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PubMed1979

Ontogenetic changes in the modulation of taste aversion learning by home environmental cues in rats.

Eight experiments using 611 rats as subjects were conducted to define and analyze an age-related phenomenon of conditioned taste aversion. When consumption of sucrose solution was followed by LiCl-induced illness in the animals' home, acquisition of the aversion to sucrose solution was retarded in preweanling (18-day-old) rats. This effect was not found in adults or in slightly older (21-day-old) rats. Place of testing had no effect in the younger two age-groups, but in adults manifestation of the acquired aversion was retarded when they were tested in the home. There was no interaction between place of conditioning and testing for any age. The locus of the environmental influence on conditioning in preweanling rats was found to be the place of tasting rather than place of illness, retention interval, or testing. Also, the effect was found to be invariant under minor variations in familiarization of the animal with the non-home environment. The principle emerging from these data and others is that the home environment can have a significant influence on learning and conditioning in the immature rat.

Animals↗
PubMed1980

Aversion learning in 5-day-old rats: taste-toxicosis and texture-shock associations.

Five-day-old rats that received a single pairing of a novel saccharin flavor with lithium treatment learned to suppress ingestion of saccharin on subsequent occasions (Experiment 1). This flavor aversion learning was inversely related to the interval between the novel flavor experience and drug administraton, wit h significant aversions being learned with intervals of 0 and 30 min but not with intervals of 60 and 90 min (experiment 2). The conditioning was observed when hypertonic lithium served as the unconditioned stimulus but did not occur with isotonic lithium or hypertonic saline injections (Experiment 3). These results indicate that flavor aversion learning in infant rats is a result of the joint action of two factors--pure drug effects and the somatic pain and irritation produced by the tonicity of the injected agent. The taste aversion learning was specific to the drug-paired flavor, and evidence was presented suggesting that 5-day-old rats display a natural hesitancy to consume novel edibles (neophobia) (Experiment 4). Experiment 5 demonstrated that 5-day-old rats selectively associate tactile stimuli with shock but not with the gastrointestinal consequences of lithium. Implications of the mechanisms involved in flavor aversion learning in infant rats are discussed as they relate to adaptation and food selection in adult animals.

Animals↗
PubMed1980

Effects of interference stimuli on the acquisition of learned aversions to foods in the rat.

A learned food aversion paradigm was developed to investigate characteristics of aversion learning likely to be involved in nutrient selection. The development of aversions to a relatively familiar, complete food was examined in rats with continuous access to that food. Learned food aversions were observed which were specific to the particular diet present during a sequence of toxic drug injections. In subsequent studies, novel liquids and solids were introduced in association with drug treatment to examine their effectiveness as interference stimuli. Flavored solutions, which have previously been reported to interfere with conditioned taste aversions, had little or no effect on learned aversions to the diet. This lack of interference by novel flavored liquids was coupled with significant conditioned aversions to the novel liquids themselves. Novel flavored solutions were contrasted with novel foods, which were extremely effective as interference stimuli in this paradigm. Possible bases for the observed differences in interference effects of foods and drinks are examined.

Animals↗
PubMed1980

Specificity of acquired aversions to taste qualities in hamsters and rats.

Nine groups of rats and 27 groups of hamsters (n = 12/group) each tasted 1 from among 27 different solutions before receiving an ip injection of apomorphine, then were tested for aversions to 4 solutions prototypic of human beings' four taste qualities (S, sucrose; N, NaCl; H, Hcl; Q, quinine hydrochloride). With most of the solutions that are described as sweet by humans employed as a conditional stimulus (CS), the rodents acquired an S aversion (exceptions occurring for some artificial sweeteners). With CSs described as either predominantly salty or sour by humans, the rodents acquired an N aversion in the former case or an H aversion in the latter case; a Q aversion was also acquired with two (including H) of the three CSs described as sour. With most of the CSs described as predominantly bitter or as having a considerable bitter component by humans, the rodents acquired a Q aversion (as well as a weaker H aversion). Considerable parallels among the taste sensations of humans, rats, and hamsters are indicated. Patterns of activity evoked across four classes of peripheral gustatory neurons (those responding best to lingual stimulation with S, N, H, or Q) in rodents when the CSs were applied to the tongue were similar to the patterns of aversions across the four test stimuli for the CSs. This suggests that these four neural channels mediate the sensations evoked by S, N, H, and Q in rats and hamsters, perhaps even in human beings.

Animals↗
PubMed1982

Selective associations in one-day-old rats: taste-toxicosis and texture-shock aversion learning.

One-day-old rats learned aversions to a novel taste paired with lithium-induced distress and to a tactile stimulus paired with brief electric shocks. However, aversions did not develop when taste was paired with shock or when the tactile stimulus was paired with lithium treatment. The aversions occurred only when lithium treatment immediately followed taste exposure and when shock was concurrent with exposure to the tactile stimulus. These findings indicate that selective associations in aversion learning are mediated by innate mechanisms that govern conditioning in the absence of extensive ontogenetic experience. The present research also shows that selective associations are sufficient for the occurrence of long-delay learning.

Animals↗
PubMed1982

Flavor-illness aversions: potentiation of odor by taste with toxin but not shock in rats.

Potentiation of odor by taste in rats was tested in a variety of situations. In three experiments, almond odor and saccharin taste were presented either as a single conditioned stimulus (CS) or as a compound CS and followed by either toxic lithium chloride or footshock. Extinction tests with the almond and saccharin components were then given. In single CS-toxin experiments, taste was more effective than odor, and after compound conditioning, the taste component potentiated the odor component. Conversely, in single CS-shock experiments, odor was more effective than taste, and after compound conditioning, no potentiation was observed. Rather, interference effects were observed. In Experiments 1 and 2, the addition of taste disrupted odor CS-shock conditioning, and in Experiment 3, odor interfered with taste CS-shock conditioning. Visceral feedback is apparently a necessary unconditioned stimulus for the potentiation of odor by taste. These data support the neural convergence and gating hypothesis of flavor aversion conditioning.

Animals↗
PubMed1982

Flavor-illness aversions: gustatory neocortex ablations disrupt taste but not taste-potentiated odor cues.

Two experiments evaluated the contribution of the gustatory neocortex (GN) to the potentiation of odor by taste during illness-induced aversions in rats. In Experiment 1, rats lacking GN and control rats were given an odor, a taste, or an odor-taste compound cue followed by intragastric gavage of lithium chloride. Prior to conditioning, neophobia for flavored solutions was absent in rats with GN lesions. After pairing with LiCl, GN rats developed normal conditioned odor aversions (Experiment 1B), whereas conditioned taste aversions were attenuated (Experiment 1A) or totally blocked (Experiment 1B). Potentiation of odor by taste after compound conditioning was evident in both control and GN rats, although GN lesions attenuated the effect slightly in Experiment 1B. In Experiment 2, normal rats were given compound conditioning to induce potentiated odor aversions and then given GN lesions prior to tests with the odor and taste components. Taste aversion retention was disrupted totally by GN ablation; potentiated odor aversions were retained by both groups, although the GN group extinguished faster. Gustatory neocortex ablations produced differential effects on odor and taste, disrupting taste memorial and associative processes but leaving odor conditioning and the potentiation of odor by taste processes relatively unaffected. Integrity of the GN apparently is not necessary for the acquisition or retention of potentiation odor aversions.

Animals↗
PubMed1982

Contribution of the rat's neocortex to ingestive control: I. Latent learning for the taste of sodium chloride.

Neocortical mechanisms do not directly contribute to the execution of taste discrimination, sodium appetite, or the acquisition of a taste aversion in the rat. Examination of previous studies led to the question of whether some permanent ingestive control deficit would be revealed if elements of these experimental paradigms were combined. A latent learning paradigm for the taste of salt was applied to decorticate rats. The ability of decorticate rats to associate how they obtained the taste of NaCl when sodium replete was assessed by examining bar presses during extinction when sodium depleted. Intact rats exposed to 4-6 hr of NaCl taste training retained the association after decortication; decorticate rats exposed to the same training acquired the association. What was most striking was that decorticate rats exposed to as little as 2 min of NaCl taste training demonstrated the ability to associate bar pressing with NaCl by their resistance to extinction. The association was specific to NaCl training; training with distilled water or KCl did not yield resistance to extinction during sodium depletion. Subcortical structures are therefore adequate for latent learning involving NaCl taste. Conversely, data of other investigators have revealed that the neocortex is required for the retention of taste aversion learning for the same taste.

Animals↗
PubMed1982

Long-delay associations between drug states produced in rats by injecting two drugs in sequence.

Injection of pentobarbital after a rat has consumed saccharin solution usually produces a mild aversion to the saccharin. However, the pentobarbital-produced aversion is eliminated or attenuated by prior pairings of pentobarbital injections with lithium injections. This is called the Avfail (aversion failure) effect. The present experiments dealt with the effect of the temporal relation of the pentobarbital injection to the lithium injection. After forward pairings (pentobarbital before lithium) with delays between the two injections varying among groups from 2.5 min to 320 min, Avfail was invariably obtained. There was little effect of the length of the forward delay, although the Avfail effect appeared to be slightly stronger at 30-40 min or so. When the two drugs were injected simultaneously or in a backward sequence, there was a weakening of the flavor aversion produced by pentobarbital, but this is attributable to habituation to the drugs, not to Avfail.

Animals↗
PubMed1982

Potentiation of odor by taste in rats: tests of some nonassociative factors.

The contribution of nonassociative neophobia and sensitization to the potentiation of odor by taste in rats was tested in three experiments. In Experiment 1, neophobia for almond odor (O), saccharin taste (T), and odor-taste compound (OT) cues was tested before and after noncontingent lithium chloride poisoning and compared with conditioned aversions produced by OT-LiCl temporal pairing. The OT compound potentiated unconditioned neophobia, but there was no evidence of poison-enhanced neophobia, disinhibition of neophobia, or sensitization by noncontingent LiCl; temporal pairing produced aversions for the compound and its elements. In Experiment 2, generalization to a novel odor was tested after O-LiCl or compound OT-LiCl pairing. The potentiated odor aversion did not generalize to the novel odor; it was specific to the odor paired with taste and LiCl. In Experiment 3, potentiation of the odor component by a discriminant or nondiscriminant taste component was tested. Potentiation was evident only when a novel discriminant taste was in compound with odor prior to LiCl poisoning. These studies support an associative "indexing" hypothesis of the potentiation effect in rats.

Animals↗
PubMed1982

Acquisition and extended retention of a conditioned taste aversion in preweanling rats.

The time course of memory decay for infant rats may shed light on the processes responsible for infantile amnesia. A taste aversion conditioning procedure appropriate for both neonatal and adult rats was employed in four experiments to investigate the ontogeny of extended retention. In Experiment 1, rats trained at 1, 10, 20, or 60 days of age were tested for retention of the taste aversion 25 days later. At testing, only those rats conditioned when 20 or 60 days old demonstrated significant taste aversions. Experiments 2 and 3 established that rats 14-15 days old and older were able to retain significant taste aversions following a 25-day retention interval. Younger rats did, however, acquire and retain the aversion for several days and showed a gradual retention loss over progressively longer retention intervals (Experiment 4). These findings suggest that preweanling rats demonstrate initial consolidation, storage, and retrieval of conditioned taste aversions. It is only after this initial period that retention deficits become evident.

Aging↗
PubMed1989

Recovery of spatial learning deficits after decay of electrically induced synaptic enhancement in the hippocampus.

A widespread interest in a long-lasting form of synaptic enhancement in hippocampal circuits has arisen largely because it might reflect the activation of physiological mechanisms that underlie rapid associative learning. As its induction normally requires the 'Hebbian' association of activity on a number of input fibres, we refer to the process as long-term enhancement (LTE) rather than long-term potentiation (LTP), to emphasize its distinction from the ubiquitous, non-associative 'potentiation' phenomena that occur at most synapses, including those exhibiting LTE. Among other evidence that LTE might actually have a role in associative memory is the demonstration that repeated high-frequency stimulation, which saturated the inducible LTE, caused a severe deficit in spatial learning, although it had no effect on well established spatial memory. These results were consistent with a widespread view that information need only temporarily be stored in the hippocampal formation in order for long-term memories to be established in neocortical circuits. In this context, it is important to understand whether the possible underlying synaptic changes are of a permanent character, or are relatively transient. A second question is whether the actual cause of the observed learning deficit is the distruption of the synaptic weight distribution, and/or the limitation of further synaptic change, which presumably results from experimental saturation of the LTE mechanism. Alternatively, the deficit could be a consequence of some unobserved secondary effect of the high-frequency electrical stimulation. Here we demonstrate that learning capacity recovers in about the same time that it takes LTE to decay, which strongly favours the first possibility and supports the idea that LTE-like processes actually underlie associative memory.

Animals↗
PubMed2001

Multiple benefits of gregariousness cover detectability costs in aposematic aggregations.

Understanding the early evolution of aposematic (warning) coloration has been a challenge for scientists, as a new conspicuous morph in a population of cryptic insects would have a high predation risk and would probably die out before local predators learnt to avoid it. Fisher presented the idea of aggregation benefit through the survival of related individuals; however, his theory has been strongly debated as the mechanisms that favour grouping have never been explored experimentally with the incorporation of detectability costs. Here we create a comprehensive 'novel world' experiment with the great tit (Parus major) as a predator to explore simultaneously the predation-related benefits and costs for aposematic aggregated prey, manipulating both group size and signal strength. Our results show that grouping would have been highly beneficial for the first aposematic prey individuals surrounded by naive predators, because (1) detectability risk increased only asymptotically with group size; (2) additional detectability costs due to conspicuous signals were marginal in groups; (3) even naive predators deserted the group after detecting unpalatability (dilution effect); and (4) avoidance learning of signal was faster in groups. None of these mechanisms require kin selection.

Animals↗
PubMed1997

Influence of olfactory bulbectomy and subsequent imipramine treatment on 5-hydroxytryptaminergic presynapses in the rat frontal cortex: behavioural correlates.

1. Alterations of 5-hydroxytryptaminergic mechanisms are thought to play a special role in the pathogenesis of depression and antidepressant treatments are assumed to restore these changes. 2. We have used one of the most reliable models of depression, the olfactory bulbectomized rat to study the long term consequences of this manipulation and of subchronic imipramine treatment on two parameters of 5-hydroxytryptaminergic presynapses, 5-hydroxytryptamine (5-HT) transporter density and tryptophan hydroxylase apoenzyme concentration, in the frontal cortex as well as on active avoidance learning several weeks after bulbectomy. 3. The Bmax value of [3H]-paroxetine binding and the concentration of the 5-HT synthesizing enzyme were both significantly elevated in the frontal cortex of bulbectomized rats compared to sham-operated controls. 4. Imipramine treatment, either by daily injections or by subcutaneous implantation of slow release imipramine-containing polymers reduced the elevated tryptophan hydroxylase apoenzyme levels in the frontal cortex of bulbectomized, but not of sham-operated control rats and restored the deficient learning performance of bulbectomized rats. 5. Both effects were more pronounced after continuous drug administration by imipramine-releasing polymers compared to daily i.p. injections. 6. These findings indicate that bulbectomy leads to a compensatory 5-hydroxytryptaminergic hyperinnervation of the frontal cortex. Chronic antidepressant treatment seems to attenuate the increased output of the 5-hydroxytryptaminergic projections in the frontal cortex through the destabilization of the rate limiting enzyme of 5-HT synthesis of the 5-hydroxytryptaminergic nerve endings in this brain region.

Adrenergic Uptake Inhibitors↗
PubMed2006

Neuroprotective effect of exogenous microglia in global brain ischemia.

Exogenous microglia pass through the blood-brain barrier and migrate to ischemic hippocampal lesions when injected into the circulation. We investigated the effect of exogenous microglia on ischemic CA1 pyramidal neurons. Microglia were isolated from neonatal mixed brain cultures, labeled with the fluorescent dye PKH26, and injected into the subclavian artery of Mongolian gerbils subjected to ischemia reperfusion neuronal injury. PKH26-labeled microglia migrated to the ischemic hippocampal lesion, resulting in increased numbers of surviving neurons compared with control animals, even when injected 24 h after ischemia. Interferon-gamma stimulation of isolated microglia enhanced the neuroprotective effect. Administration of exogenous microglia resulted in normal performance in a passive avoidance-learning task. Additionally, administration of exogenous microglia increased the expression of brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor in the ischemic hippocampus, and thus might have induced neurotrophin-dependent protective activity in damaged neurons. Peripherally injected microglia exhibited a specific affinity for ischemic brain lesions, and protected against ischemic neuronal injury in vivo. It is possible that administration of exogenous microglia can be developed as a potential candidate therapy for central nervous system repair after transitory global ischemia.

Animals↗