Pavlovian conditioning processes contribute to the etiology of nicotine dependence. Conditioning involving interoceptive stimuli is increasingly recognized as playing a role in many diseases and psychopathologies, including drug addiction. Previous animal research on diminishing the influence of interoceptive conditioning has been limited to antagonism and nonreinforced exposures to the drug stimulus. The goal of the present research was to determine whether interoceptive conditioning with a nicotine stimulus could be diminished through an unconditioned stimulus (US) devaluation procedure. In two separate experiments, male Sprague-Dawley rats received nicotine injections (0.4 mg base/kg) followed by intermittent sucrose (26%) access in a conditioning chamber. On intermixed saline sessions, sucrose was withheld. Conditioning was demonstrated by a reliable increase in head entries in the dipper receptacle on nicotine versus saline sessions. After conditioning, rats in a devaluation condition were given access to sucrose in their home cages immediately followed by a lithium chloride (LiCl) injection on 3 consecutive days. On subsequent test days, nicotine-evoked conditioned responding was significantly attenuated. Within-subject (Experiment 1) and between-subjects (Experiment 2) controls revealed that the diminished responding was not attributable to mere exposure to the sucrose US in the devaluation phase. Experiment 2 included a LiCl-alone control group. Repeated illness induced by LiCl did not reduce later nicotine-evoked responding. These findings suggest that there is a direct association between the interoceptive stimulus effects of nicotine and the appetitive sucrose US (i.e., stimulus-stimulus) rather than a stimulus-response association. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

The anterior thalamic nuclei form part of a network for episodic memory in humans. The importance of these nuclei for recognition and recency judgments remains, however, unclear. Rats with anterior thalamic nuclei lesions and their controls were tested on object recognition, along with two types of recency judgment. The spontaneous discrimination of a novel object or a novel odor from a familiar counterpart (recognition memory) was not affected by anterior thalamic lesions when tested after retention delays of 1 and 60 min. To measure recency memory, rats were shown two familiar objects, one of which had been explored more recently. In one condition, rats were presented with two lists (List A, List B) of objects separated by a delay, thereby creating two distinct blocks of stimuli. After an additional delay, rats were presented with pairs of objects, one from List A and one from List B (between-block recency). No lesion-induced deficit was apparent for recency discriminations between objects from different lists, despite using three different levels of task difficulty. In contrast, rats with anterior thalamic lesions were significantly impaired when presented with a continuous list of objects and then tested on their ability to distinguish between those items early and late in the same list (within-block recency). The contrasting effects on recognition and recency support the notion that interlinked hippocampal-anterior thalamic interconnections support aspects of both spatial and nonspatial learning, although the role of the anterior thalamic nuclei may be restricted to a subclass of recency judgments (within-block). (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Reports an error in "Ventral pallidum mediates amygdala-evoked deficits in prepulse inhibition" by Patrick A. Forcelli, Elizabeth A. West, Alice T. Murnen and Ludise Malkova (Behavioral Neuroscience, 2012[Apr], Vol 126[2], 290-300). It was incorrectly stated in the introduction and discussion that Alsene et al. (2011) had found that blockade of adrenergic neurotransmission in amygdala disrupted PPI. In fact, contrary to this statement, they found that infusion of a combination of alpha and beta adrenoceptor agonists (phenylephrine and isoproterenol) disrupted PPI. This oversight does not alter the results, nor the conclusions/interpretations presented in the article. (The following abstract of the original article appeared in record 2012-00555-001.) Prepulse inhibition (PPI) is an operational measure of sensorimotor gating. It is defined as a reduction in magnitude of a startle response when a startling stimulus is preceded by a weaker "prepulse." PPI has been found to be altered in patients with schizophrenia, autism spectrum disorders, and other neuropsychiatric illnesses. As such, the neural substrates regulating PPI are of particular interest. Previous studies using lesions, selective blockade of N-methyl-d-aspartate (NMDA) receptors, and pharmacological disinhibition have demonstrated that impairment of the function of the basolateral and lateral nuclei of the amygdala (BLA) disrupts PPI. However, transient gamma aminobutyric acid-mediated (GABA-mediated) inactivation of BLA has not been evaluated for effects on PPI. Furthermore, the downstream projection targets that mediate BLA-evoked disruptions of PPI have not been elucidated. Thus, in the present study, we evaluated the effect on PPI of bilateral and unilateral inactivation of BLA, by microinfusion of the GABA-A receptor agonist, muscimol. We found that either bilateral or unilateral inactivation impaired PPI. Because unilateral inactivation was sufficient to impair PPI, we hypothesized that this was due to an indirect activation of a downstream target of BLA, the ventral pallidum (VP). Because VP inhibition normalizes PPI deficits evoked from nucleus accumbens (Kodsi & Swerdlow, 1994), we next tested the degree to which VP inhibition would normalize PPI deficits evoked from BLA. We unilaterally inactivated BLA with concurrent inactivation of VP and found that VP inactivation blocked BLA-evoked deficits in PPI. We suggest that BLA inactivation disrupts PPI through disinhibition of VP. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Disgust extinction is an important mechanism relevant for the treatment of psychiatric disorders. However, only a few studies have investigated disgust extinction. Moreover, because disgust sensitivity (DS) is considered as a relevant factor for learning processes, this study also investigated the potential relationship between DS and disgust extinction learning. The aim of this study was to explore the neuronal correlates of disgust extinction, as well as changes in skin conductance responses (SCRs) and evaluative conditioning. Twenty subjects were exposed to a differential extinction paradigm, in which a previous conditioned, and now unreinforced, stimulus (conditioned stimulus, CS+) was compared to a second stimulus (CS-), which was previously not associated with the unconditioned stimulus (UCS). Extinction learning was measured on three different response levels (BOLD responses, SCRs, and evaluative conditioning). Regarding evaluative conditioning, the CS+ was rated as more unpleasant than the CS-. Interestingly, significantly increased amygdala responses and SCRs toward to the CS- were observed. Finally, a (negative) trend was found between DS scores and BOLD responses of the prefrontal cortex. The present findings showed a dissociation of different response levels. The increased CS- responses could be explained by the assumption that the increased amygdala activity may reflect a safety learning signal during the first extinction trials and the subjective focus may therefore shift from the CS+ to the CS-. The correlation finding supports previous studies postulating that DS hampers extinction processes. The present results point toward dissociations between the response levels in context of extinction processes. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

The nature of the relationship between explicit and implicit learning is a topic of considerable debate. To investigate this relationship we conducted two experiments on postconditioning revaluation of the unconditional stimulus (UCS) in human fear conditioning. In Experiment 1, the intensity of the UCS was decreased after acquisition for one group (devaluation) and held constant for another group (control). A subsequent test revealed that even though both groups exhibited similar levels of UCS expectancy, the devaluation group had significantly smaller conditional skin conductance responses. The devaluation effect was not explained by differences in the explicit estimates of UCS probability or explicit knowledge that the UCS intensity had changed. In Experiment 2, the value of the UCS was increased after acquisition for one group (inflation) and held constant for another group (control). Test performance revealed that UCS inflation did not alter expectancy ratings, but the inflation group exhibited larger learned skin conductance responses than the control group. The inflation effect was not explained by differences in the explicit estimates of UCS probability or explicit knowledge that the UCS intensity had changed. The SCR revaluation effect was not dependent on explicit memory processes in either experiment. In both experiments we found differences on an implicit measure of learning in the absence of changes in explicit measures. Together, the differences observed between expectancy measures and skin conductance support the idea that these responses might reflect different types of memory formed during the same training procedure and be supported by separate neural systems. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Alzheimer's disease (AD) affects 5.4 million Americans. Evidence suggests that individuals who are positive for the apolipoprotein E (ApoE) ε4 allele are at higher risk for developing the disease. Studies have also shown that the ε4 allele is linked to olfactory decline. Olfactory functioning may be investigated using olfactory event-related potentials (OERPs). The high temporal resolution of OERPs enables an understanding of the neural correlates of olfactory processing and functioning. This study investigated the effects of age, ApoE ε4 status, response type, and electrode site on OERP latency and amplitude during encoding and retrieval in an odor recognition memory task. The 60 participants were equally divided into 3 age groups matched on ε4 status: younger, middle, and older. Odors were presented using a computer-controlled olfactometer. Participants were notified during encoding that this was a task of odor memory. Results indicated differences in OERP activity as a function of age, ApoE ε4 status, response type, and electrode site. These findings highlight the potential of OERPs to distinguish ε4- and ε4+ individuals and to contribute to an earlier diagnosis of AD. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Benzodiazepines have been demonstrated to have a high abuse liability in persons suffering from anxiety but have demonstrated mixed abuse liability findings in preclinical models. We hypothesized that by modeling anxiety in a male C57BL/6 mouse model it would be possible to reveal a preference for benzodiazepines within this subpopulation through negative reinforcement. Using the Tube Test of Social Dominance and the Resident/Intruder Paradigm we investigated whether animals identified as dominant or submissive/defeated would differentially display a preference for midazolam (a short acting benzodiazepine) in a conditioned place preference paradigm. Consistent with our hypotheses, benzodiazepine conditioned motivation was mediated by negative reinforcement as submissive but not dominant mice displayed a preference for midazolam. Furthermore, different neural systems mediated midazolam conditioned motivation depending on the stress status of the animal (single vs. repeated stress-as induced by the Resident/Intruder Paradigm). Singly stressed animals showed midazolam place preferences through a dopamine-independent pathway, whereas the place preferences of repeatedly stressed animals were mediated through a dopamine-dependent pathway. This demonstrates that stress is sufficient for switching the neural system mediating midazolam conditioned motivation. Finally, midazolam reinforcement in the conditioned place preference paradigm was shown to be predictive for dominance/submission status. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Estrogens have been shown to rapidly promote male copulatory behaviors with a time-course that suggests rapid signaling events are involved. The present study tested the hypothesis that estrogen acts through a novel Gq protein-coupled membrane estrogen receptor (ER). Thus, either estradiol (E2), STX (a diphenylacrylamide compound that selectively activates a membrane ER pathway), or vehicle were administered acutely to castrated male rats that bore subcutaneous (sc) dihydrotestosterone implants to maintain genital sensitivity. Appetitive (level changes, genital investigation) and consummatory (mounts, intromissions, ejaculations) components of male sexual behavior were measured in a bilevel testing apparatus. Testing showed that E2 treatment promoted olfactory and mounting behaviors, but had no effect on motivation as measured by anticipatory level changes. STX treatment showed no effect on either component of male sexual behavior. These results support previous results that showed that E2 can rapidly affect male sexual behaviors but fail to support a role for the specific membrane-initiated pathway activated by STX. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Navigation depends on a network of neural systems that accurately monitor an animal's spatial orientation in an environment. Within this navigation system are head direction (HD) cells which discharge as a function of an animal's directional heading, providing an animal with a neural compass to guide ongoing spatial behavior. Experiments were designed to test this hypothesis by damaging the dorsal tegmental nucleus (DTN), a midbrain structure that plays a critical role in the generation of the rodent HD cell signal, and evaluating landmark based navigation using variants of the Morris water task. In Experiments 1 and 2, shams and DTN-lesioned rats were trained to navigate toward a cued platform in the presence of a constellation of distal landmarks located outside the pool. After reaching a training criteria, rats were tested in three probe trials in which (a) the cued platform was completely removed from the pool, (b) the pool was repositioned and the cued platform remained in the same absolute location with respect to distal landmarks, or (c) the pool was repositioned and the cued platform remained in the same relative location in the pool. In general, DTN-lesioned rats required more training trials to reach performance criterion, were less accurate to navigate to the platform position when it was removed, and navigated directly to the cued platform regardless of its position in the pool, indicating a general absence of control over navigation by distal landmarks. In Experiment 3, DTN and control rats were trained in directional and place navigation variants of the water task where the pool was repositioned for each training trial and a hidden platform was placed either in the same relative location (direction) in the pool or in the same absolute location (place) in the distal room reference frame. DTN-lesioned rats were initially impaired in the direction task, but ultimately performed as well as controls. In the place task, DTN-lesioned rats were severely impaired and displayed little evidence of improvement over the course of training. Together, these results support the conclusion that the DTN is required for accurate landmark navigation. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Differences in an animal's spatial environment can have dramatic effects on the hippocampus, an area of the brain involved with spatial processing. Animals in spatially impoverished environments have decreased hippocampal attributes. However, we do not know if differences in the spatial environment differentially interact with territorial status, which also covaries with hippocampal attributes. Here, we asked whether territoriality and differential spatial-area use interact to generate different effects on cortical attributes (reptilian hippocampal homologue) in lizards. We compared medial and dorsal cortical attributes between territorial and nonterritorial morphotypes of side-blotched lizards, Uta stansburiana, in larger versus smaller (i.e., spatially impoverished) enclosures. We found that territorial males had increased neurogenesis rates in their medial cortices in larger enclosures when compared with their siblings in smaller enclosures; nonterritorial males had low levels of neurogenesis regardless of enclosure size. Enclosure size had no significant effect on cortical volumes or the total number of neurons in either cortical region. These results suggest that territorial morphotypes may be more sensitive to changes in the spatial environment, thus leading to increases in regulation of neurogenesis in the face of increased spatial processing and physical activity demands. (PsycINFO Database Record (c) 2013 APA, all rights reserved).