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Behavioral Neuroscience - Vol 131, Iss 2

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Behavioral Neuroscience The primary mission of Behavioral Neuroscience is to publish original research papers in the broad field of the biological bases of behavior.
Copyright 2017 American Psychological Association
  • Effects of inference on dopaminergic prediction errors depend on orbitofrontal processing.
    Dopaminergic reward prediction errors in monkeys reflect inferential reward predictions that well-trained animals can make when associative rules change. Here, in a new analysis of previously described data, we test whether dopaminergic error signals in rats are influenced by inferential predictions and whether such effects depend on the orbitofrontal cortex (OFC). Dopamine neurons were recorded from controls or rats with ipsilateral OFC lesions during performance of a choice task in which odor cues signaled the availability of sucrose reward in 2 wells. To induce prediction errors, we manipulated either the timing or number of rewards delivered in each well across blocks of trials. Of importance, a change in reward at 1 well predicted a change in reward at the other on later trials. We compared behavior and neural activity on trials when such inference was possible versus trials involving the same reward change when inference was not possible. Rats responded faster when they could infer an increase in reward compared to when the same reward was coming but they could not infer a change. This inferential prediction was reflected in the firing of dopamine neurons in controls, which changed less to unexpected delivery (or omission) of reward and more to the new high-value cue on inference versus noninference trials. These effects were absent in dopamine neurons recorded in rats with ipsilateral OFC lesions. Thus, dopaminergic error signals recorded in rats are influenced by both experiential and inferential reward predictions, and the effects of inferential predictions depend on OFC. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Partial lesion of the nigrostriatal dopamine pathway in rats impairs egocentric learning but not spatial learning or behavioral flexibility.
    Degeneration of the nigrostriatal dopaminergic system in Parkinson’s disease (PD) causes motor dysfunction and cognitive impairment, but the etiology of the cognitive deficits remains unclear. The present study investigated the behavioral effects of partial lesions of the nigrostriatal dopamine (DA) pathway. Rats received bilateral infusions of either 6-hydroxydopamine (6-OHDA) or vehicle into the dorsolateral striatum and were tested in spatial and procedural learning tasks. Compared with intact rats, DA-depleted rats were impaired when the first task they learned required egocentric responses. Intact rats that received prior training on a spatial task were impaired while learning a subsequent body-turn task, suggesting that prior spatial training may compete with egocentric learning in intact but not DA-depleted rats. Spatial discrimination, reversal learning, and switching between allocentric and egocentric strategies were similar in both groups. The results suggest that DA loss that is not associated with gross motor pathology temporarily impairs egocentric, but not allocentric, learning or subsequent behavioral flexibility. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Differential effects of neural inactivation of the dorsolateral striatum on response and latent extinction.
    The present study examined the role of the dorsolateral striatum (DLS) in extinction behavior. Male Long-Evans rats were initially trained on the straight alley maze, in which they were reinforced to traverse a straight runway and retrieve food reward at the opposite end of the maze. After initial acquisition, animals were given extinction training using 1 of 2 distinct protocols: response extinction or latent extinction. For response extinction, the animal was released from the same starting position and had the opportunity to perform the originally reinforced approach response to the goal end of the maze, which no longer contained food. For latent extinction, the animal was confined to the original goal location without food, allowing the animal to form a new cognitive expectation (i.e., that the goal location is no longer reinforced). Immediately before response or latent extinction training, animals received bilateral intra-DLS administration of the sodium channel blocker bupivacaine or control injections of physiological saline. Results indicated that neural inactivation of the DLS with bupivacaine impaired response extinction, but did not influence latent extinction. The dissociation observed indicates that the DLS selectively mediates extinction mechanisms involving suppression of the original response, as opposed to cognitive mechanisms involving a change in expectation. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Auditory cue absence as a conditioned stimulus for delay eyeblink conditioning.
    The present experiment was designed to determine if the absence of an auditory cue (i.e., a “tone-off” cue) would be an effective conditioned stimulus (CS) for delay eyeblink conditioning and to test if the medial geniculate nucleus (MGN) is part of the sensory pathway for tone-off conditioning. Rats were given paired or unpaired delay eyeblink conditioning to examine if responding to a tone-off CS was due to an associative process. An inactivation technique was performed on a separate group of rats to determine if the MGN is needed to express tone-off conditioning. The results showed that rats given paired conditioning acquired robust conditioned eyeblink responses (CRs) compared with rats given unpaired conditioning and that expression of tone-off elicited CRs was impaired when the MGN was inactivated. The findings suggest that tone-on and tone-off eyeblink conditioning may share a common neural pathway. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Cue-induced food seeking after punishment is associated with increased Fos expression in the lateral hypothalamus and basolateral and medial amygdala.
    In humans, relapse to unhealthy eating habits following dieting is a significant impediment to obesity treatment. Food-associated cues are one of the main triggers of relapse to unhealthy eating during self-imposed abstinence. Here we report a behavioral method examining cue-induced relapse to food seeking following punishment-induced suppression of food taking. We trained male rats to lever press for food pellets that were delivered after a 10-s conditional stimulus (CS) (appetitive). Following training, 25% of reinforced lever presses resulted in the presentation of a compound stimulus consisting of a novel CS (aversive) and the appetitive CS followed by a pellet and footshock. After punishment-imposed abstinence, we tested the rats in an extinction test where lever pressing resulted in the presentation of either the appetitive or aversive CS. We then compared activity of lateral hypothalamus (LH) and associated extrahypothalamic regions following this test. We also assessed Fos expression in LH orexin and GABA neurons. We found that cue-induced relapse of food seeking on test was higher in rats tested with the appetitive CS compared to the aversive CS. Relapse induced by the appetitive CS was associated with increased Fos expression in LH, caudal basolateral amygdala (BLA), and medial amygdala (MeA). This relapse was also associated with increased Fos expression in LH orexin and VGAT-expressing neurons. These data show that relapse to food seeking can be induced by food-associated cues after punishment-imposed abstinence, and this relapse is associated with increased activity in LH, caudal BLA, and MeA. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Threat intensity widens fear generalization gradients.
    Research in nonhuman animals reveals threat-sensitive generalization of defensive behavior that favors widespread generalization when threat intensity is high and limited generalization (i.e., specificity) when threat intensity is low. Here, we used Pavlovian fear conditioning to systematically investigate whether threat intensity widens behavioral generalization gradients to stimuli that decreasingly resemble a learned threat cue. Using a between-subjects design, volunteers underwent fear conditioning with a tone paired with either a high-intensity or low-intensity aversive stimulus prior to a test of fear generalization to novel tones. Results showed no effect of threat intensity on initial acquisition of conditioned fear. However, volunteers who underwent fear conditioning with a high-intensity aversive stimulus exhibited widespread generalization of autonomic arousal (skin conductance responses) as compared to volunteers who received a low-intensity aversive stimulus. These results show a transition from normal (selective) to overgeneralized fear as threat intensity increases, and have implications for understanding overgeneralization characteristic of trauma- and stress-related disorders. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Involvement of serotonin and oxytocin in neural mechanism regulating amicable social signal in male mice: Implication for impaired recognition of amicable cues in BALB/c strain.
    Social signals play a primary role in regulating social relationships among male mice. The present series of experiments investigated the neural mechanisms underlying an induction of amicable cues that facilitate social approach in male mice of the C57BL/6 (B6) and BALB/c (BALB) strains. Male mice exhibit approach behavior and suppression of territorial scent marking toward amicable counterparts. Exposure of a group-housed mouse that maintains an amicable relationship induced social approach in B6 recipient mice, as expressed by increased preference of stay in proximity and decreased scent marks relevant to those of a single-housed mouse. Nasal administration of oxytocin (OT) to stimulus mice appeared to enhance social approach in B6 recipient mice. Systemic administration of buspirone (5-HT1A agonist) to stimulus mice also increased approach in B6 recipient mice, whereas a nasal OT antagonist infusion followed by systemic buspirone injection of stimulus mice blocked this buspirone-induced approach in B6 recipient mice. BALB mice likely possess an intact signaling system as shown in B6 mice, in which the 5-HT → OT pathway is a primary modulator for social amicable signals. However, BALB mice could not exhibit signal-dependent change in approach behavior. No impairment in olfactory discrimination or approach behavior toward social stimuli was found in BALB mice. It is concluded that social cues for facilitating social approach are eliminated via the 5-HT → OT pathway, and BALB mice as a low social strain have a deficit in recognition of specific signals associated with amicability. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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  • Blockade of glutamatergic transmission in the primate basolateral amygdala suppresses active behavior without altering social interaction.
    The amygdala is an integrator of affective processing, and a key component of a network regulating social behavior. While decades of lesion studies in nonhuman primates have shown alterations in social interactions after amygdala damage, acute manipulations of the amygdala in primates have been underexplored. We recently reported (Wellman, Forcelli, Aguilar, & Malkova, 2016) that acute pharmacological inhibition of the basolateral complex of the amygdala (BLA) or the central nucleus of the amygdala increased affiliative social interactions in experimental dyads of macaques; this was achieved through microinjection of a GABA-A receptor agonist. Prior studies in rodents have shown similar effects achieved by blocking NMDA receptors or AMPA receptors within the BLA. Here, we sought to determine the role of these receptor systems in the primate BLA in the context of social behavior. In familiar dyads, we microinjected the NMDA receptor antagonist 2-amino-7-phosphonoheptanoic acid (AP7) or the AMPA receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) and observed behaviors and social interactions in the immediate postinjection period. In striking contrast with our prior report using GABA agonists, and in contrast with prior reports in rodents using glutamate antagonists, we found that neither NMDA nor AMPA blockade increase social interaction. Both treatments, however, were associated with decreases in locomotion and manipulation and increases in passive behavior. These data suggest that local blockade of glutamatergic neurotransmission in BLA is not the functional equivalent of local activation of GABAergic signaling, and raise interesting questions regarding the functional microcircuitry of the nonhuman primate amygdala in the context of social behavior. (PsycINFO Database Record (c) 2017 APA, all rights reserved)
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