical changes were clearly revealed in the auditory cortex. At later developmental stages (starting the 3rd, more prominently the 4th and 5th week) the wave following primary positive - negative complex was shifted toward the negativity if the animal responded by an avoidance; on the contrary an ample positive, often a double-peak wave arose if the response was extinguished. The stimulus and reaction dependence in the cortical EP showed the role of not yet fully mature cerebral cortex in avoidance learning. Both, fast as well as with some delay running processes participated in the observed phenomena during the ontogenetical development.

Animals↗

PubMed1989

Comparative effects of quisqualic and ibotenic acid-induced lesions of the substantia innominata and globus pallidus on the acquisition of a conditional visual discrimination: differential effects on cholinergic mechanisms.

Two experiments tested the hypothesis that the deficits in conditional discrimination learning produced by ibotenic acid-induced lesions of the ventral pallidum and substantia innominata are produced by loss of the magnocellular cholinergic cells in the nucleus basalis and adjacent regions. Experiment 1 replicated the previously reported deficit in conditional learning produced by ibotenate-induced lesions of the ventral pallidum/substantia innominata, but failed to demonstrate any restoration of learning by a subchronic regimen of the acetylcholinesterase inhibitor physostigmine sufficient to produce significant (30%), but equivalent, degrees of inhibition in the frontal cortex of ventral pallidum/substantia innominata-lesioned or sham-operated rats. Experiment 2 examined the effects of quisqualic acid-induced lesions of the ventral pallidum/substantia innominata. According to most of the measures of learning employed, the quisqualic acid-induced lesion of the ventral pallidum/substantia innominata failed to impair conditional learning, even though the quisqualate-induced lesion produced greater degrees of cholinergic neuron destruction than the ibotenate-induced lesion, as measured in terms of reductions in cortical choline acetyltransferase activity (44% vs 27%). Although consideration of individual data suggested that very high (60%) levels of choline acetyltransferase reduction in Experiment 2 might have detrimental effects of conditional learning, the overall failure of the quisqualate-induced lesions of the ventral pallidum/substantia innominata to impair learning is to be contrasted with the significant behavioural effects of ibotenate-induced lesions. Histological and immunocytochemical analysis showed that the quisqualate-induced lesion, unlike that produced by ibotenate, tended to produce less damage to the overlying dorsal globus pallidus and to parvocellular neurons of the ventral pallidum/substantia innominata, thus implicating these nonspecific effects of ibotenate-induced lesions in their behavioural effects. The present results question previous interpretations of the behavioural effects of ibotenate-induced lesions of the ventral pallidum/substantia innominata in terms of damage inflicted on the cortically-projecting cholinergic cells of the nucleus basalis, and suggest that quisqualic acid, although also nonspecific in its excitotoxic effects, is nevertheless more selective for producing damage to cholinergic neurons in the ventral pallidum/substantia innominata than ibotenic acid.

Animals↗

PubMed2005

Behavioral and neurophysiological analyses of dynamic learning processes.

In this article, the authors address two topics relevant to the study of the brain basis of associative learning. In Part 1, they compare and contrast the patterns and time course of dynamic learning-related neural activity that have been reported in the medial temporal lobe, premotor cortex, prefrontal cortex, and striatum during various associative learning tasks. In Part 2, they examine the statistical methodologies that have been used to analyze both behavioral learning and learning-related neural activity. They describe a state-space model of behavioral learning that provides accurate estimates of dynamic learning processes and a point-process filter algorithm that tracks the dynamic changes in neural activity on a millisecond time scale. Future challenges for these statistical methodologies and their application to the study of the brain basis of associative learning are discussed.

Association Learning↗

PubMed2005

Lesions of orbitofrontal cortex impair rats' differential outcome expectancy learning but not conditioned stimulus-potentiated feeding.

Patients with damage to the orbitofrontal cortex (OFC) display various impairments in cognitive and affective function, including a reduced ability to use information about the consequences of their actions to guide their behavior. In this study, rats with neurotoxic lesions of the OFC failed to use specific expectancies about outcomes to guide their learning of an instrumental discrimination task. In contrast, lesioned rats were unimpaired in a measure of learned motivational function, the potentiation of feeding under conditions of food satiation, by a conditioned stimulus that had been paired with food while the rats were food deprived. Notably, performance of both of these tasks has been shown to depend on the function of the basolateral amygdala (BLA), a region that is richly interconnected with the OFC. Thus, the present results are consistent with the view that the acquisition and use of specific outcome expectancies to guide behavior critically involve a neural system that includes the BLA and the OFC, but they indicate that certain motivational properties acquired by cues on the basis of appetitive learning involve BLA circuitry apart from the OFC.

Animals↗

PubMed1989

Effects of desipramine on rat behavior are prevented by concomitant treatment with ethanol.

Ethanol prevents the decrease of the number of beta-adrenoceptors in the cerebral cortex induced by chronic treatment of rats with desipramine. The activation of the adenylate cyclase, the second messenger, by beta-adrenergic agonists is reduced somewhat less than after treatment with desipramine alone. The present paper examined the hypothesis that ethanol inhibits the neuronal adaptation to desipramine chronic treatment at the functional level as well. Desipramine reduced exploratory behavior (crossings, rearings) as did ethanol. Combined treatment attenuated the effect of desipramine. Cognitive performance was investigated using an active avoidance paradigm. Desipramine-treated rats did not learn the task in contrast to control animals. Again, combination treatment with ethanol improved the ability of the rats to perform the task. The activity of cerebral beta-adrenergic mechanisms was assessed by injection of salbutamol, a beta-adrenoceptor agonist in rats pretreated with 5-hydroxytryptophan (5-HTP). The augmentation of the 5-HTP-induced wet dog shake behavior by salbutamol was observed in all animals independent of the chronic treatment. However, rats treated with desipramine were less active than those treated with tap water or ethanol. The effect of desipramine in the presence of a high concentration of salbutamol was attenuated by ethanol. The observed increase of the number of wet dog shakes correlates with the function of these receptors. In two paradigms, spontaneous motility and apomorphine-induced hypothermia, ethanol did not affect the action of desipramine. It is noteworthy that desipramine acted in both situations within a short time period (minutes to hours). The findings strongly suggest that ethanol can prevent adaptive changes in the brain induced by chronic treatment with the antidepressant desipramine. This is of special interest since the adaptation of beta-adrenoceptors is thought to be critical for the antidepressant efficacy of various therapeutic interventions applied in psychiatric practice.

5-Hydroxytryptophan↗

PubMed2000

Molecular overexpression of extracellular superoxide dismutase increases the dependency of learning and memory performance on motivational state.

Extracellular superoxide dismutase (EC-SOD) controls the availability of extracellular superoxide and appears to play a role in controlling intercellular signaling. In this role EC-SOD can have potent effects on neurobehavioral function. In previous studies, we have found that either over- or under-expression of EC-SOD in mice significantly impairs spatial learning on the radial-arm maze. In the current study, the neurobehavioral nature of the EC-SOD role in cognitive function was determined. EC-SOD overexpression altered the relationship between both learning and memory with motivational state. Mice were tested in the radial-arm maze under a high motivational state (22-24 hours of food restriction) or a low motivational state (4-6 hours of food restriction). Under a high motivational state, the EC-SOD overexpressing mice were able to learn in the radial-arm maze, albeit at a slightly lower rate than wild-type controls. This contrasts with the failure to learn by EC-SOD overexpressing mice in our previous study conducted with the low motivational state. The change in motivational state did not significantly alter the learning rate of controls. Similarly, during postacquisition memory phase of testing, the EC-SOD overexpressing mice were significantly worse than controls when tested in a low motivational state but not under a high motivation state. As with learning, motivational state did not significantly affect memory performance in controls. This study shows that mice with EC-SOD overexpression are not incapable of learning and memory in the radial-arm maze, but that the mechanisms which allow control animals to perform this task well under low motivational states are deficient in the mice with EC-SOD overexpression.

Animals↗