Neurotoxic lesions of the dorsal hippocampus disrupt auditory-cued trace heart rate (fear) conditioning in rabbits

McEchron, Matthew D.; Tseng, Wilbur; Disterhoft, John F.

doi:10.1002/1098-1063(2000)10:6<739::aid-hipo1011>3.0.co;2-i

Cited by 80 publications

(63 citation statements)

References 47 publications

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“…2 and 3). This task is dependent on an intact hippocampus, as are other trace conditioned responses (Solomon et al, 1986;Weiss et al, 1999;McEchron et al, 1998McEchron et al, , 2000Beylin et al, 2001). Moreover, it was previously reported that a similar reduction in cell proliferation impairs trace conditioning of the eyeblink response ).…”

Section: Discussionmentioning

confidence: 98%

Neurogenesis may relate to some but not all types of hippocampal‐dependent learning

et al. 2002

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ABSTRACT:The hippocampal formation generates new neurons throughout adulthood. Recent studies indicate that these cells possess the morphology and physiological properties of more established neurons. However, the function of adult generated neurons is still a matter of debate. We previously demonstrated that certain forms of associative learning can enhance the survival of new neurons and a reduction in neurogenesis coincides with impaired learning of the hippocampal-dependent task of trace eyeblink conditioning. Using the toxin methylazoxymethanol acetate (MAM) for proliferating cells, we tested whether reduction of neurogenesis affected learning and performance associated with different hippocampal dependent tasks: spatial navigation learning in a Morris water maze, fear responses to context and an explicit cue after training with a trace fear paradigm. We also examined exploratory behavior in an elevated plus maze. Rats were injected with MAM (7 mg/kg) or saline for 14 days, concurrent with BrdU, to label new neurons on days 10, 12, and 14. After treatment, groups of rats were tested in the various tasks. A significant reduction in new neurons in the adult hippocampus was associated with impaired performance in some tasks, but not with others. Specifically, treatment with the antimitotic agent reduced the amount of fear acquired after exposure to a trace fear conditioning paradigm but did not affect contextual fear conditioning or spatial navigation learning in the Morris water maze. Nor did MAM treatment affect exploration in the elevated plus maze. These results combined with previous ones suggest that neurogenesis may be associated with the formation of some but not all types of hippocampal-dependent memories.

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Section: Discussionmentioning

confidence: 98%

Neurogenesis may relate to some but not all types of hippocampal‐dependent learning

et al. 2002

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“…It is also recognized that the hippocampus plays a critical role in trace conditioning (McEchron, Bouwmeester, Tseng, Weiss, & Disterhoft, 1998;McEchron, Tseng, & Disterhoft, 2000;Quinn, Oommen, Morrison, & Fanselow, 2002;Solomon, Vander Schaaf, Thompson, & Weisz, 1986). It has been hypothesized that a hippocampal-dependent short-term memory system is necessary to create and maintain a representation of the CS during the trace interval, allowing for the integration of the temporally discontiguous CS and US events (Rodriguez & Levy, 2001;Wallenstein, Eichenbaum, & Hasselmo, 1998).…”

Section: Discussionmentioning

confidence: 99%

Trace and long-delay fear conditioning in the developing rat

Barnet

Hunt

2005

Learning & Behavior

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“…A widely employed procedure with rodents is the passive (or inhibitory) avoidance task (Grossman et al, 1975;McEchron et al, 2000;Nader et al, 2000;Nagel and Kimble, 1976), in which the animal's response (e.g. entering a dark compartment of a box when placed in an adjacent lighted compartment, or stepping down from a platform onto a grid floor) is followed by a footshock.…”

Section: What Is Fear Conditioning?mentioning

confidence: 99%

“…Additionally, lesions to the nucleus accumbens (a target of hippocampal efferents) obstruct contextual fear conditioning without affecting auditory fear conditioning (Riedel et al, 1997). Analogous to trace eyeblink conditioning in rabbits (Kim et al, 1995;Moyer et al, 1990;Solomon et al, 1986), hippocampal lesions have also been shown to impair trace (but not delay) fear conditioning to an auditory CS in rats (as measured by freezing) (McEchron et al, 1998) and rabbits (as measured by heart rate) (McEchron et al, 2000). The notion that the hippocampus is involved in contextual and trace fear conditioning are also supported by various knockout/transgenic mice studies.…”

Section: Hippocampusmentioning

confidence: 99%

Neural circuits and mechanisms involved in Pavlovian fear conditioning: A critical review

Kim

Jung

2006

Neuroscience & Biobehavioral Reviews

525

438

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Pavlovian or classical fear conditioning is recognized as a model system to investigate the neurobiological mechanisms of learning and memory in the mammalian brain and to understand the root of fear-related disorders in humans. In recent decades, important progress has been made in delineating the essential neural circuitry and cellular-molecular mechanisms of fear conditioning. Converging lines of evidence indicate that the amygdala is necessarily involved in the acquisition, storage and expression of conditioned fear memory, and long-term potentiation (LTP) in the lateral nucleus of the amygdala is often proposed as the underlying synaptic mechanism of associative fear memory. Recent studies further implicate the prefrontal cortexamygdala interaction in the extinction (or inhibition) of conditioned fear. Despite these advances, there are unresolved issues and findings that challenge the validity and sufficiency of the current amygdalar LTP hypothesis of fear conditioning. The purpose of this review is to critically evaluate the strengths and weaknesses of evidence indicating that fear conditioning depend crucially upon the amygdalar circuit and plasticity. KeywordsFear conditioning; Amygdala; Prefrontal cortex; LTP; NMDA Fear is considered a defensive mechanism that evolved because of its evolutionary success in protecting animals from danger. While fear to certain kinds of stimuli is innately hardwired (e.g. a loud noise evoking fear in newborn infants, a cat inducing fear in naïve laboratory-reared rats), fear can also be acquired rapidly and lastingly to different stimuli allowing animals to respond adaptively to new or changing environmental situations. In the laboratory setting, Pavlovian or classical fear conditioning has become the par excellence task for studying the anatomical, cellular and molecular bases of fear memory formation in the brain.

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Neurotoxic lesions of the dorsal hippocampus disrupt auditory-cued trace heart rate (fear) conditioning in rabbits

Cited by 80 publications

References 47 publications

Neurogenesis may relate to some but not all types of hippocampal‐dependent learning

Neurogenesis may relate to some but not all types of hippocampal‐dependent learning

Trace and long-delay fear conditioning in the developing rat

Neural circuits and mechanisms involved in Pavlovian fear conditioning: A critical review

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