Learning in the Africanized honey bee: Apis mellifera L

Several series of experiments are reported that investigate learning in the Africanized honey bee. In the first series, classical conditioning of proboscis extension was studied by confining bees to small metal tubes where they received pairings of an odor with a 3-s feeding of sucrose. After a number of odor-sucrose pairings, the bees began to extend their proboscis to the odor. Controls include Unpaired, Discrimination, and Pseudoconditioning Groups. This technique was used to look at conditioning to a light CS, and to the odors of beeswax, geraniol, citral, and hexanal. The results indicate that acquisition was best when sucrose was paired with the odor of beeswax. Conditioning to the remaining odors was roughly similar, but acquisition did not occur using a light. In a second series of experiments, odors were no longer followed by sucrose feedings and the conditioned response slowly disappeared. With the exception of geraniol as a CS, this extinction effect did not occur if the animals continued to be fed on an unpaired schedule. In a third series of experiments, conditioned inhibition was demonstrated when geraniol was used as conditioned stimuli, but no effect was found when the odors of hexanal, citral and wax were used. In a fourth series of experiments, unrestrained bees flew back and forth from the laboratory to the hive, where they were taught to distinguish targets based on color and odor. With this technique, color and odor discrimination in the Africanized bees was demonstrated. In addition, it was found that more intruder bees visited the experimental station when the stimuli used were olfactory rather than visual.     

Behavioral expression of learned fear: Updating of early memories.

The expression of learned fear emerges in a response-specific sequence where freezing occurs before fear potentiated startle (FPS) to an odor conditioned stimulus (CS; Postnatal Day [PN] 16 vs. PN 23; e.g., Hunt, 1997; Richardson, Paxinos, & Lee, 2000). Studies have shown that learned fear is expressed in a manner appropriate to the animal's age at training and not its age at test (Richardson & Fan, 2002; Richardson et al., 2000). Specifically, animals trained with an odor CS at PN 16 exhibit avoidance but not FPS when tested at PN 23. The present study shows that subsequent training with a different CS can "update" an early memory, allowing it to be expressed in a manner appropriate to the animal's age at test. This updating effect appears to be modality specific, whereby the subsequent training must involve a CS of the same sensory modality as the original training. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The expression of fear-potentiated startle during development: Integration of learning and response systems.

Relative to freezing, fear-potentiated startle (FPS) is developmentally delayed. Rats trained on Postnatal Day (PD) 18 expressed conditioned stimulus learning on PD 19 in freezing but not in FPS, whereas rats trained on PD 24 and tested on PD 25 expressed both freezing and FPS (Experiment 1). According to a neural maturation hypothesis, this delay results from functional immaturity of pathways mediating FPS. When rats were trained on PD 18, neither delaying the FPS test, allowing FPS pathways to develop, nor administrating the "reminder" treatment, the expression of FPS was promoted (Experiments 1, 2, and 2A). PD 18 learning was expressed in FPS on PD 25 when nontarget conditioned stimulus-unconditioned stimulus training occurred prior to the test, and this effect was modality dependent (Experiments 3 and 4). The authors conclude that engaging mechanisms of associative encoding when FPS pathways are functional is a critical condition for integrating learning and FPS response systems in development. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Odor-guided fear conditioning in rats: 2. Lesions of the anterior perirhinal cortex disrupt fear conditioned to the explicit conditioned stimulus but not to the training context.

Previous studies examining the neural substrates of fear conditioning have indicated unequivocally that the acquisition and expression of conditioned fear depends critically on the integrity of the amygdala. The extent to which the rhinal cortical areas contribute to fear conditioned to either the explicit conditioned stimulus (CS) or to the training context is less clear, however. The effects of pretraining lesions of the anterior perirhinal (PRH) cortex on fear conditioned to an explicit odor CS and to the context in which CS–unconditioned stimulus pairing took place was examined in rats. Rats with PRH cortex lesions demonstrated a robust attenuation of fear conditioned to the explicit CS, but no attenuation of fear conditioned to the training context. These data suggest that the PRH cortex is an important component of the neural system supporting the association between olfactory cues and footshock and add to a growing body of evidence implicating the rhinal cortical regions in associative learning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Memory effects on symptom reporting in a respiratory learning paradigm.

With odors as conditioned stimuli (CSs) and CO?-enriched air as the unconditioned stimulus, participants learned to exhibit respiratory responses and somatic complaints on presentation of only the odor CS+. Studied was whether complaints during CS+-only trials were inferred from the conditioned somatic responses or were based on activated memory of the complaints during acquisition. Participants (N?=?56) were either attentionally directed away or not from the complaints during acquisition, and the effects on somatic complaints during test were studied. Respiratory responses, heart rate, and somatic complaints were measured. No physiological conditioning effects were found. However, more complaints were reported to the CS+ than to the CS– odor, but only when the CS+ was foul smelling. This effect was modulated by the attention manipulation, showing that the learned complaints during the test phase were based on memory of the acquisition complaints and not on physiological responses during the test. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Basolateral amygdala NMDA receptors are selectively involved in the acquisition of taste-potentiated odor aversion in the rat.

In the taste-potentiated odor aversion (TPOA) paradigm, animals acquire a strong aversion to an odor that is followed by delayed intoxication only if a gustatory stimulus is presented with the odor during conditioning. Although previous work has shown that N-methyl-D-aspartate (NMDA) receptors in the basolateral nucleus of the amygdala (BLA) play a role in the acquisition of TPOA, the present study aimed at.describing the process in which NMDA receptors in the BLA are involved during acquisition of TPOA. Male Long-Evans rats received intra-BLA infusions of the competitive NMDA receptor antagonist {d},{l}-2-2-amino-5-phosphonovalerate ({d}-APV; 0.05 and 0.50 μg) immediately before or after the odor–taste conditioned stimulus (CS) presentation, or immediately before the test. Results showed that {d}-APV impaired acquisition of TPOA when infused before, but not after, the CS presentation, but did not affect retrieval. These results suggest that NMDA receptors of the BLA are involved in the formation of potentiation—by taste—of the olfactory memory trace, but not in the maintenance of this process. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Facilitation of conditioned odor aversion by entorhinal cortex lesions in the rat.

This study examined the role of the entorhinal cortex (EC) in conditioned odor aversion learning (COA). Lateral EC lesions did not impair but rather facilitated COA. In the experiments the delay separating the odor cue presentation from the subsequent toxicosis was varied during acquisition. EC-lesioned rats demonstrated COA for delays up to 2 hr, whereas sham-operated rats displayed COA only if toxicosis immediately followed the odor cue. This facilitation was not dependent on the intensity of the odor and corresponded to a facilitated long-delay learning. EC lesion did not affect conditioned taste aversion, confirming that the facilitation effect does not correspond to a general facilitation of conditioned aversion learning. Taken together, these results indicate that the removal of the EC may allow odor-toxicosis associations across longer delays by extending the duration of the olfactory trace. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste-potentiated odor aversion learning: Role of the amygdaloid basolateral complex and central nucleus.

Examined the relative contributions of the amygdaloid basolateral complex (ABL) and central nucleus (CN) to taste-potentiated odor aversion (TPOA) learning, an associative learning task that is dependent on information processing in 2 sensory modalities. In Exp 1, rats with neurotoxic lesions of these systems were trained on the TPOA task by presenting a compound taste–odor conditioned stimulus (CS), which was followed by LiCl administration. Results showed that ABL damage caused an impairment in potentiated odor aversion learning but no deficit in the conditioned taste aversion. In contrast, rats with CN damage learned both tasks. Exp 2 examined the effects of ABL damage on TPOA and odor discrimination learning. The odor discrimination procedure used a place preference task to demonstrate normal processing of olfactory information. Results indicated that although ABL-lesioned animals were impaired on TPOA, there was no deficit in odor discrimination learning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Carbohydrate-conditioned odor preferences in rats.

The effectiveness of odor cues to support nutrient-conditioned flavor preferences in rats was studied. When the rats drank fluid, the CS+ odor was paired with intragastric (IG) infusions of Polycose, and the CS– odor with IG water. In Experiment 1, rats trained with almond and anise odors presented with plain drinking water failed to acquire a CS+ odor preference. In contrast, rats in Experiment 2 formed a strong aversion to anise (or almond) paired with lithium chloride, which indicated that the odors were distinguishable to the rats. Experiment 3 showed that providing unique tastes (bitter or sour) in combination with the odors during training potentiated odor conditioning. The rats displayed a strong preference for the odor?+?taste CS+ and for the odor component alone. Experiment 4 showed that with another pair of odors (peppermint and vanilla), CS+ preferences could be conditioned in the absence of taste cues during training. These results demonstrate that rats can acquire strong nutrient-conditioned odor preferences. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Age-related differences in short-term retention of separable elements of an odor aversion.

The rate of forgetting over short intervals was tested in preweanling rats, 8, 12, or 18 days postnatal, using procedures that may have analytical advantages over other tests of short-term retention. Separate tests of retention were conducted for the simple occurrence of an odor and for the occurrence of an odor paired with a mild footshock. Forgetting of odors with either of two histories, incidental or target, was more rapid the younger the preweanling, over intervals of less than an hour. There was some indication of more rapid forgetting for incidental than target odors. Finally, although exposure to a CS– (conditioned stimulus [an odor not paired with footshock]) was necessary for conditioning of the CS+ (an odor paired with footshock) in rats 8 or 12 days of age, exposure to a CS– had no influence on conditioning of the CS+ in preweanlings 18 days of age. The age-related differences in forgetting over intervals less than an hour long suggest that substantial age-related differences in forgetting can occur that, it is likely, are not accounted for by differential growth. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Visual cortical lesions in the rat and a conditioned emotional response.

Reports results of 11 experiments with Long-Evans rats (N = 105). Visual decortication failed to affect rate of acquisition of 1-min delayed CERs when either light alone or noise alone provided the CS. However, CER paradigms involving a combination of light and noise CSs revealed differences in behavior between experimental and control Ss. Decorticate Ss transferred the CER from light to noise (although not from noise to light); normal Ss showed no transfer. Decorticate Ss were conditioned to a noise CS in a paradigm which prevented conditioning in normal Ss. Also, decorticate Ss were better able to discriminate a compound light-noise CS from light-alone and noise-alone CS. Based on the findings and the fact that abnormal behavior of the decorticate Ss was mimicked by normal Ss wearing light-diffusing eye occluders, it is speculated that vision as a qualitatively unique sensory modality is undermined by visual cortex destruction. (21 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of posttraining damage to the pedunculopontine tegmental nucleus on conditioned stimulus transfer in two-way active avoidance in rats.

The effects of posttraining excitotoxic lesions of the pedunculopontine tegmental nucleus (PPTg) on two-way active avoidance after changing the conditioned stimulus (CS) used during prelesion training were examined. Prelesion training was carried out with either a tone or a light as the CS, and this CS was changed during postlesion training. Replacing the tone with a light reduced the performance of control and lesioned rats, but the degree of reduction was higher in the latter. Replacing the light with a tone had slight detrimental effects in lesioned rats but not in controls. Thus, posttraining PPTg lesions slowed down the reacquisition of shuttle-box avoidance under conditions of CS transfer, an effect that may be attributable to disruption of attention and/or gating of sensory stimuli. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of the hippocampus in blocking and conditioned inhibition of the rabbit's nictitating membrane response.

In Exp I, bilateral aspiration of the dorsal hippocampus produced a disruption of blocking of 30 New Zealand rabbits' nictitating membrane response in L. J. Kamin's (1968, 1969) 2-stage paradigm, but had no effect on the formation of a Pavlovian conditioned inhibitor in Exp II (27 Ss). Results of Exp I indicate that normal Ss and those with cortical lesions given conditioning to a light-plus-tone CS gave CRs to both light and tone during nonreinforced presentations of each (test phase). If, however, compound conditioning was preceded by tone acquisition, only the tone elicited a CR during testing; that is, blocking was observed. In Ss with hippocampal lesions, however, CRs were given to both light and tone during testing whether or not compound conditioning was preceded by tone acquisition. Data from Exp II show that Ss with hippocampal lesions could discriminate as well as normal Ss and those with cortical lesions between a light (CS+) and light plus tone (CS-). In addition, when the inhibitory tone was subsequently paired with the UCS in retardation testing, Ss in all 3 lesion conditions acquired the CR at the same rate. Thus, it appears that hippocampal lesions do not disrupt conditioned inhibition. Results are taken as support for the view that the hippocampus is responsible for "tuning out" stimuli that have no adaptive value to the organism. (27 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Inhibition as a "slave" process: Deactivation of conditioned inhibition through extinction of conditioned excitation.

In 4 experiments with 176 male albino Sprague-Dawley rats, a conditioned-suppression paradigm was used to investigate why a conditioned inhibition (CS–) does not extinguish when presented alone. Exp I assessed the role of blocking by excitatory contextual cues and/or an evoked representation of the conditioned excitor (CS+), which had been nonreinforced in conjunction with the CS–. When the CS+ and context were extinguished prior to presentations of the CS– alone, the CS– showed a retardation effect, reflecting latent inhibition, because no inhibition was detected in controls for which presentation of the CS– alone had been omitted. Exp II showed that the loss of conditioned inhibition (CI) was due to excitatory extinction and not to time since conditioning. When excitation was reconditioned to the extinguished CS+ (Exp I) or to a novel CS in the same context (Exp II), CI was restored. Exps III and IV evaluated whether the maintenance of CI depended on excitation that was generic in form or associatively tied to the training context. Results indicate no loss of CI when groups received CS+ extinction in that context, with concomitant presentations in a different context of the UCS by itself, for a novel CS, or correlated either positively or negatively with the original CS+. Overall findings suggest that CI is dependent on excitation: When excitation is extinguished, CI is deactivated; when excitation is reconditioned to the original or a new CS+ in the same or a different context, CI is restored. (41 ref) (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Cerebellar inactivation impairs cross modal savings of eyeblink conditioning.

Eyeblink conditioning using a conditioned stimulus (CS) from one sensory modality (e.g., an auditory CS) is greatly enhanced when the subject is previously trained with a CS from a different sensory modality (e.g., a visual CS). The enhanced acquisition to the second modality CS results from cross modal savings. The current study was designed to examine the role of the cerebellum in establishing cross modal savings in eyeblink conditioning with rats. In the first experiment rats were given paired or unpaired presentations with a CS (tone or light) and an unconditioned stimulus. All rats were then given paired training with a different modality CS. Only rats given paired training showed cross modal savings to the second modality CS. Experiment 2 showed that cerebellar inactivation during initial acquisition to the first modality CS completely prevented savings when training was switched to the second modality CS. Experiment 3 showed that cerebellar inactivation during initial cross modal training also prevented savings to the second modality stimulus. These results indicate that the cerebellum plays an essential role in establishing cross modal savings of eyeblink conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Differential Effects of 8-OH-DPAT on Two Forms of Appetitive Pavlovian Conditioning in the Rat.

Rats were trained on an appetitive Pavlovian conditioning task in which the conditioned stimulus (CS) was either localized (a light in the food tray) or nonlocalized (an increase in the general level of illumination). The conditioned response (CR) of approaching the site of food delivery in the presence of the CS was monitored. Presession treatment with the 5-HT1A agonist 8-OH-DPAT (subcutaneous injections at a dose of 0.15 mg/kg) retarded acquisition of the CR, but only when the localized CS was used. The results confirm the general proposal that serotonergic processes are involved in learning. The selective effect of the drug is not to be explained in terms of its motor effects and is consistent with the specific suggestion that systemic administration of 8-OH-DPAT is especially effective in disrupting learning tasks mediated by hippocampal mechanisms. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gustatory thalamus lesions in the rat: II. Aversive and appetitive taste conditioning.

The learning capacities of rats with electrolytic lesions of the gustatory thalamus (GT) were investigated in 3 experiments. In Experiment 1, the presence of a taste cue failed to overshadow odor aversion learning in the lesioned rats, yet these same animals acquired normal taste and odor aversions. Thalamic lesions had no discernible effect on the acquisition of a conditioned flavor preference in Experiment 2. Finally, GT lesions completely reversed the anticipatory contrast effect shown by control subjects in Experiment 3. These results suggest that damage to the GT spares taste detection and recognition and simple associative learning but interferes with learning that involves more complex gustatory information processing. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Functional inactivation of the lateral and basal nuclei of the amygdala by muscimol infusion prevents fear conditioning to an explicit conditioned stimulus and to contextual stimuli.

The GABAa agonist, muscimol (0.5 μg in 0.5 μl saline), or vehicle was infused into the lateral and basal amygdala nuclei prior to fear conditioning or testing in rats. Rats given muscimol before conditioning and saline before testing showed much less freezing to the conditioned stimulus (CS) and the context than did controls given saline before training and testing. Rats given saline before training and muscimol prior to testing also showed low levels of freezing to the CS and the context. In follow-up procedures, rats with acquisition initially blocked by pretraining muscimol infusions froze in a manner similar to that of controls when retrained and retested with saline infusions. Rats trained with saline but tested with muscimol presumably became conditioned but could express the learning. When retested with saline, they froze in the same manner as controls. Thus, activity in the lateral and basal amygdala appears to play an essential role in the acquisition and expression of fear conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neurotoxic lesions of basolateral, but not central, amygdala interfere with Pavlovian second-order conditioning and reinforcer devaluation effects

Considerable evidence suggests that various discrete nuclei within the amygdala complex are critically involved in the assignment of emotional significance or value to events through associative learning. Much of this evidence comes from aversive conditioning procedures. For example, lesions of either basolateral amygdala (ABL) or the central nucleus (CN) interfere with the acquisition or expression of conditioned fear. The present study examined the effects of selective neurotoxic lesions of either ABL or CN on the acquisition of positive incentive value by a conditioned stimulus (CS) with two appetitive Pavlovian conditioning procedures. In second-order conditioning experiments, rats first received light-food pairings intended to endow the light with reinforcing power. The acquired reinforcing power of the light was then measured by examining its ability to serve as a reinforcer for second-order conditioning of a tone when tone-light pairings were given in the absence of food. Acquisition of second-order conditioning was impaired in rats with ABL lesions but not in rats with CN lesions. In reinforcer devaluation procedures, conditioned responding of rats with ABL lesions was insensitive to postconditioning changes in the value of the reinforcer, whereas rats with CN lesions, like normal rats, were able to spontaneously adjust their CRs to the current value of the reinforcer. The results of both test procedures indicate that ABL, but not CN, is part of a system involved in CSs' acquisition of positive incentive value. Together with evidence that identifies a role for CN in certain changes in attentional processing of CSs in conditioning, these results suggest that separate amygdala subsystems contribute to a variety of processes inherent in associative learning.     

Function of the "onset of illness" in the preference changes of alloxan-diabetic rats.

144 male Sprague-Dawley rats were given access to saccharin or NaCl solutions as a conditioned stimulus (CS) at 1 of several times before and after injection with alloxan as an unconditioned stimulus (UCS) and were compared with controls (given UCS but no CS exposure) on their preference for the CS 7 days after the diabetes was well established. Results indicate that Ss exposed to the UCS at 1 or 2 hrs prior to the CS or at 1, 2, or 6 hrs following the CS all formed a conditioned aversion, whereas those with 6, 24, or 48 hrs between UCS and CS showed no greater aversion to the CS than controls. It is suggested that while the onset of alloxan diabetes can serve as the UCS for a conditioned taste aversion, the behavior of alloxan-diabetic rats towards saccharin does not depend upon this process. (PsycINFO Database Record (c) 2010 APA, all rights reserved)