Lesions of the Caudal Area of Rabbit Medial Prefrontal Cortex Impair Trace Eyeblink Conditioning

Kronforst-Collins, M. A.; Disterhoft, John F.

doi:10.1006/nlme.1997.3818

Cited by 180 publications

(175 citation statements)

References 55 publications

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“…The frontal working memory system is critical for a variety of reinforcement learning functions. For example, as noted earlier, it can support trace conditioning by maintaining active representations of stimuli after they disappear from the environment (e.g., Kronforst & Collins & Disterhoft, 1998;Weible et al, 2000). Without this system, the basic PVLV model with immediate sensory inputs can only support delay conditioning.…”

Section: ϭ Patch-like Neurons In the Ventral Striatummentioning

confidence: 99%

PVLV: The Primary Value and Learned Value Pavlovian Learning Algorithm.

O’Reilly

Frank

Hazy

et al. 2007

Behavioral Neuroscience

112

115

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The authors present their primary value learned value (PVLV) model for understanding the rewardpredictive firing properties of dopamine (DA) neurons as an alternative to the temporal-differences (TD) algorithm. PVLV is more directly related to underlying biology and is also more robust to variability in the environment. The primary value (PV) system controls performance and learning during primary rewards, whereas the learned value (LV) system learns about conditioned stimuli. The PV system is essentially the Rescorla-Wagner/delta-rule and comprises the neurons in the ventral striatum/nucleus accumbens that inhibit DA cells. The LV system comprises the neurons in the central nucleus of the amygdala that excite DA cells. The authors show that the PVLV model can account for critical aspects of the DA firing data, making a number of clear predictions about lesion effects, several of which are consistent with existing data. For example, first-and second-order conditioning can be anatomically dissociated, which is consistent with PVLV and not TD. Overall, the model provides a biologically plausible framework for understanding the neural basis of reward learning.Keywords: basal ganglia, dopamine, reinforcement learning, Pavlovian conditioning, computational modeling An important and longstanding challenge for both the cognitive neuroscience and artificial intelligence communities has been to develop an adequate understanding (and a correspondingly robust model) of Pavlovian learning. Such a model should account for the full range of signature findings in the rich literature on this phenomenon. Pavlovian conditioning refers to the ability of previously neutral stimuli that reliably co-occur with primary rewards to elicit new conditioned behaviors and to take on reward value themselves (e.g., Pavlov's famous case of the bell signaling food for hungry dogs; Pavlov, 1927).Pavlovian conditioning is distinguished from instrumental conditioning in that the latter involves the learning of new behaviors that are reliably associated with reward, either first order (US), or second order (CS). Although Pavlovian conditioning also involves behaviors (conditioned and unconditioned responses), reward delivery is not contingent on behavior but is instead reliably paired with a stimulus regardless of behavior. In contrast, instrumental conditioning explicitly makes reward contingent on a particular "operant" or "instrumental" response. Both stimulus-reward (Pavlovian) and stimulus-response-reward (instrumental) associations, however, are thought to be trained by the same phasic dopamine signal that occurs at the time of primary reward (US) as described below. In practice, the distinction is often blurry as the two types of conditioning interact (e.g., second-order instrumental conditioning and so-called Pavlovian instrumental transfer effects).The dominant theoretical perspective for both Pavlovian and instrumental conditioning since the seminal Rescorla and Wagner (1972) model, is that learning is based on the discrepancy between act...

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Section: ϭ Patch-like Neurons In the Ventral Striatummentioning

confidence: 99%

PVLV: The Primary Value and Learned Value Pavlovian Learning Algorithm.

O’Reilly

Frank

Hazy

et al. 2007

Behavioral Neuroscience

112

115

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“…For example, several studies have demonstrated that the medial PFC (mPFC) is intimately involved in the acquisition of pavlovian-conditioned autonomic responses (Buchanan and Powell, 1982;Buchanan et al, 1985;Neafsey, 1991, 1994;Powell et al, 1994), but other studies have shown that mPFC damage has no effect on simple somatomotor eyeblink (EB) classical conditioning (Buchanan and Powell, 1982;Weible et al, 2000;McLaughlin et al, 2002;Powell et al, 2005). However, it has also been reported that, under conditions that are less than optimal for learning to occur, such as during trace conditioning or partial reinforcement, mPFC lesions also impair EB conditioning (Kronforst-Collins and Disterhoft, 1998;Weible et al, 2000;McLaughlin et al 2002;Powell et al, 2005). During trace conditioning, a temporal gap occurs between the termination of the conditioned stimulus (CS) and the onset of the unconditioned stimulus (US), which can be contrasted with delay conditioning, in which the CS overlaps the US and the two stimuli coterminate.…”

Section: Introductionmentioning

confidence: 99%

Post-Training Lesions of the Medial Prefrontal Cortex Interfere with Subsequent Performance of Trace Eyeblink Conditioning

Simon¹,

Knuckley²,

Churchwell³

et al. 2005

J. Neurosci.

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Rabbits were trained on trace eyeblink (EB) conditioning until they reached a criterion of 10 consecutive EB conditioned responses (CRs). Electrolytic lesions were made in the medial prefrontal cortex (mPFC) centered on the prelimbic area (Brodmann's area 32), at five different intervals after training. These included immediately, 24 h, 1 and 2 weeks, and 1 month after training. Separate groups of animals received sham lesions at these same intervals after training. After a 2 week postoperative recovery period, all animals were retested for 3 d on trace conditioning, using the same parameters used during preoperative training. Mean EB conditioning performance deficits occurred in the animals with mPFC lesions compared with sham-lesioned animals on the first day of retesting in all five groups. However, by the second or third day of retesting, the rabbits with lesions were performing at a level that was comparable with that of sham animals. Rabbits that received more posterolateral lesions of the neocortex did not, however, show postoperative conditioning deficits. A comparison of percentage EB CRs of animals with postoperative training with that of animals that received mPFC lesions before training suggests that the mPFC post-training lesions produce damage to a retrieval process and not to a storage site or an acquisition process.

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“…In this paradigm, the conditioned stimulus (CS) and the unconditioned stimulus (US) are separated by a stimulus-free trace interval. Previous studies using permanent lesion methods have revealed that pre-conditioning lesioning of the hippocampus (Solomon et al 1986;Moyer et al 1990;McGlinchey-Berroth et al 1997;Beylin et al 2001), the medial prefrontal cortex (mPFC) (Kronforst-Collins and Disterhoft 1998;Weible et al 2000Weible et al , 2003McLaughlin et al 2002), the entorhinal cortex (Ryou et al 2001), and the mediodorsal thalamus all impair acquisition of the trace eyeblink-conditioned response (CR), suggesting that the circuitry for this learning covers multiple regions of the brain, as others have previously proposed (Weiss and Disterhoft 1996;Green and Woodruff-Pak 2000). Furthermore, this circuitry is reorganized after the CR has been completely acquired.…”

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confidence: 99%

NMDA receptor-dependent processes in the medial prefrontal cortex are important for acquisition and the early stage of consolidation during trace, but not delay eyeblink conditioning

Takehara‐Nishiuchi¹,

Kawahara²,

Kirino³

2005

Learn. Mem.

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Permanent lesions in the medial prefrontal cortex (mPFC) affect acquisition of conditioned responses (CRs) during trace eyeblink conditioning and retention of remotely acquired CRs. To clarify further roles of the mPFC in this type of learning, we investigated the participation of the mPFC in mnemonic processes both during and after daily conditioning using local microinfusion of the GABA A receptor agonist muscimol or the NMDA receptor antagonist APV into the rat mPFC. Muscimol infusions into the mPFC before daily conditioning significantly retarded CR acquisition and reduced CR expression if applied after sufficient learning. APV infusion also impaired acquisition of CRs, but not expression of well-learned CRs. When infusions were made immediately after daily conditioning, acquisition of the CR was partially impaired in both the muscimol and APV infusion groups. In contrast, rats that received muscimol infusions 3 h after daily conditioning exhibited improvement in their CR performance comparable to that of the control group. Both the pre-and post-conditioning infusion of muscimol had no effect on acquisition in the delay paradigm. These results suggest that the mPFC participates in both acquisition of a CR and the early stage of consolidation of memory in trace, but not delay eyeblink conditioning by NMDA receptor-mediated operations.

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Lesions of the Caudal Area of Rabbit Medial Prefrontal Cortex Impair Trace Eyeblink Conditioning

Cited by 180 publications

References 55 publications

PVLV: The Primary Value and Learned Value Pavlovian Learning Algorithm.

PVLV: The Primary Value and Learned Value Pavlovian Learning Algorithm.

Post-Training Lesions of the Medial Prefrontal Cortex Interfere with Subsequent Performance of Trace Eyeblink Conditioning

NMDA receptor-dependent processes in the medial prefrontal cortex are important for acquisition and the early stage of consolidation during trace, but not delay eyeblink conditioning

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