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Jerry W Rudy

Publications and source records attributed to Jerry W Rudy.

27 records · Page 2Linked to original sources
PubMed2004

Damage to the hippocampal formation does not disrupt representational flexibility as measured by a novelty transfer test.

Rats were trained on a set of visual discrimination problems (A+B-, C+D-, E+F-). The choice stimuli were then recombined to create novel combination tests (A+D-, C+F-, E+B-). Rats with damage to the hippocampus showed perfect transfer on these tests, always choosing A, C, and E, but were not able to learn the spatial location of the platform, indicating that damage to the hippocampus was functional. These results question the generality of H. Eichenbaum, P. Mathews, and N. J. Cohen's (1989) findings and the theoretical claim that choice behavior with novel combinations is based on inferential-like hippocampus-dependent processes (H. Eichenbaum, 1992). They are consistent with the view that simple associative processes guide choice behavior in animals with hippocampal damage that are confronted with novel combinations.

Animals↗
PubMed2003

Transitivity, flexibility, conjunctive representations, and the hippocampus. I. An empirical analysis.

After training on a set of four ordered, simultaneous, odor discrimination problems (A+B-, B+C-, C+D-, D+E), intact rats display transitivity: When tested on the novel combination BD, they choose B. Rats with damage to the hippocampus, however, do not show transitivity (Dusek and Eichenbaum, 1997. Proc Natl Acad Sci U S A 94:7109-7114). These results have been interpreted as support for the idea that the hippocampus is a relational memory storage system that enables the subject to make comparisons among representations of the individual problems and choose based on inferential logic. We provide evidence for a simpler explanation. Specifically, subjects make their choices based on the absolute excitatory value of the individual stimuli. This value determines the ability of that stimulus to attract a response. This conclusion emerged because after training on a five-problem set (A+B-, B+C-, C+D-, D+E-, E+F-) rats preferred B when tested with BE, but not when tested with BD. The implication of these results for how to conceptualize the role of the hippocampus in transitive-like phenomena is discussed.

Animals↗
PubMed2003

Transitivity, flexibility, conjunctive representations, and the hippocampus. II. A computational analysis.

A computational neural network model is presented that explains how the hippocampus can contribute to transitive inference performance observed in rats (Dusek and Eichenbaum, 1997. Proc Natl Acad Sci U S A 94:7109-7114; Van Elzakker et al., 2003. Hippocampus 12:this issue). In contrast to existing theories that emphasize the idea that the hippocampus contributes by flexibly relating previously encoded memories, we find that the hippocampus contributes by altering the elemental associative weights of individual stimulus elements during learning. We use this model to account for a range of existing data and to make a number of distinctive predictions that clearly contrast these two views.

Animals↗
PubMed2002

Memory for context is impaired by a post context exposure injection of interleukin-1 beta into dorsal hippocampus.

Prior research has revealed that treatments that elevate the level of the pro-inflammatory cytokine IL-1beta in the brain, if given after training, impair contextual but not auditory-cue fear conditioning. The present experiments add to these finding by showing that, (a) IL-1beta exerts its effect on contextual fear conditioning by impairing consolidation processes that support the storage of the memory representation of the context; (b) the dorsal hippocampus is a critical site for the effect of IL-1beta; (c) the effect of IL-1beta cannot be attributed to its effect on glucocorticoid levels; and (d) IL-1beta injected into dorsal hippocampus either, immediately, 3, or 24 h, but not 48 h, after training produces this impairment. At this time the mechanisms responsible for this impairment are not understood, but may involve late-phase protein synthesis processes associated with LTP, because later consolidation processes are being disrupted.

Animals↗
PubMed2002

Memory for context is impaired by injecting anisomycin into dorsal hippocampus following context exploration.

Pre-exposure to the context facilitates the small amount of contextual fear conditioning that is normally produced by immediate shock. This context pre-exposure facilitation effect provides a convenient way to study the rat's learning about context. We recently reported that anterograde damage to dorsal hippocampus prevents this facilitation. The present experiments strengthen this conclusion by showing that the protein synthesis inhibitor, anisomycin, injected bilaterally into the dorsal hippocampus following context pre-exposure also significantly reduces the facilitation effect. The same treatment given immediately after immediate shock, however, had no effect on facilitation. These results support theories that assume that, (a) contextual fear involves two processes, acquiring and storing a conjunctive representation of a context and associating that representation with fear; and (b) the hippocampus contributes to contextual fear by participating in the storage of the memory representation of the context.

Animals↗
PubMed2002

Neonatal handling enhances contextual fear conditioning and alters corticosterone stress responses in young rats.

Previous studies have indicated that neonatal handling influences development of hypothalamic-pituitary-adrenal (HPA) control of corticosterone. In addition, corticosterone influences memory consolidation processes in contextual fear conditioning. Therefore, neonatal handling may affect hippocampal-dependent memory processes present in contextual fear conditioning by influencing the development of HPA control of corticosterone. To investigate the effects of neonatal handling on early learning, rat pups were either handled (15-min removal from home cage) on the first 15 days after birth or left undisturbed in their home cage. Handled rats and nonhandled rats were fear conditioned at 18, 21, or 30 days of age and then tested at two time points--24 h following conditioning and at postnatal day 45. Subsequently, at approximately postnatal day 60, rats were exposed to restraint stress and corticosterone levels were assessed during restraint and recovery. Handled and nonhandled rats did not differ significantly in their freezing response immediately following footshock on the conditioning day. However, when tested for contextual fear conditioning at 24 h following conditioning and at postnatal day 45, handled rats showed more freezing behavior than nonhandled rats. When exposed to restraint stress, handled rats had a more rapid return of corticosterone to basal levels than nonhandled rats. These results indicate that neonatal handling enhances developmentally early memory processes involved in contextual fear conditioning and confirms previously reported effects of neonatal handling on HPA control of corticosterone.

Animals↗
PubMed2002

Hippocampal formation supports conditioning to memory of a context.

It has been proposed that contextual fear conditioning depends on 2 processes: (a) construction of a conjunctive representation of the features that make up the context and (b) association of the representation with shock. Support for this view comes from studies indicating that prior exposure to the conditioning context facilitates contextual fear conditioning supported by immediate shock. Thus, conditioning produced by immediate shock is to the memory representation of the preexposed context, which is activated by retrieval cues associated with this context. The authors' experiments support this interpretation and indicate that this process depends on an intact hippocampal formation. These results support the hypothesis that the hippocampal formation supports contextual fear conditioning by storing a conjunctive representation of context.

Animals↗
PubMedDate not supplied

Context pre-exposure obscures amygdala modulation of contextual-fear conditioning.

We report that post-training inactivation of basolateral amygdala region (BLA) with muscimol impaired memory for contextual-fear conditioning (as measured by freezing) and intra-BLA norepinephrine enhanced this memory. However, pre-exposure to the context eliminated both of these effects. These findings provide a likely explanation of why an earler study failed to observe that the BLA modulates contextual fear conditioning-they pre-exposed their rats to the context. These results also suggest that the amygdala modulates the storage of the context fear memory and may do so by influencing the storage of the representation of the context in which the shock occurred.

Amygdala↗