Ibotenate lesions of the hippocampus enhance latent inhibition in conditioned taste aversion and increase resistance to extinction in conditioned taste preference.

Reilly, Steve; Harley, Carolyn W.; Revusky, Sam

doi:10.1037/0735-7044.107.6.996

Cited by 112 publications

(106 citation statements)

References 69 publications

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“…However, the effects of hippocampal lesions on latent inhibition of conditioned taste aversions are equivocal (McFarland et al, 1978;Reilly et al, 1993;Gallo and Cándido, 1995), which may explain the lack of effect observed in that study. In contrast, the current results are consistent with a disruption in latent inhibition produced by neurotoxic hippocampal lesions in our appetitive within-subject procedure (Han et al, 1995).…”

Section: Behavioral Datacontrasting

confidence: 50%

Disruption of Decrements in Conditioned Stimulus Processing by Selective Removal of Hippocampal Cholinergic Input

1997

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The attention directed to environmental stimuli can be modified by experience. For example, preexposure of a conditioned stimulus (CS) in the absence of reinforcement can retard subsequent conditioning of that stimulus when it is paired directly with an unconditioned stimulus, a phenomenon referred to as latent inhibition. Similarly, consistent pairings of a CS with another event can slow the acquisition of new information about that CS. Such phenomena suggest that reductions in the processing of CSs occur when they are made behaviorally irrelevant or consistent predictors of other events. On the basis of the observation that hippocampal lesions prevented such reductions in CS processing, we hypothesized that damage to basal forebrain cholinergic neurons that project to the hippocampus, using microinjections of the selective immunotoxin 192 IgG-saporin into the medial septum/vertical limb of the diagonal band (MS/VDB), also would disrupt normal reductions in CS processing. Lesions of hippocampal cholinergic input disrupted decreases in CS processing, manifested in both an absence of latent inhibition and a lack of reduced processing of a CS that had been a consistent predictor of another CS. These results indicate that cholinergic neurons in the MS/VDB play a role in the regulation of CS processing. Furthermore, these findings (in conjunction with previous findings) implicate both rostral (hippocampal-projecting) and caudal (corticalprojecting) regions of the basal forebrain cholinergic system in the modulation of attention.

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Section: Behavioral Datacontrasting

confidence: 50%

Disruption of Decrements in Conditioned Stimulus Processing by Selective Removal of Hippocampal Cholinergic Input

1997

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“…This pattern of results has also been observed in rats (Ellenbroek et al 1997;Russig et al 2003). Second, there is increasing evidence that depending on the specific paradigms, the same treatment (drugs, selective brain lesions, or environmental manipulations) can result in differing patterns of LI modulation (Reilly et al 1993;Purves et al 1995;Gallo and Candido 1995;Buhusi et al 1998;Schmajuk et al 2000Schmajuk et al , 2001Oswald et al 2002;Schmajuk 2005;Meyer et al 2006b;Pothuizen et al 2006). Our data (in this paper and in Meyer et al 2004) further indicate that this impression is not unprecedented in either rats or mice.…”

Section: Avoidance Learning After Amphetamine Treatmentsupporting

confidence: 62%

Disruption of the US pre-exposure effect and latent inhibition in two-way active avoidance by systemic amphetamine in C57BL/6 mice

et al. 2006

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Rationale Pre-exposure to either one of the two to-beassociated stimuli alone is known to reduce the efficiency of the learning of their association when they are subsequently paired explicitly. In classical conditioning, pre-exposure to the conditioned stimulus (CS) gives rise to latent inhibition (LI); and pre-exposure to the unconditioned stimulus (US) results in the US pre-exposure effect (USPEE). Considerable evidence supports an important role of central dopamine in the regulation and modulation of LI; it has been suggested that the USPEE may be similarly controlled by dopamine, but this parallelism has only been directly demonstrated in the conditioned taste aversion paradigm. Objective The present study tested this hypothesis by comparing the efficacy of systemic amphetamine treatment to affect the expression of LI and the USPEE in a two-way active avoidance paradigm. Methods C57BL/6 male mice were tested in active avoidance using a tone CS and a foot-shock US. Twenty-four hours before, they were pre-exposed to 100 presentations of the CS or the US, or to the test apparatus only. Amphetamine (2.5 mg/kg) or saline was administered before stimulus preexposure and conditioned avoidance test, in which the mice learned to avoid the shock by shuttling in response to the tone. Results Amphetamine disrupted both stimulus pre-exposure effects, thus, lending further support to the hypothesis that the USPEE is similar to LI in its sensitivity to dopamine receptor agonist. Hence, the USPEE paradigm may represent a valuable addition to the study of dopamine-sensitive processes of selective learning currently implicated in LI and Kamin blocking.

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“…4C). Although CTA extinction is attributed primarily to cortical regions, including the PFC (59), studies have indicated that hippocampal lesions slow CTA extinction (29,30), suggesting a potential interaction between the hippocampus and the PFC. Recent studies also suggested that the hippocampus participates in consolidating CTA extinction (60).…”

Section: Discussionmentioning

confidence: 99%

“…These results indicate that BDNF-KIV mice retain short-term fear extinction but may be inefficient in long-term fear extinction. Finally, we determined whether the extinction deficit extends to conditioned taste aversion (CTA), a process that involves the mPFC (27,28) and hippocampus (29,30). Animals were offered a sweetened solution during a pretraining trial (trial 1: P = 0.52; t test) (Fig.…”

Section: Impairment Of Activity-driven Expression Of Bdnf Protein In Thementioning

confidence: 99%

Role of activity-dependent BDNF expression in hippocampal–prefrontal cortical regulation of behavioral perseverance

Sakata

Martinowich²,

Woo

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

121

131

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Activity-dependent gene transcription, including that of the brainderived neurotrophic factor (Bdnf) gene, has been implicated in various cognitive functions. We previously demonstrated that mutant mice with selective disruption of activity-dependent BDNF expression (BDNF-KIV mice) exhibit deficits in GABA-mediated inhibition in the prefrontal cortex (PFC). Here, we show that disruption of activity-dependent BDNF expression impairs BDNF-dependent late-phase long-term potentiation (L-LTP) in CA1, a site of hippocampal output to the PFC. Interestingly, early-phase LTP and conventional L-LTP induced by strong tetanic stimulation were completely normal in BDNF-KIV mice. In parallel, attenuation of activity-dependent BDNF expression significantly impairs spatial memory reversal and contextual memory extinction, two executive functions that require intact hippocampal-PFC circuitry. In contrast, spatial and contextual memory per se were not affected. Thus, activity-dependent BDNF expression in the hippocampus and PFC may contribute to cognitive and behavioral flexibility. These results suggest distinct roles for different forms of L-LTP and provide a link between activity-dependent BDNF expression and behavioral perseverance, a hallmark of several psychiatric disorders.

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Ibotenate lesions of the hippocampus enhance latent inhibition in conditioned taste aversion and increase resistance to extinction in conditioned taste preference.

Cited by 112 publications

References 69 publications

Disruption of Decrements in Conditioned Stimulus Processing by Selective Removal of Hippocampal Cholinergic Input

Disruption of Decrements in Conditioned Stimulus Processing by Selective Removal of Hippocampal Cholinergic Input

Disruption of the US pre-exposure effect and latent inhibition in two-way active avoidance by systemic amphetamine in C57BL/6 mice

Role of activity-dependent BDNF expression in hippocampal–prefrontal cortical regulation of behavioral perseverance

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