Hippocampectomy and the attenuation of blocking

Rickert, Edward J.; Bennett, Thomas L.; Lane, Patrick; French, John D.

doi:10.1016/s0091-6773(78)92170-3

Cited by 210 publications

(57 citation statements)

References 16 publications

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“…The results of several studies have implicated the hippocampus in blocking (Rickert et al, 1978;Solomon, 1977). In a better controlled study, however, Garrud et al (1984) failed to find such an effect.…”

Section: B Septal-hippocampal System For Decremental But Not Incrementioning

confidence: 98%

Brain mechanisms for changes in processing of conditioned stimuli in Pavlovian conditioning: Implications for behavior theory

Holland

1997

Animal Learning & Behavior

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This article is a review of the results of a series of experiments designed to identify brain systems involved in appetitive conditioning of rats. It discusses some of their implications for behavioral theories of learning, especially those that concern changes in processing of conditioned stimuli (CSs). Evidence is presented which suggests that separable brain circuits are involved in (1) the production of CS-dependent conditioned orienting responses, (2) the enhancement of CS associability produced when expectancies about upcoming events are violated, (3) the reduction of CS associability produced when stimuli are consistent predictors of other events or are presented without consequence, and (4) the abilities of CSs to serve as reinforcers for second-order conditioning and to be sensitive to postconditioning changes in the value of the unconditioned stimulus (US). Finally, none of these circuits seems critical for normal acquisition of the most common indicator of Pavlovian conditioning, US-dependent conditioned responses (CRs). Although the independence of brain pathways does not demand independence of behavioral function, clustering of behavioral phenomena on anatomical grounds may provide useful guides for constructing behavior theories.

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Section: B Septal-hippocampal System For Decremental But Not Incrementioning

confidence: 98%

Brain mechanisms for changes in processing of conditioned stimuli in Pavlovian conditioning: Implications for behavior theory

Holland

1997

Animal Learning & Behavior

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“…This result is evident in habituation of spontaneous orienting to neutral cues, in blocking itself, and in the effects of repeated exposure to cues on subsequent conditioning (e.g., latent inhibition), all of whjch proceed normally in rats with neurotoxic lesions ofthe CN (7,44). Interestingly, effects on those functions spared by CN damage are often impaired by lesions ofanother brain system studied in associative learning, the hippocampal formation including the septohippocampal pathway (48)(49)(50)(51)(52). This result raises the possibility that incremental and decremental regulation of attention is served by separate neural systems.…”

Section: A Neuroanatomical Framework For Cn Functionmentioning

confidence: 99%

The amygdala complex: multiple roles in associative learning and attention.

Gallagher

Holland

1994

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

275

187

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Although certain neurophysiological functions of the amygdala complex in learning seem well established, the purpose of this review is to propose that an additional conceptualization of amygdala function is now needed. The research we review provides evidence that a subsystem within the amygdala provides a coordinated regulation of attentional processes. An important aspect of this additional neuropsychology of the amygdala is that it may aid in understanding the importance of connections between the amygdala and other neural systems in information processing.Kluver and Bucy (1) Perhaps the most frequently cited measure of a cue's changed motivational value, as a consequence of its pairing with a biologically meaningful stimulus, such as food, is its ability to reinforce subsequent learning-for example, the phenomenon known as second-order conditioning. We tested a cue's ability to support Pavlovian second-order conditioning in rats with CN damage. As shown in Fig. 1, second-order conditioning was as robust in rats with CN lesions as it was in normal control rats (see legend to Fig. 1 for description of task).Thus, CN damage did not interfere with a cue's ability to acquire reinforcing power when paired with food.We also tested whether a cue's acquisition of motivational properties remains intact in rats with CN damage by using a procedure called "conditioned potentiation of feeding." In this procedure, sated rats are induced to eat by presenting a previously trained cue for food (9). To test for this effect, rats were placed back on ad libitum feeding after standard appetitive training and exposed repeatedly to the test chamber with food available to eliminate all tendency to consume food in that environment. Two test sessions were then conducted, during which 20 food pellets were made available. In one session the formerly trained cue was presented; in the other no cue presentations occurred during the test. Our experiment showed that feeding was potentiated substantially by the cue in normal rats; whereas an average of 0.2 pellet was consumed in the unsignaled test, on average, 15.2 pellets were consumed in the cue-signaled condition. The rats with CN damage showed a comparable effect of cue presentations; lesioned rats ate 3.8 pellets in the unsignaled condition and 16.9 pellets in the signaled condition (10).These results provide strong support for the conclusion that the motivational value associated with cues during appetitive learning is acquired normally by rats with amygdala CN damage. Taken together with research conducted in other laboratories (e.g., refs. 6 and 8), it appears that a separate subsystem within the amygdala is necessary for this function. Despite the normal appearance of rats with CN damage on the tests described above, the lesions were highly effective in producing other behavioral impairments. One that can be observed during simple appetitive conditioning will be described here; others will be introduced in a later section of the paper.We observed that neurotoxic damage to t...

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“…If so, does damage in the hippocampus disrupt it? The data are presently confusing (Rickert, Bennett, Lane, & French, 1978;Solomon, 1977;Mackintosh, Note 2). Although there may, indeed, be a defect in blocking after hippocampal disruption, as the latter two studies suggest, it cannot be attributed to some lesion-induced failure in assessing or reacting to changing salience.…”

Section: Context In Conditioningmentioning

confidence: 99%