The possibility of neurotoxicity in the hippocampus in major depression: a primer on neuron death.

By R. Sapolsky. Biological Psychiatry, 2000

721 citations recorded by the source corpus.

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

View Paper: https://www.semanticscholar.org/paper/796ef88b22a358dd8ca32d638a44daa0c20b768d

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In Behavioral Neuroscience

In Cellular and Molecular Neuroscience

In Developmental Neuroscience

Citations in the corpus

A Unified Model of Depression (2016, positive): “Over time, elevated cortisol can lead to neural atrophy (mediated by glutamate, and particularly in the hippocampus;5 see McEwen, 2003; Sapolsky, 2000) that could further exacerbate HPA dysregulation (as the hippocampus plays a key role in HPA feedback inhibition; see Mahar, Bambico, Mechawar, & Nob”
Brain-Derived Neurotrophic Factor Produces Antidepressant Effects in Behavioral Models of Depression (2002, background): “Another possibility is that BDNF makes hippocampal neurons more resilient and able to oppose the effects of stress (e.g., oppose the downregulation of neurotrophic factor support, inhibit potential excitoxic damage, and block neuronal atrophy; Duman et al., 2000; McEwen, 2000; Sapolsky, 2000).”
Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior (2012, background): “More recently, human imaging and post mortem studies have suggested that there is increased occupancy of nAChRs by ACh that is highest in individuals who are actively depressed and intermediate in those who have a history of depression with no change in overall nAChR number (Saricicek et al., 2012).”
The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007, background): “First, if a stress-induced increase in hippocampal activation, with its increase in glutamate levels and enhanced calcium influx, were to continue unabated, hippocampal neurons would be at an increased risk for glutamate-induced neurotoxicity (Sapolsky [298]; Slemmer et al.”
Stress and Memory: Behavioral Effects and Neurobiological Mechanisms (2007, background): “Nowadays, there is great consensus in the literature that stress is a potent modulator of cognitive function in general, and more precisely, of learning and memory processes McEwen and Sapolsky [1]; de Kloet et al. [2]; Lupien and Lepage [3]; Sandi [4, 5]; Diamond et al. [6]; Fuchs et al. [7]; Joël”
The role of the hippocampus in the pathophysiology of major depression. (2004, neutral): “Whether genetic vulnerability is expressed in part through a small HC that confers vulnerability to MDD is unknown, but the sample in which this may be most readily tested comprises individuals with strong family histories of MDD.”
Neurobiological and Neuropsychiatric Effects of Dehydroepiandrosterone (DHEA) and DHEA Sulfate (DHEAS) (2008, background): “endogenous and/or exogenously-supplemented DHEA(S) concentrations and depression [81,82,142,220,253,267,273,300,332,334, 339].”
Limbic-frontal circuitry in major depression: a path modeling metanalysis (2004, background): “, 1998 ; Sapolsky , 2000 ) .”
Why Does Schizophrenia Develop at Late Adolescence?: A Cognitive-Developmental Approach to Psychosis (2003, background): “There is evidence that stress hormones (glucocorticoids) can bring about reduced hippocampus volume (Sapolsky, 2000), and that this reduction is also reversible (i.e. when glucocorticoids are stabilised; Sapolsky, 2000).”