Dorsal hippocampal involvement in conditioned-response timing and maintenance of temporal information in the absence of the CS

Tam, Shu K. E.; Jennings, Dómhnall J.; Bonardi, Charlotte

doi:10.1007/s00221-013-3530-4

Cited by 21 publications

(42 citation statements)

References 36 publications

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“…Importantly, both pre-training and post-training DH lesions produced leftward shifts in peak times, confirming previous investigations and suggesting a possible role for the DH in the cortical-striatal-based timing mechanisms [16,20,22,23,25,70]. Importantly, examination of the individual-trial performance revealed that earlier 'start' times rather than earlier 'stop' times or a combination of both could well be the reason for the observed leftward shifts of peak times.…”

Section: Discussion (A) Dorsal and Ventral Hippocampal Lesions Differsupporting

confidence: 87%

“…B 369: 20120466 after the mice had already received FI training and 20 sessions of bipeak training. Such post-training lesions are the most common procedure used to evaluate the effects of hippocampal damage on timing behaviour [20,[52][53][54][55], but see 22,23]. Behavioural training was resumed after the mice recovered from the surgery and no reversal learning was conducted.…”

Section: Training Ventral Hippocampus Lesionsmentioning

confidence: 99%

“…Interestingly, although neglected by many of the current models of interval timing [17], the hippocampus has long been considered a site of spatial-temporal interaction, which provides a basis for generation, maintenance and retrieval of episodic memories [18,19]. Since the initial evaluation of the effects of post-training fimbria-fornix lesions on timing and temporal memory [20], studies investigating the role of the hippocampus in the temporal control of behaviour have generated consistent, though not always conclusive, results [21][22][23][24]. Specifically, both humans and rodents with a variety of different types of hippocampal lesions have been shown to underestimate target durations, and/or to exhibit increased sensitivity to signal duration [25,26].…”

Section: Introductionmentioning

confidence: 99%

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Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Yin

Meck

2014

Phil. Trans. R. Soc. B

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Mice with cytotoxic lesions of the dorsal hippocampus (DH) underestimated 15 s and 45 s target durations in a bi-peak procedure as evidenced by proportional leftward shifts of the peak functions that emerged during training as a result of decreases in both ‘start’ and ‘stop’ times. In contrast, mice with lesions of the ventral hippocampus (VH) displayed rightward shifts that were immediately present and were largely limited to increases in the ‘stop’ time for the 45 s target duration. Moreover, the effects of the DH lesions were congruent with the scalar property of interval timing in that the 15 s and 45 s functions superimposed when plotted on a relative timescale, whereas the effects of the VH lesions violated the scalar property. Mice with DH lesions also showed enhanced reversal learning in comparison to control and VH lesioned mice. These results are compared with the timing distortions observed in mice lacking δ -opioid receptors (Oprd1 −/− ) which were similar to mice with DH lesions. Taken together, these results suggest a balance between hippocampal–striatal interactions for interval timing and demonstrate possible functional dissociations along the septotemporal axis of the hippocampus in terms of motivation, timed response thresholds and encoding in temporal memory.

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Section: Discussion (A) Dorsal and Ventral Hippocampal Lesions Differsupporting

confidence: 87%

Section: Training Ventral Hippocampus Lesionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Yin

Meck

2014

Phil. Trans. R. Soc. B

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“…It may also be that impaired timing abilities in the CA3 NR1-deleted mice are expressed as a greater tendency to exhibit premature responses, as may be expected if the mice are unable to judge whether sufficient time has passed to expect the onset of another trial. The latter interpretation is consistent with (1) an emerging behavioral literature indicating that the dorsal hippocampus plays a role in response timing that is independent of a role in response inhibition (Tam and Bonardi, 2012a; Tam and Bonardi, 2012b; Tam et al, 2013) and (2) research indicating that systemic NMDAR antagonists affect both response inhibition and timing in rats performing a DRL task (Welzl et al, 1991). Our data are not consistent with recent studies in which excitotoxic lesions of the dorsal hippocampus failed to affect premature responding in rats previously trained on the 5-CSRTT (Abela et al, 2013; Chudasama et al, 2012).…”

Section: Discussionsupporting

confidence: 81%

Effects of prefrontal cortex and hippocampal NMDA NR1-subunit deletion on complex cognitive and social behaviors

et al. 2015

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Glutamate N-methyl-D-aspartate receptors (NMDARs) in the medial prefrontal cortex (mPFC) and hippocampus may play an integral role in complex cognitive and social deficits associated with a number of psychiatric illnesses including autism, mood disorders, and schizophrenia. We used localized infusions of adeno-associated virus Cre-recombinase in adult, targeted knock-in mice with loxP sites flanking exons 11-22 of the NR1 gene, to investigate the effects of chronic NMDAR dysfunction in the mPFC and CA3 hippocampus on cognitive and social behavior. A 5-choice serial reaction time task (5-CSRTT) was used to monitor aspects of cognitive function that included attention and response inhibition. Social behavior was assessed using Crowley's sociability and preference for social novelty protocol. Chronic NMDAR dysfunction localized to the anterior cingulate/prelimbic mPFC or dorsal CA3 hippocampus differentially affected response inhibition and social interaction. mPFC NR1-deletion increased perseverative responding in the 5-CSRTT and enhanced preference for social novelty, whereas CA3 NR1-deletion increased premature responding in the 5-CSRTT and decreased social approach behavior. These findings suggest that mPFC and CA3 NMDARs may play selective roles in regulating compulsive and impulsive behavior, respectively. Furthermore, these findings are consistent with emerging evidence that these behaviors are mediated by distinct, albeit overlapping, neural circuits. Our data also suggest that NMDARs in these regions uniquely contribute to the expression of normal social behavior. In this case, mPFC and CA3 NMDARs appear to inhibit and facilitate aspects of social interaction, respectively. The latter dissociation raises the possibility that distinct circuits contribute to the expression of social intrusiveness and impoverished social interaction.

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“…Until recently there was almost no behavioral evidence that could unequivocally establish that damage to the hippocampus, and more specifically the DHPC, is sufficient to produce a temporal deficit (although see Jaldow et al, ; Balci et al, ; Yin and Meck, ). To address this deficiency, we examined the effect of ibotenic‐acid lesions of the DHPC in an appetitive conditioning task, in which a fixed‐duration, 15‐s CS was followed by a food pellet at its termination (Tam and Bonardi, ; Tam et al, ). On subsequent non‐reinforced test trials we found that, while sham‐lesioned subjects showed maximal responding at the time point at which food had been delivered during training, subjects with DHPC damage showed maximal responding at significantly earlier time points (i.e.…”

Section: Introductionmentioning

confidence: 99%

Effects of dorsal hippocampal damage on conditioning and conditioned‐response timing: A pooled analysis

2014

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Charlotte (2015) Effects of dorsal hippocampal damage on conditioning and conditioned-response timing: a pooled analysis. Hippocampus, 25 (4 A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription. AbstractBehavioral findings suggest that the dorsal hippocampus (DHPC) plays a role in timing of appetitive conditioned responding. The present article explored the relationship between the extent of DHPC damage and timing ability, in a pooled analysis of three published studies from our laboratory. Initial analyses of variance confirmed our previous reports that DHPC damage reduced peak times (a measure of timing accuracy). However, the spread (a measure of timing precision) was unchanged, such that the coefficient of variation (spread / peak time) was significantly larger in DHPC-lesioned animals. This implies that, in addition to the wellestablished effect of DHPC lesions on timing accuracy, DHPC damage also produced a deficit in precision of timing. To complement this analysis, different generalized linear mixed-effects models (GLMMs) were performed on the combined dataset, to examine which combinations of the different behavioral measures of timing were the best predictors of the degree of hippocampal damage. The results from the GLMM analysis suggested that the greater the DHPC damage, the greater the absolute difference between the observed peak time and reinforced duration. Nevertheless, this systematic relationship between damage and performance was not specific to the temporal domain: paradoxically the greater the damage the greater the magnitude of peak responding. We discuss these lesion effects in terms of scalar timing theory.3

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Dorsal hippocampal involvement in conditioned-response timing and maintenance of temporal information in the absence of the CS

Cited by 21 publications

References 36 publications

Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Effects of prefrontal cortex and hippocampal NMDA NR1-subunit deletion on complex cognitive and social behaviors

Effects of dorsal hippocampal damage on conditioning and conditioned‐response timing: A pooled analysis

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