The hippocampus and appetitive Pavlovian conditioning: Effects of excitotoxic hippocampal lesions on conditioned locomotor activity and autoshaping

Ito, Rutsuko; Everitt, Barry J.; Robbins, Trevor W.

doi:10.1002/hipo.20094

Cited by 77 publications

(59 citation statements)

References 53 publications

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“…Weakening of such an association may serve to reduce "signtracking" (e.g., Hearst and Jenkins 1974) to the goal box, and thereby extinguish the instrumental approach response exhibited in the maze runway. However, this alternative is inconsistent with evidence that lesions of hippocampus impair latent runway extinction (Gabriele and Packard 2006) but do not impair acquisition of sign-tracking (Bussey et al 2000;Parkinson et al 2000;Ito et al 2005). To our knowledge, the effects of hippocampal lesions on extinction of sign-tracking behavior have not been investigated.…”

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confidence: 74%

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Gabriele¹,

Packard²

2007

Learn. Mem.

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Adult male Long-Evans rats were trained to run in a straight-alley maze for food reward and subsequently received hippocampus-dependent latent extinction training. Immediately following latent extinction, rats received peripheral injections of the NMDA receptor partial agonist D-cycloserine (DCS, 15 mg/kg), or saline. Twenty-four hours later, rats received four extinction "probe" trials. Relative to saline controls, latencies to reach the goal box on probe trials were significantly higher in rats that had received DCS. These findings indicate that memory consolidation underlying hippocampus-dependent latent extinction, a cognitive form of learning in which the previously rewarded response is not made during extinction training, can be enhanced by NMDA-receptor agonism.Behavioral extinction is operationalized as a reduction of a previously acquired response, and this process can involve new learning (for review, see Bouton 2004). The initial acquisition of learned behavior involves multiple memory systems (for review, see Packard 2001) and we have recently expanded this view to the study of the new learning underlying behavioral extinction (Gabriele and Packard 2006). We used a task in which extinction of the same overt behavior could be achieved using either a "response" or "latent" extinction training procedure. In contrast to typical extinction training that involves performance of a previously reinforced response, during latent extinction training no overt response is made. For example, a food-rewarded approach response in a straight-alley maze can be extinguished by placing the animal in the goal box in the absence of reward (Seward and Levy 1949). Consistent with the hypothesis that multiple memory systems play a role in the learning that occurs during extinction, we observed that the learning underlying response and latent extinction of runway behavior is neuroanatomically dissociable. Specifically, neural inactivation of the hippocampus prevented latent extinction of maze runway behavior, but did not block response extinction of the same behavior (Gabriele and Packard 2006). Latent extinction is conducive to a cognitive learning process in which an expectancy (Tolman 1932) of food reward can be altered without performance of the previously acquired response (Seward and Levy 1949). According to the multiple memory systems hypothesis, the hippocampus is selectively involved in cognitive learning and memory (e.g., Hirsh 1974;Mishkin and Petri 1984), and the impairment of latent extinction produced by hippocampal inactivation is consistent with this view.Although our previous study using a reversible lesion technique implicates the hippocampus in latent extinction, the findings do not provide any information concerning the neurochemical basis of this form of cognitive learning. Various neurotransmitter systems play a role in extinction (for review, see Mason 1983) and several recent studies have focused on the role of glutamatergic neurotransmission (for review, see Davis and Myers 2002). For example, adminis...

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confidence: 74%

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Gabriele¹,

Packard²

2007

Learn. Mem.

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“…This area of the mPFC is connected with the hippocampal formation (Swanson et al, 1987;Van Groen and Wyss, 1990;Condé et al, 1995), relevant for contextual information, and its integration in motivational processing associated with appetitive learning and the control of ingestive behavior (Ito et al, 2005;Davidson et al, 2005). Similarly, the ILA, ventral (but not dorsal) PL, and medial (but not lateral) OFC all send output to the nucleus accumbens (ACB) (Sesack et al, 1989;Hurley et al, 1991;Petrovich et al, 2005a), which, itself, has been heavily implicated in feeding behavior (Baldo and Kelley, 2007).…”

Section: Discussionmentioning

confidence: 99%

Medial Prefrontal Cortex Is Necessary for an Appetitive Contextual Conditioned Stimulus to Promote Eating in Sated Rats

Petrovich

Ross

Holland³

et al. 2007

Journal of Neuroscience

103

105

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Motivation plays an important role in the control of food intake. A cue that acquires motivational properties through pairings with food consumption when an animal is hungry can override satiety and promote eating in sated rats. This phenomenon of conditioned potentiation of feeding is mediated by connections between the forebrain and the lateral hypothalamic area (LHA). In a recent study using markers for cellular activation, neurons in the ventral medial prefrontal cortex (vmPFC) that project directly to the LHA were strongly engaged after exposure to a conditioned cue that stimulates eating in sated rats. Here, we examined whether those vmPFC neurons are necessary for conditioned potentiation of eating. We trained rats in a paradigm in which the context provided conditioning cues. Rats with bilateral neurotoxic lesions of vmPFC were impaired in context-enhanced food consumption in tests when the rats were sated. At the same time, vmPFC lesions did not produce changes in food consumption in the home cage or changes in body weight during training. Thus, vmPFC neurotoxic lesions produced impairment in food consumption specifically driven by conditioned motivational cues. The current findings suggest a critical role for vmPFC in the brain network that mediates control of conditioned motivation to eat perhaps by a mechanism akin to appetite or craving.

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“…Of course, the circuitry described here is not complete. The ventral pallidum (Smith et al 2009), anterior cingulate cortex (Cardinal et al 2003), and hippocampus (Ito et al 2005;Gilboa et al 2014), to name a few, have all been implicated in Pavlovian conditioning and more work is needed to fully delineate the entire circuit.…”

Section: Circuitry Of Outcome Representationsmentioning

confidence: 99%

The Origins and Organization of Vertebrate Pavlovian Conditioning

Fanselow

Wassum

2015

Cold Spring Harb Perspect Biol

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Pavlovian conditioning is the process by which we learn relationships between stimuli and thus constitutes a basic building block for how the brain constructs representations of the world. We first review the major concepts of Pavlovian conditioning and point out many of the pervasive misunderstandings about just what conditioning is. This brings us to a modern redefinition of conditioning as the process whereby experience with a conditional relationship between stimuli bestows these stimuli with the ability to promote adaptive behavior patterns that did not occur before the experience. Working from this framework, we provide an in-depth analysis of two examples, fear conditioning and food-based appetitive conditioning, which include a description of the only partially overlapping neural circuitry of each. We also describe how these circuits promote the basic characteristics that define Pavlovian conditioning, such as error-correction-driven regulation of learning.

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The hippocampus and appetitive Pavlovian conditioning: Effects of excitotoxic hippocampal lesions on conditioned locomotor activity and autoshaping

Cited by 77 publications

References 53 publications

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Medial Prefrontal Cortex Is Necessary for an Appetitive Contextual Conditioned Stimulus to Promote Eating in Sated Rats

The Origins and Organization of Vertebrate Pavlovian Conditioning

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