Impaired Recognition Memory in Rats after Damage to the Hippocampus

By R. E. Clark, S. Zola, L. R. Squire. Journal of Neuroscience, 2000

759 citations recorded by the source corpus.

Rats with radio-frequency or ibotenic acid lesions of the hippocampus and rats with radio-frequency lesions of the fornix were tested on the visual paired comparison task (VPC), a test of recognition memory. Memory was assessed at five different delay intervals ranging from 10 sec to 24 hr. All operated groups performed normally at the shorter delays (10 sec and 1 min). Across longer delays, the two groups with hippocampal damage were impaired. Rats with fornix lesions performed well on the VPC task but were impaired on a spatial task (spontaneous alternation). The results show that the hippocampus is essential for normal recognition memory. Moreover, fornix lesions need not mimic the effects of direct damage to hippocampal tissue. The findings are discussed in the context of the contribution of the hippocampus to recognition memory.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Developmental Neuroscience

View Paper: https://www.semanticscholar.org/paper/ca3e83f9f253a410f9b192865bd0d267da7d3caa

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Citations in the corpus

When Is the Hippocampus Involved in Recognition Memory? (2011, background): “When Is the Hippocampus Involved in Recognition Memory?”
Hippocampal damage and exploratory preferences in rats: memory for objects, places, and contexts. (2002, background): “However, it was recently reported that cytotoxic lesions of the HPC caused deficits after a 24-hr retention delay (Clark et al. 2000), although rats in the same study that had fornix lesions or radiofrequency lesions of the HPC performed normally after the 24-hr delay.”
New neurons in the dentate gyrus are involved in the expression of enhanced long‐term memory following environmental enrichment (2005, background): “…a review), other studies have found a delay-dependent impairment in long-term (24 h) recognition memory in rats with hippocampal lesions (Vnek & Rothblat, 1996; Clark et al., 2000; but see Gaskin et al., 2003) and mice with lidocaine-induced inactivation of the hippocampus (Hammond et al., 2004).”
The stressed hippocampus, synaptic plasticity and lost memories (2002, background): “Recently, stress has also been found to impair hippocampus-dependent object-recognition memor”
The medial temporal lobe and recognition memory. (2007, background): “…no deficit (e.g., Mumby et al. 2002, Winters et al. 2004; reviewed in Mumby 2001) whereas other studies have observed impairment at long delays (Clark et al. 2000, Hammond et al. 2004), and observation of the deficit may depend on the amount of damage to the hippocampus (e.g., Broadbent et al.…”
Hippocampal Sharp Waves and Reactivation during Awake States Depend on Repeated Sequential Experience (2006, background): “Analogous deficits are observed in both humans and animals after hippocampal lesions (Scoville and Milner, 1957; O’Keefe and Nadel, 1978; Kesner and Novak, 1982; Morris et al., 1982; Redish, 1999; Clark et al., 2000; Fortin et al., 2002).”
Epigenetic Modulation of Seizure-Induced Neurogenesis and Cognitive Decline (2007, methodology): “We tested all rats in the survival groups 5 weeks after seizure induction in a hippocampus-dependent object recognition test (Clark et al., 2000).”
Dentate gyrus-specific knockdown of adult neurogenesis impairs spatial and object recognition memory in adult rats. (2009, methodology): “We scored object exploration (nose within 2 cm of object and vibrissae moving) (see Clark et al. 2000 ) until the rat accumulated 30 sec of contact time with the objects.”