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At least 1,711 records · Page 95Linked to original sources
PubMed1994

Archistriatal lesions impair the acquisition of filial preferences during imprinting in the domestic chick.

The avian archistriatum has been demonstrated to play a role in agonistic behaviours and avoidance learning. However, the extent of its role in learning is unknown. The involvement of the archistriatum in the learning process of filial imprinting was therefore investigated in day-old chicks. Bilateral archistriatal lesions, lateral cerebral area lesions or sham archistriatal penetrations were made in dark-reared, day-old chicks, which were subsequently exposed to either a rotating red box or blue cylinder for 2 x 1 h training sessions. Three hours later, the approach of chicks to their training object and to the other, novel object was measured. Chicks with archistriatal lesions ran a similar distance towards each stimulus and therefore failed to display a preference for their training object. However, chicks with sham archistriatal penetrations or lateral cerebral area lesions exhibited a significant preference for the object they had been trained upon. These results demonstrate that the archistriatum is essential for the expression of an imprinted preference. All chicks approached their training object significantly more on their second compared to their first training exposure, suggesting that some aspects of imprinting behaviour remain intact in chicks with archistriatal lesions. Taken together with the results of previous work, the current data suggest that the archistriatum may be involved in retention of significant aspects of the imprinting experience, or in motivation to approach imprinting objects.

Animals↗
PubMed1996

Acquisition of conditioned inhibition in rats is impaired by ablation of serotoninergic pathways.

The effects of chronically ablating the serotoninergic inputs to various regions of the rat brain on the ability to solve a feature-negative discrimination was measured. After intracerebroventricular administration of the specific neurotoxin 5,7-dihydroxytryptamine, the rats exhibited an impaired capacity to solve such a discrimination, irrespective of whether auditory or visual stimuli were used. Further behavioural analysis revealed that this effect was not due to a reduced capacity to form excitatory associations, since both groups responded equally to reinforced stimuli. By contrast, the lesion more likely resulted in a failure to endow the non-reinforced stimuli with inhibitory properties. This suggestion was supported by the observation that, in a retardation test, the conditioned inhibitor aroused less inhibition in the lesioned group than in vehicle-injected controls. Furthermore, the conditioned inhibitor failed to pass a summation test in lesioned animals, again indicating that their hampered ability to master the discrimination was the result of an impairment in the formation of inhibitory associations. It is concluded that destruction of central 5-hydroxytryptamine-containing pathways impairs the functioning of brain areas underlying inhibitory associative learning.

5,7-Dihydroxytryptamine↗
PubMed1991

Aversive and compensatory classical conditioning with diazepam as conditional stimulus.

The purpose of the first experiment was to investigate whether diazepam could acquire anxiogenic properties by signalling an aversive event. Rats were trained in an operant chamber in the pentylenetetrazol (PTZ) model of anxiety. Thereafter the animals were divided into groups that received classical diazepam conditioning (Group 1), and conditioning of diazepam + tone (Group 2). In the test phase diazepam was injected prior to placement in the operant chamber. Group 2 selected the PTZ-appropriate lever more often than the other groups, indicating that the tone induced anxiety, and diazepam did not. Tones and shock may therefore be more easily associated than diazepam and shock. The second experiment investigated this. Rats were trained the same way as in the first experiment. Thereafter the experimental group received injections of a small dose of diazepam prior to a second injection of a large dose of diazepam. The hypothesis was that a compensatory anxiogenic conditional response to diazepam's anxiolytic effect should be elicited by the small dose. There were no differences between the groups in lever selection, indicating that a compensatory anxiogenic response was not elicited.

Animals↗
PubMed1992

Characterisation and regional localisation of pre- and postsynaptic glycoproteins of the chick forebrain showing changed fucose incorporation following passive avoidance training.

To identify those glycoproteins whose synthesis or modification is necessary for memory formation, we have studied the uptake of radiolabelled fucose into synaptic plasma membranes (SPMs) and postsynaptic densities (PSDs) derived from two specific left and right forebrain loci, at two different times after training of 1-day-old chicks on a one-trial passive avoidance learning task. To increase the reliability of the comparison, a double-labelling method was used. Tissue samples from intermediate medial hyperstriatum ventrale (IMHV) and lobus parolfactorius (LPO) were isolated at 6 and 24 h after training. At both times, training resulted in region-specific changes, both increases and decreases, in incorporated radioactivity into pre- and postsynaptic glycoproteins. After 6 h, there was a relative decline in incorporation into both SPMs and PSDs of the right IMHV of trained chicks, a decline that persisted in the PSDs until 24 h. A small decline in incorporation in SPMs from the right LPO of trained chicks at 6 h was reversed by 24 h, by which time there was a 64% increase in incorporation into SPMs and a 24% increase into PSDs of the left LPO. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analysis of left and right hemisphere samples containing LPO revealed that 6 h after training the main effect was presynaptic, including a reduction of incorporation into high molecular mass glycoproteins, of 150-180 kDa, and an increase in a lower molecular mass (41 kDa) fraction. By 24 h after training, a left hemisphere presynaptic glycoprotein of molecular mass approximately 50 kDa showed the biggest increase in fucosylation. In addition, a wide group of postsynaptic glycoproteins of both hemispheres, in the ranges 150-180, 100-120, and 33 kDa now showed increases in incorporation. Some other fractions showed decreases. These results are in accord with previous data on incorporation obtained using the amnesic agent 2-deoxygalactose. They also support the hypothesis that memory formation involves the strengthening of connections between pre- and postsynaptic neurons of the LPO by growth or modulation of pre- and postsynaptic structures.

Animals↗
PubMed1992

Ambient temperature effects on taste aversion conditioned by ethanol: contribution of ethanol-induced hypothermia.

Six experiments examined the effects of low (5-10 degrees C), normal (21 degrees C), or high (32 degrees) ambient temperature on conditioned taste aversion and body temperature changes produced by ethanol, lithium chloride, or morphine sulfate. Fluid-deprived rats received five to seven taste conditioning trials at 48-hr intervals. On each trial, access to saccharin at normal ambient temperature was followed by injection of drug or saline and placement for 6 hr into a temperature-controlled enclosure. Exposure to low ambient temperature facilitated, whereas exposure to high ambient temperature retarded acquisition of ethanol-induced conditioned taste aversion. The ability of an alteration in ambient temperature to influence conditioned taste aversion varied as a function of ethanol dose and was related to ambient temperature's effect on ethanol-induced hypothermia. More specifically, strength of conditioned taste aversion was negatively correlated with core body temperature after ethanol injection. Alterations in ambient temperature alone did not affect ingestion of a paired flavor solution in the absence of drug. Moreover, alterations in ambient temperature did not appear to influence conditioned taste aversion by changing ethanol pharmacokinetics. Finally, high and low ambient temperature did not affect development of taste aversion conditioned by lithium chloride or morphine sulfate. The overall pattern of data presented by these experiments supports the hypothesis that ambient-temperature influences strength of ethanol-induced conditioned taste aversion by altering the hypothermic response to ethanol. More generally, these data support the suggestion that body temperature change induced by ethanol is related to ethanol's aversive motivational effects and may be involved in modulating ethanol intake.

Animals↗
PubMed1993

State-dependent stimulus control: cueing attributes of ethanol "hangover" in rats.

In Experiment 1, twelve Sprague-Dawley rats were trained in a two-choice food-reinforced drug discrimination task (10-min sessions) using the state-dependent interoceptive stimulus attributes of ethanol's (ETOH) delayed or rebound effects (EDE) versus "normal" basal homeostasis. Rats were injected with either 4 g/kg ETOH or equivalent volumes of saline (SAL) 18 hr before the sessions. Each rat was injected with an additional 1 ml/kg injection of SAL 15 min before the sessions. EDE training sessions were always followed by a "day off." SAL sessions were conducted between 36-96 hr after an EDE training session. Rats demonstrated > 90% discriminative accuracy. Test sessions showed a time-dependent, cyclic, return from the experimental "hangover" state to the "normal" state, by 48 hr. The acute (immediate) effects of ETOH and chlordiazepoxide (0.75 g/kg or 0.18 mg/kg, respectively; @15 min) did not cross-generalize with the "hangover" state. Both these low-dose ETOH and chlordiazepoxide pretreatments blocked the stimulus attributes of "hangover." All subjects responded on the EDE-appropriate lever at 5.6 mg/kg pentylenetetrazole and exhibited an increase in susceptibility to clonic seizures. In Experiment 2 blood alcohol concentration kinetics functions were quantified in three groups (n = 8/group) of age-matched cohorts to Experiment 1 subjects (2, 3, and 4 g/kg ETOH) using a head-space gas chromatographic technique. The training stimulus state associated with 4 g/kg, at 18 hr postinjection intervals, in Experiment 1, did not produce any chromatogram peaks for ETOH or any its active metabolite (acetaldehyde, acetone, nor methanol).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Reduced sensitivity to ethanol reward, but not ethanol aversion, in mice lacking 5-HT1B receptors.

Various serotonergic receptor systems are thought to influence the motivational effects of ethanol. This experiment characterized the acquisition of ethanol-induced conditioned taste aversion and ethanol-induced conditioned place reference in mutant knockout mice lacking 5-HT1b receptors. In the taste conditioning procedure, adult homozygous knockout mice (-/-) and homozygous wild-type mice (+/+) received access to 0.2 M NaCl solution, followed immediately by intraperitoneal injection of 0 to 4 g/kg of ethanol. Ethanol produced dose-dependent conditioned taste aversion that was the same in both genotypes. In the place conditioning procedure, knockout and wild-type mice received six pairings of a tactile stimulus with ethanol (2 g/kg, i.p.). A different tactile stimulus was paired with saline. Ethanol produced increases in locomotor activity, with wild-type mice showing higher levels of ethanol-stimulated activity than knockout mice during conditioning trials 5 and 6. Wild-type mice demonstrated conditioned place preference for the ethanol-paired stimulus. In contrast, knockout mice showed no evidence of place conditioning. These results are generally consistent with an important role for serotonergic systems in ethanol reward and specifically indicate that 5-HT1b receptors are important for ethanol's rewarding effects but not for ethanol's aversive effects.

Alcoholism↗
PubMed2004

Convergent analysis of cDNA and short oligomer microarrays, mouse null mutants and bioinformatics resources to study complex traits.

Gene expression data sets have recently been exploited to study genetic factors that modulate complex traits. However, it has been challenging to establish a direct link between variation in patterns of gene expression and variation in higher order traits such as neuropharmacological responses and patterns of behavior. Here we illustrate an approach that combines gene expression data with new bioinformatics resources to discover genes that potentially modulate behavior. We have exploited three complementary genetic models to obtain convergent evidence that differential expression of a subset of genes and molecular pathways influences ethanol-induced conditioned taste aversion (CTA). As a first step, cDNA microarrays were used to compare gene expression profiles of two null mutant mouse lines with difference in ethanol-induced aversion. Mice lacking a functional copy of G protein-gated potassium channel subunit 2 (Girk2) show a decrease in the aversive effects of ethanol, whereas preproenkephalin (Penk) null mutant mice show the opposite response. We hypothesize that these behavioral differences are generated in part by alterations in expression downstream of the null alleles. We then exploited the WebQTL databases to examine the genetic covariance between mRNA expression levels and measurements of ethanol-induced CTA in BXD recombinant inbred (RI) strains. Finally, we identified a subset of genes and functional groups associated with ethanol-induced CTA in both null mutant lines and BXD RI strains. Collectively, these approaches highlight the phosphatidylinositol signaling pathway and identify several genes including protein kinase C beta isoform and preproenkephalin in regulation of ethanol- induced conditioned taste aversion. Our results point to the increasing potential of the convergent approach and biological databases to investigate genetic mechanisms of complex traits.

Animals↗
PubMed2006

Early genomics of learning and memory: a review.

The characterization of the molecular mechanisms whereby our brain codes, stores and retrieves memories remains a fundamental puzzle in neuroscience. Despite the knowledge that memory storage involves gene induction, the identification and characterization of the effector genes has remained elusive. The completion of the Human Genome Project and a variety of new technologies are revolutionizing the way these mechanisms can be explored. This review will examine how a genomic approach can be used to dissect and analyze the complex dynamic interactions involved in gene regulation during learning and memory. This innovative approach is providing information on a new class of genes associated with learning and memory in health and disease and is elucidating new molecular targets and pathways whose pharmacological modulation may allow new therapeutic approaches for improving cognition.

Animals↗
PubMed1985

Neural mediation of conditioned food aversions.

The above discussion is only a brief review of what is known about the neural mediation of conditioned food aversions. Although several other approaches were not mentioned (e.g. biochemical studies), one can still appreciate the value of the aversion paradigm for providing important information about neural mechanisms in learning and memory. A theoretical approach that may be valuable in understanding brain function in conditioned food aversion data is Hughlings Jackson's hierarchical notions of nervous organization. Hedonic responses to food stimuli appear to be brainstem reflexes. On top of these are rostral brain structures that add greater complexity to the consummatory behavior of the organism. An important aspect of this complexity is reflected in an animal's ability to form conditioned food aversions, a process undoubtedly tied intimately to particular neural mechanisms.

Afferent Pathways↗
PubMed2003

Consideration of a unified model of amygdalar associative functions.

This paper considers issues arising from presentations by Barry Everitt and Gorica Petrovich concerning amygdalar involvement in appetitive conditioning. Studies reported by these researchers are beginning to unravel the distribution of associative functions among amygdalar nuclei and their efferent targets. The main issue addressed here concerns how to integrate the information from studies of appetitive conditioning with conclusions from studies of other forms of associative learning, including pavlovian fear conditioning and instrumental conditioning. Most students of this issue will agree that no prima facie integration is readily apparent in current scholarship. Although we do not here provide the definitive integration, we do attempt to take some preliminary, broad-brush steps towards that goal.

Amygdala↗