Hippocampal synaptic plasticity, spatial memory and anxiety

Bannerman, David M.; Sprengel, Rolf; Sanderson, David J.; McHugh, Stephen B.; Rawlins, J. N. P.; Monyer, Hannah; Seeburg, Peter H.

doi:10.1038/nrn3677

Cited by 544 publications

(419 citation statements)

References 145 publications

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“…Lesions of the hippocampus, in particular the ventral hippocampus, decrease anxiety-related behavior, indicating a role for the hippocampus in generating anxiety (Bannerman et al, 2014;Deacon et al, 2002), suggesting that neurogenesis might also play a role in anxiety. However, several studies have failed to find any effect of genetic or irradiation-induced ablation of adult neurogenesis on anxiety-like behavior in the open field test or elevated plus maze, either in naive animals (Jaholkowski et al, 2009;Saxe et al, 2006;Snyder et al, 2011;Wei et al, 2011) or after acute stress (Snyder et al, 2011).…”

Section: Anxietymentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

155

108

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Several lines of evidence suggest that adult neurogenesis, the production of new neurons in adulthood, may play a role in psychiatric disorders, including depression, anxiety, and schizophrenia. Medications and other treatments for mental disorders often promote the proliferation of new neurons; the time course for maturation and integration of new neurons in circuitry parallels the delayed efficacy of psychiatric therapies; adverse and beneficial experiences similarly affect development of mental illness and neurogenesis; and ablation of new neurons in adulthood alters the behavioral impact of drugs in animal models. At present, the links between adult neurogenesis and depression seem stronger than those suggesting a relationship between new neurons and anxiety or schizophrenia. Yet, even in the case of depression there is currently no direct evidence for a causative role. This article reviews the data relating adult neurogenesis to mental illness and discusses where research needs to head in the future.

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Section: Anxietymentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

155

108

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“…However, a context is much more complex than a discrete cue and due to this complexity, context conditioning requires additional processes and brain structures (Fanselow 2010). Both the amygdala and the hippocampus are mandatory for such contextual conditioning, as demonstrated by animal studies revealing deficits in the acquisition of conditioned anxiety when the hippocampus and/or the amygdala were lesioned before context conditioning (Fanselow 2010;Maren et al 2013;Bannerman et al 2014). Corroborating these results, we and others found greater hippocampal activation triggered by CTX+ when compared with CTX2 (Marschner et al 2008;Lang et al 2009;Andreatta et al 2015b) in humans.…”

mentioning

confidence: 99%

“…The hippocampus is crucially involved in the formation of spatial (O'Keefe and Dostrovsky 1971;Schiller et al 2015) and cognitive maps (Rudy 2009;Bannerman et al 2014), and such processes are likely to be essential for the discrimination between threatening and safety contexts. Moreover, the hippocampus plays a fundamental role in memory processes in general (Squire and Zola-Morgan 1991;Squire 2004).…”

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confidence: 99%

Effects of context preexposure and delay until anxiety retrieval on generalization of contextual anxiety

et al. 2016

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Animal studies suggest that time delay between acquisition and retrieval of contextual anxiety increases generalization. Moreover, such generalization is prevented by preexposure to the context (CTX), presumably due to an improved representation of such context. We investigated whether preexposure and time-passing modulate generalization of contextual anxiety, in humans. On Day 1, 42 participants (preexposure group) explored two virtual offices, while 41 participants (no-preexposure group) explored a virtual stadium. On Day 2 (24 h later), all participants learned to associate one office (CTX+) with unpredictable unconditioned stimuli (USs), and another office (CTX2) with safety. On Day 3, either 24 h (recent test) or 2 wk (remote test) later, participants revisited CTX2 and CTX+ without USs, as well as a generalization context (G-CTX). Results revealed successfully conditioned anxiety and anxiety generalization for ratings (G-CTX was as aversive as CTX+ was), while safety generalization was found for startle responses (G-CTX elicited startle attenuation as CTX2 did). Time between learning and testing enhanced generalization as reflected by comparable startle responses to all three offices in the remote test. Contextual preexposure facilitated extinction of explicit conditioned anxiety assessed with ratings. These results suggest that memory trace of a context degrades with passage of time in humans like in animals and, consequently, anxiety generalization enhances. After context preexposure, high cognitive processes seem to be crucially involved in facilitating extinction (or safety) learning.

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“…Indeed the harmful impact of treating the SVZ is not surprising since neural stem cell compartments have been implicated in neurocognitive decline due to hints of memory preservation observed when conformal avoidance strategies were designed to shield the dentate gyrus of the hippocampus among patients referred for whole brain irradiation [9,10]. Can the new neurobiology be selectively harnessed to protect patients from toxicity in the case of brain metastases and to augment the control of a devastating entity like GBM?…”

Section: Editorialmentioning

confidence: 99%