Conditioned taste aversions and neophobia in rats with hippocampal lesions.

Krane, Richard V.; Sinnamon, Harry M.; Thomas, Garth J.

doi:10.1037/h0077236

Cited by 82 publications

(32 citation statements)

References 45 publications

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“…The range of defensive responses influenced by the hippocampus remains to be determined. Rats with large hippocampal lesions exhibit less food neophobia (17)(18)(19) and less predator-induced freezing (20), but do avoid predators when escape is possible (20), suggesting that not all defensive reactions depend on the ventral hippocampus.…”

Section: Discussionmentioning

confidence: 99%

“…This view is based particularly on the similar effects that anxiolytic drugs and septal-hippocampal lesions have on behavior in aversively motivated tasks. However, except for early studies showing that rats with large nonselective hippocampal lesions exhibit reduced food neophobia (17)(18)(19) and reduced freezing in the presence of a predator (20), direct evidence is absent. We now show (i) that the hippocampus controls defensive fear responses during exposure to a potentially threatening environment, (ii) that the relevant circuitry is located at the ventral pole of the hippocampus, and (iii) that this circuit may be dissociable from the associative circuits involved in contextual fear conditioning.…”

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confidence: 99%

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Reduced fear expression after lesions of the ventral hippocampus

Kjelstrup

Tuvnes

Steffenach

et al. 2002

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

766

567

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The hippocampus has a critical role in several fundamental memory operations, including the conditioning of fear to contextual information. We show that the hippocampus is necessary also for unconditioned fear, and that the involved circuitry is at the ventral pole of the hippocampus. Rats with selective hippocampal lesions failed to avoid open arms in an elevated plus-maze and had decreased neuroendocrine stress responses during confinement to a brightly lit chamber. These effects were reproduced by lesions of the ventral half of the hippocampus, but not by damage to the dorsal three-quarters of the hippocampus or the amygdala. Ventral lesions failed to impair contextual fear conditioning or spatial navigation, suggesting that the ventral hippocampus may specifically influence some types of defensive fear-related behavior.defensive ͉ rat ͉ plus-maze ͉ water maze ͉ corticosterone T he experience of anxiety and fear is controlled by a modular neural system including regions in the brainstem, hypothalamus, and deeper parts of the temporal lobe (1-4). The amygdala plays a pivotal role in this system. It controls a broad range of fear reactions, and exhibits neural plasticity that may permit fear responses to be conditioned to new types of experience (refs. 1-5; but see ref. 6). Conditioned fear depends strongly on the basolateral complex of the amygdala (the lateral, basolateral, and basomedial nuclei), whereas the central nucleus and the bed nucleus of the stria terminalis are thought to be the principal output structures, mediating fear-related signals to behavioral, autonomic, and endocrine response systems in the hypothalamus and brainstem (1-5).Conditioning of fear to multimodal stimuli such as context and spatial location also requires the integrity of the hippocampus (7-9). The hippocampus is strongly involved in the encoding of spatial and episodic memories (10-12), and contextual fear conditioning is thought to require many of the associative algorithms responsible for these types of memory (13)(14)(15). Although the hippocampal influence on fear reactions may be a necessary consequence of its mnemonic operations, it is also possible that the hippocampus controls fear and anxiety independently of learning (16). This view is based particularly on the similar effects that anxiolytic drugs and septal-hippocampal lesions have on behavior in aversively motivated tasks. However, except for early studies showing that rats with large nonselective hippocampal lesions exhibit reduced food neophobia (17)(18)(19) and reduced freezing in the presence of a predator (20), direct evidence is absent. We now show (i) that the hippocampus controls defensive fear responses during exposure to a potentially threatening environment, (ii) that the relevant circuitry is located at the ventral pole of the hippocampus, and (iii) that this circuit may be dissociable from the associative circuits involved in contextual fear conditioning. Methods Subjects.A total of 187 male Long Evans rats (250-450 g) were housed individually in tran...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Reduced fear expression after lesions of the ventral hippocampus

Kjelstrup

Tuvnes

Steffenach

et al. 2002

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

766

567

View full text Add to dashboard Cite

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“…However, it should be noted that several researchers have used CTA procedures (e.g., discrimination between different tastes using multiple bottle tests or aversion produced in a particular context) that are hippocampusdependent (Best and Orr 1973;Krane et al 1976). …”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids enhance taste aversion memory via actions in the insular cortex and basolateral amygdala

Miranda¹,

Quírarte²,

Rodriguez-Garcia³

et al. 2008

Learn. Mem.

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It is well established that glucocorticoid hormones strengthen the consolidation of hippocampus-dependent spatial and contextual memory. The present experiments investigated glucocorticoid effects on the long-term formation of conditioned taste aversion (CTA), an associative learning task that does not depend critically on hippocampal function. Corticosterone (1.0 or 3.0 mg/kg) administered subcutaneously to male Sprague-Dawley rats immediately after the pairing of saccharin consumption with the visceral malaise-inducing agent lithium chloride (LiCl) dose-dependently increased aversion to the saccharin taste on a 96-h retention test trial. In a second experiment, rats received corticosterone either immediately after saccharin consumption or after the LiCl injection, when both stimuli were separated by a 3-h time interval, to investigate whether corticosterone enhances memory of the gustatory or visceral stimulus presentation. Consistent with the finding that the LiCl injection, but not saccharin consumption, increases endogenous corticosterone levels, corticosterone selectively enhanced CTA memory when administered after the LiCl injection. Suppression of this training-induced release of corticosterone with the synthesis-inhibitor metyrapone (35 mg/kg) impaired CTA memory, and was dose-dependently reversed by post-training supplementation of corticosterone. Moreover, direct post-training infusions of corticosterone into the insular cortex or basolateral complex of the amygdala, two brain regions that are critically involved in the acquisition and consolidation of CTA, also enhanced CTA retention, whereas post-training infusions into the dorsal hippocampus were ineffective. These findings provide evidence that glucocorticoid effects on memory consolidation are not limited to hippocampus-dependent spatial/contextual information, but that these hormones also modulate memory consolidation of discrete-cue associative learning via actions in other brain regions.

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“…Lesions to many brain regions, including but not restricted to the amygdala, parabrachial nucleus, hypothalamus, medial thalamus, hippocampus and gustatory cortex, all diminish CTA responses (Yamamoto & Fujimoto 1991, Yamamoto et al 1995, arguing that several brain regions are involved in sensing noxious metabolic stimuli or processing such information, and not just the hippocampus. Lesions to the hippocampus alone do affect CTA, but in a complex manner (Krane et al 1976, Kimble et al 1979, Miller et al 1986, Reilly et al 1993. However, from an evolutionary standpoint, CTA may be a primitive response that pre-dates the divergence and specialisation of the chemosensory regions of the brain.…”

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confidence: 99%

Hormones and the hippocampus

Lathe

2001

Journal of Endocrinology

222

161

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Hippocampal lesions produce memory deficits, but the exact function of the hippocampus remains obscure. Evidence is presented that its role in memory may be ancillary to physiological regulation. Molecular studies demonstrate that the hippocampus is a primary target for ligands that reflect body physiology, including ion balance and blood pressure, immunity, pain, reproductive status, satiety and stress. Hippocampal receptors are functional, probably accessible to their ligands, and mediate physiological and cognitive changes. This argues that an early role of the hippocampus may have been in sensing soluble molecules (termed here 'enteroception') in blood and cerebrospinal fluid, perhaps reflecting a common evolutionary origin with the olfactory system ('exteroception').Functionally, hippocampal enteroception may reflect feedback control; evidence is reviewed that the hippocampus modulates body physiology, including the activity of the hypothalamus-pituitary-adrenal axis, blood pressure, immunity, and reproductive function. It is suggested that the hippocampus operates, in parallel with the amygdala, to modulate body physiology in response to cognitive stimuli. Hippocampal outputs are predominantly inhibitory on downstream neuroendocrine activity; increased synaptic efficacy in the hippocampus (e.g. long-term potentiation) could facilitate throughput inhibition. This may have implications for the role of the hippocampus and long-term potentiation in memory. Journal of Endocrinology (2001) 169, 205-231The hippocampus and memory Attention has focused on the hippocampus in view of its likely role in memory encoding and its dysfunction in Alzheimer's disease. The hippocampal formation undoubtedly contributes to the encoding of long-term memories, but an exclusive focus on memory would be a mistake. The present review emphasises an important aspect of hippocampal function: that of responding to and governing body physiology. What follows briefly revisits the role of the hippocampus in learning and memory, and the electrophysiological correlates of memory processes, before considering how the spectrum of genes expressed in the hippocampal formation may cast light on the involvement of the hippocampus in other processes. (In this paper, 'hippocampus' and 'hippocampal formation' are used interchangably to denote the juxtaposition of the fields of the cornu ammonis with the dentate gyrus.) Memory and the hippocampusThe hippocampus, located beneath the cerebral hemispheres, resembles a large 'wishbone' (the curved Y-shaped bone in the chicken neck), but takes its name from the appearance of its arms in cross-section -the interlocking double-U formed by the tightly aligned cell bodies of ammon's horn (cornu ammonis) and the dentate gyrus -reminiscent of the shape of Hippocampus spp. ( Fig. 1; for detailed reviews of hippocampal structure see Amaral 1987, Amaral & Witter 1989. Memory problems in a patient with limbic damage (i.e. at the edge of the forebrain) were first recorded in 1898; another 60 years elapsed be...

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Conditioned taste aversions and neophobia in rats with hippocampal lesions.

Cited by 82 publications

References 45 publications

Reduced fear expression after lesions of the ventral hippocampus

Reduced fear expression after lesions of the ventral hippocampus

Glucocorticoids enhance taste aversion memory via actions in the insular cortex and basolateral amygdala

Hormones and the hippocampus

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