Research Topics
Species | Robert SapolskySummaryAffiliation: Stanford University Country: USA Publications
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Publications
Organismal stress and telomeric aging: an unexpected connectionRobert M Sapolsky
Department of Biological Sciences, Stanford University, Gilbert Lab MC 5020, Stanford, CA 94305-5020, USA
Proc Natl Acad Sci U S A 101:17323-4. 2004
General versus specific actions of mild-moderate hypothermia in attenuating cerebral ischemic damageHeng Zhao
Department of Neurosurgery, Stanford University, Stanford, California 94305 5327, USA
J Cereb Blood Flow Metab 27:1879-94. 2007....- Alzheimer's disease and some speculations about the evolution of its modifiersR M Sapolsky
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA
Ann N Y Acad Sci 924:99-103. 2000..We analyze this in the context of the altricial nature of new-born primates, their long period of dependency on competent maternal care, and the requirement of cognitive intactness for such competency... - Neuroprotective gene therapy against acute neurological insultsRobert M Sapolsky
Department of Biological Sciences, Stanford University, Gilbert Laboratory, Stanford, California 94305-5020, USA
Nat Rev Neurosci 4:61-9. 2003 - Altering behavior with gene transfer in the limbic systemRobert M Sapolsky
Department of Biological Sciences, Gilbert Lab, MC 5020, Stanford University, Stanford, CA 94305 5020, USA
Physiol Behav 79:479-86. 2003..These involve altering (a) cognition, (b) the rewarding properties of addictive substances, (c) patterns of social affiliation, and (d) responses to stress... - Gene therapy for psychiatric disordersRobert M Sapolsky
Department of Biological Sciences, Stanford University School of Medicine, CA 94305 5020, USA
Am J Psychiatry 160:208-20. 2003..In particular, the author considers the role of stress as a predisposing factor in certain psychiatric disorders and the ways in which stress signals can be harnessed as inducers of conditional expression systems in gene therapy... - The frontal cortex and the criminal justice systemRobert M Sapolsky
Department of Biological Sciences, Stanford University School of Medicine, Gilbert Laboratory, MC 5020, Stanford, CA 94305 5020, USA
Philos Trans R Soc Lond B Biol Sci 359:1787-96. 2004.... - The influence of social hierarchy on primate healthRobert M Sapolsky
Departments of Biological Sciences, Neurology and Neurological Sciences, Stanford University, MC 5020, Stanford, CA 94305 5020, USA
Science 308:648-52. 2005..Finally, I consider how these findings apply to the human realm of health, disease, and socioeconomic status... 
A pacific culture among wild baboons: its emergence and transmissionRobert M Sapolsky
Department of Biological Sciences, Stanford University, Stanford, California, USA
PLoS Biol 2:E106. 2004....- Stress and plasticity in the limbic systemRobert M Sapolsky
Department of Biological Sciences, Stanford University, Gilbert Laboratory, MC 5020, Stanford, California 94305 5020, USA
Neurochem Res 28:1735-42. 2003.... - Marked differences in the efficacy of post-insult gene therapy with catalase versus glutathione peroxidasePearl Chang
Departments of Biological Sciences, Neurology, and Neurological Sciences, Stanford University, Gilbert Laboratory, MC 5020, Stanford, CA 94305-5020, USA
Brain Res 1063:27-31. 2005..Thus, we speculated that the post-insult decline in glutathione compromises the protective potential of GPX. Supporting this, reversing the post-insult glutathione decline with glutathione supplementation was neuroprotective... - Gene therapy in the nervous system with superoxide dismutaseIlona Zemlyak
Dept. of Biological Sciences, Stanford University, Gilbert Lab, MC 5020, Stanford, CA 94305-5020, USA
Brain Res 1088:12-8. 2006..These studies can be viewed as a cautionary note concerning gene therapy intervention against necrotic insults... - Over-expression of antioxidant enzymes protects cultured hippocampal and cortical neurons from necrotic insultsHui Wang
Department of Biological Sciences, and Neurology and Neurological Sciences, Stanford University, Gilbert Laboratory, Stanford, California 94305, USA
J Neurochem 87:1527-34. 2003..These studies not only underline the key role played by ROS in the neurotoxicity of necrotic insults, but also suggest potential gene therapy approaches... 
Overexpression of mineralocorticoid and transdominant glucocorticoid receptor blocks the impairing effects of glucocorticoids on memoryDeveroux Ferguson
Department of Biological Sciences, Stanford University, California, USA
Hippocampus 18:1103-11. 2008..These findings illustrate the potential beneficial effects of increasing MR signaling or decreasing GR signaling to enhance specific aspects of cognitive function...- Mild postischemic hypothermia prolongs the time window for gene therapy by inhibiting cytochrome C releaseHeng Zhao
Department of Neurosurgery, Stanford University, Stanford, CA 94305-5327, USA
Stroke 35:572-7. 2004..CONCLUSIONS: Postischemic mild hypothermia extended the time window for gene therapy neuroprotection using Bcl-2 and reduced cytochrome c release... - Bcl-2 overexpression protects against neuron loss within the ischemic margin following experimental stroke and inhibits cytochrome c translocation and caspase-3 activityHeng Zhao
Department of Neurosurgery, Stanford University School of Medicine, 300 Pasteur Drive R200, Stanford, CA 94305 5327, USA
J Neurochem 85:1026-36. 2003..This suggests a potential therapeutic strategy for stroke... - Viral vector-mediated blockade of the endocrine stress-response modulates non-spatial memoryDeveroux Ferguson
Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
Neurosci Lett 437:1-4. 2008..These data add to the growing evidence that increasing estrogenic signaling can protect against the impairing effects of stress on non-spatial memory... - Evidence for caspase effects on release of cytochrome c and AIF in a model of ischemia in cortical neuronsManeesh H Singh
Department of Biological Sciences, and Neurology and Neurological Sciences, Stanford University, 371 Serra Street, Stanford, CA 94305, USA
Neurosci Lett 469:179-83. 2010..In addition, both crmA overexpression and DEVD inhibited cyt c release, suggesting a positive feedback loop involving activated caspases stimulating cyt c release... - Enhancing cognition after stress with gene therapyAndrea Nicholas
Department of Biological Sciences, Stanford University, Stanford, California 94305 5020, USA
J Neurosci 26:11637-43. 2006..Thus, ER/GR expression enhances spatial memory performance and blocks the impairing effects of GCs on such performance... - Resilience against predator stress and dendritic morphology of amygdala neuronsRupshi Mitra
Department of Biology, Stanford University, Stanford, CA 94305, USA
Behav Brain Res 205:535-43. 2009..These data suggest that dendritic hypotrophy in the BLA may be a resilience marker against lasting anxiogenic effects of predator stress... - Estrogenic protection against gp120 neurotoxicity: role of microgliaIlona Zemlyak
Department of Biological Sciences, Neurology and Neurological Sciences, Stanford University, CA 94305 5020, USA
Brain Res 1046:130-6. 2005.... - Bcl-2 transfection via herpes simplex virus blocks apoptosis-inducing factor translocation after focal ischemia in the ratHeng Zhao
Department of Neurosurgery, Stanford University, Stanford, CA, USA
J Cereb Blood Flow Metab 24:681-92. 2004..Our data also suggest that AIF translocated into nuclei after cytochrome c was released into the cytosol. Bcl-2 transfection in the peri-infarct region blocked nuclear AIF translocation and improved cortical neuron survival... - Glucocorticoids worsen excitotoxin-induced expression of pro-inflammatory cytokines in hippocampal culturesAnna MacPherson
Department of Biological Sciences, Stanford University, Gilbert Laboratory MC 5020, Stanford, CA 94305-5020, USA
Exp Neurol 194:376-83. 2005..These findings add to the growing picture of these classically anti-inflammatory hormones potentially having pro-inflammatory effects in the injured CNS... - Neuroprotective effects of bcl-2 overexpression in hippocampal cultures: interactions with pathways of oxidative damageSarah Howard
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA
J Neurochem 83:914-23. 2002..Thus, the antioxidant actions of Bcl-2 are neither necessary nor sufficient to explain its protective actions against these insults in hippocampal neurons... - Novel glucocorticoid effects on acute inflammation in the CNSKlaus Dinkel
Department of Biological Sciences, Gilbert Hall, Stanford University, Stanford, CA 94305 5020, USA
J Neurochem 84:705-16. 2003..These data strongly question the traditional view of GCs being uniformly anti-inflammatory and could further explain how GCs worsen the outcome of neurological insults... - Dual-gene, dual-cell type therapy against an excitotoxic insult by bolstering neuroenergeticsTonya M Bliss
Department of Biological Sciences, Stanford University, Stanford, California 94305-5020, USA
J Neurosci 24:6202-8. 2004.... - Anti-apoptotic therapy with a Tat fusion protein protects against excitotoxic insults in vitro and in vivoKevin L Ju
Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
Exp Neurol 210:602-7. 2008..This fusion protein decreased neurotoxicity caused by the excitotoxins glutamate and kainic acid in primary hippocampal cultures, and decreased hippocampal damage in vivo in an excitotoxic seizure model... - Gene therapy using SOD1 protects striatal neurons from experimental strokeAlexis S Davis
Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Drive R200, Stanford, CA 94305 5237, United States
Neurosci Lett 411:32-6. 2007..These data add to the growing literature, which suggests that an antioxidant approach, perhaps by employing gene therapy techniques, may be beneficial in the treatment of stroke... - Gene therapy and hypothermia for stroke treatmentMidori A Yenari
Department of Neurosurgery, Stanford University, California 94305, USA
Ann N Y Acad Sci 993:54-68; discussion 79-81. 2003.... - Gene therapy in neurological diseaseMidori A Yenari
Department of Neurosurgery and Neurology, Stanford University School of Medicine, CA, USA
Methods Mol Med 104:75-88. 2005..Although application to clinical stroke is probably remote, viral vector-mediated gene therapy provides a unique and powerful tool in the study of molecular mechanisms involved in brain injury... - Chaperones, protein aggregation, and brain protection from hypoxic/ischemic injuryRona G Giffard
Department of Anesthesia, Stanford University, Stanford, CA 94305, USA
J Exp Biol 207:3213-20. 2004..Protection from ischemia and ischemia-like injury by chaperones thus involves at least anti-apoptotic, anti-necrotic and anti-protein aggregation mechanisms... - gp120 neurotoxicity fails to induce heat shock defenses, while the over expression of hsp70 protects against gp120Min Chin Lim
Department of Biological Sciences, Stanford University MC 5020, Stanford, CA 94305 5020, USA
Brain Res Bull 61:183-8. 2003..Specifically, over expression of hsp70 with a herpes viral amplicon vector protected cultured hippocampal neurons from gp120 neurotoxicity... - Catalase over-expression protects striatal neurons from transient focal cerebral ischemiaWenping Gu
Departments of Neurosurgery, Stanford University School of Medicine, 300 Pasteur Drive R200, Stanford, CA 94305-5327, USA
Neuroreport 15:413-6. 2004..Thus, the timing of catalase over-expression relative to ischemia is a critical variable determining its potential therapeutic value... - Disruption of fear memory through dual-hormone gene therapySarina M Rodrigues
Department of Biological Sciences, Stanford University, Stanford, California, USA
Biol Psychiatry 65:441-4. 2009..The basolateral complex of the amygdala (BLA) is uniquely affected by steroid hormones. Whereas glucocorticoids (GCs)--the adrenal hormones released during stress--increase the excitability of BLA neurons, estrogen decreases it... - Glucocorticoids exacerbate lipopolysaccharide-induced signaling in the frontal cortex and hippocampus in a dose-dependent mannerCarolina Demarchi Munhoz
Department of Biological Sciences, Stanford University, Stanford, California 94305 5020, USA
J Neurosci 30:13690-8. 2010..These findings suggest that GCs do not uniformly suppress neuroinflammation and can even enhance it at multiple levels in the pathway linking LPS exposure to inflammation... - The neuroprotective effects of virally-derived caspase inhibitors p35 and crmA following a necrotic insultMadhuri Roy
Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
Neurobiol Dis 14:1-9. 2003..Moreover, in demonstrating the previously unexplored modulation of these processes, these data underline the capacity for classically "anti-apoptotic" proteins to alter other branches of cell death processes... - Disturbing behaviors of the orangutanAnne Nacey Maggioncalda
Department of Anthropological Sciences, Program in Human Biology, Stanford University, Department of Anatomy, Stanford University School of Medicine, USA
Sci Am 286:60-5. 2002 - Gene transfer of HSP72 protects cornu ammonis 1 region of the hippocampus neurons from global ischemia: influence of Bcl-2Stephen Kelly
Department of Neurosurgery, Stanford University, Stanford, CA 94305-5327, USA
Ann Neurol 52:160-7. 2002..We show that HSP72 overexpression protects cornu ammonis 1 region of the hippocampus neurons from global cerebral ischemia, and that this protection may be mediated in part by increased Bcl-2 expression... - Neurotoxic effects of polymorphonuclear granulocytes on hippocampal primary culturesKlaus Dinkel
Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA
Proc Natl Acad Sci U S A 101:331-6. 2004..These findings suggest that PMN might represent a harmful part of inflammation after brain injury that can contribute to secondary damage... - Effect of GP120 on glutathione peroxidase activity in cortical cultures and the interaction with steroid hormonesSheila M Brooke
Department of Biological Sciences, Stanford University, California 94305 5020, USA
J Neurochem 81:277-84. 2002..Overexpression of GSPx enzyme via herpes vector system reversed the GCs-induced loss of enzyme and eliminated the GCs exacerbation of gp120 neurotoxicity... - An inflammatory review of glucocorticoid actions in the CNSShawn F Sorrells
Department of Biological Sciences, Stanford University, Gilbert Lab MC 5020, Stanford, CA 94305 5020, USA
Brain Behav Immun 21:259-72. 2007..We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings... - Phosphoinositide-3-kinase/akt survival signal pathways are implicated in neuronal survival after strokeHeng Zhao
Departments of Neurosurgery and Stanford Stroke Center, Stanford University, Stanford, CA, USA
Mol Neurobiol 34:249-70. 2006..Together, attenuation of the Akt pathway dysfunction contributes to neuronal survival after stroke... - Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odorsAjai Vyas
Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA
Proc Natl Acad Sci U S A 104:6442-7. 2007..Proximate mechanisms of such behavioral manipulations remain unknown, although a subtle tropism on part of the parasite remains a potent possibility... - The stressed CNS: when glucocorticoids aggravate inflammationShawn F Sorrells
Department of Biological Sciences, Stanford University, Gilbert Lab MC 5020, Stanford, CA 94305 5020, USA
Neuron 64:33-9. 2009..In this minireview we discuss the contexts wherein GCs increase CNS inflammation and point out directions for future investigation... - Blocking glucocorticoid and enhancing estrogenic genomic signaling protects against cerebral ischemiaMichelle Y Cheng
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA
J Cereb Blood Flow Metab 29:130-6. 2009..Thus, gene therapeutic strategies to modulate GC and estrogen signaling can be beneficial during an ischemic insult... - Effects of enrichment predominate over those of chronic stress on fear-related behavior in male ratsRupshi Mitra
Department of Biology, Stanford University, Stanford, CA 94305, USA
Stress 12:305-12. 2009..Enhanced contextual modulation of fear memories in animals experiencing environmental enrichment while stressed could reflect an adaptive response. This could allow greater flexibility to optimize vigilance in differing spatial contexts... - Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticusNathan C Manley
Department of Biological Sciences, Stanford University, Stanford, CA, USA
Brain Res 1182:138-43. 2007.... - The exacerbation of hippocampal excitotoxicity by glucocorticoids is not mediated by apoptosisMadhuri Roy
Department of Biological Sciences, Stanford University, Stanford, Calif 94305 5020, USA
Neuroendocrinology 77:24-31. 2003..We suggest that this finding is to be expected, given some energetic features of GC action and the energetic demands of apoptosis... - Effects of overexpression of antioxidants on the release of cytochrome c and apoptosis-inducing factor in the model of ischemiaIlona Zemlyak
Department Biological Sciences, 371 Serra Street, Stanford University, Stanford, CA, United States
Neurosci Lett 453:182-5. 2009..Arguing against this, overexpression of the same antioxidants did not inhibit cytochrome c release. These findings suggest a specific interaction between ROS formation and the caspase-independent route of apoptosis... - Mineralocorticoid receptor overexpression in basolateral amygdala reduces corticosterone secretion and anxietyRupshi Mitra
Department of Biology, Stanford University, Stanford, California 94305, USA
Biol Psychiatry 66:686-90. 2009..Prolonged and heavy occupancy of GRs tends to mediate the deleterious effects of glucocorticoids on neurons, whereas MR occupancy tends to mediate beneficial effects... - Glucocorticoids influence brain glycogen levels during sleep deprivationPhung Gip
Stanford Genome Technology Center, Stanford University, CA 94304 8307, USA
Am J Physiol Regul Integr Comp Physiol 286:R1057-62. 2004..Our findings suggest that the elevated glucocorticoid secretion during SD causes brain glycogenolysis in response to energy demands... - Gene therapy in rodent amygdala against fear disordersRupshi Mitra
Stanford University, Department of Biology, Stanford, CA 94305, USA
Expert Opin Biol Ther 10:1289-303. 2010..As we obtain more information about mechanisms and brain circuits involved, treatment of these conditions will become increasingly realistic... - Sleep deprivation effects on growth factor expression in neonatal rats: a potential role for BDNF in the mediation of delta powerIlana S Hairston
Department of Biological Sciences, Stanford University, Stanford, California 94305 5020, USA
J Neurophysiol 91:1586-95. 2004..We conclude that cortical BDNF expression reflects the onset of adult sleep-homeostatic response, whereas the profile of expression of both growth factors suggests a trophic effect of mild sleep deprivation... - Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in ratsHeng Zhao
Department of Neurosurgery, Stanford University, California 94305 5327, USA
J Cereb Blood Flow Metab 26:1114-21. 2006..In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment... - Potassium channel gene therapy can prevent neuron death resulting from necrotic and apoptotic insultsAngela L Lee
Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
J Neurochem 86:1079-88. 2003..This difference raises the possibility that the means by which these channel subtypes protect may differ. With further development, potassium channel vectors may be an effective pre-emptive strategy against necrotic insults... - Neighbor effects of neurons bearing protective transgenesAngela L Lee
Department of Biology, Stanford University, Stanford, CA 94305 5020, USA
Brain Res 1339:70-5. 2010..We also characterized the necessity for cell-cell contact for these effects. These phenomena may have broad implications for the efficacy of gene overexpression strategies in the CNS... - Glucocorticoid exacerbation of gp120 neurotoxicity: role of microgliaSheila M Brooke
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA
Exp Neurol 177:151-8. 2002..Thus, GCs appear to act at a number of different sites in the multi-cellular pathway to exacerbate the neurotoxic effects of gp120... - Effects of glucocorticoids in the gp120-induced inhibition of glutamate uptake in hippocampal culturesSheila M Brooke
Department of Biological Sciences, Gilbert Building Rm 432, Stanford University, Stanford, CA 94305 5020, USA
Brain Res 972:137-41. 2003..It was found that while GCs do not exacerbate the decrease in reuptake of glutamate in glia cultures, they do enhance the decrease in mixed neuronal cultures and this latter effect appears to be energy-dependent... - Acute corticosterone treatment is sufficient to induce anxiety and amygdaloid dendritic hypertrophyRupshi Mitra
Department of Biology, Stanford University, Gilbert Building, Stanford, CA 94305, USA
Proc Natl Acad Sci U S A 105:5573-8. 2008..The effects of corticosterone were specific to anxiety, as neither acute nor chronic treatment caused any change in conditioned fear or in general locomotor activity in these animals... - Biphasic cytochrome c release after transient global ischemia and its inhibition by hypothermiaHeng Zhao
Department of Neurosurgery, Stanford University, Stanford, California 94305-5327, USA
J Cereb Blood Flow Metab 25:1119-29. 2005..Thus, biphasic cytochrome c release occurs after transient global ischemia and mild hypothermia protects against ischemic damage by blocking the second phase of cytochrome c release, possibly by blocking caspase activity... - Protection against gp120-induced neurotoxicity by an array of estrogenic steroidsIlona Zemlyak
Department of Biological Sciences, Gilbert Laboratory MC 5020, Stanford University, Stanford, CA 94305 5020, USA
Brain Res 958:272-6. 2002..These findings give insight both into the mechanisms of estrogenic protection (e.g. receptor-dependent versus independent actions) as well as into the potential therapeutic use of estrogens against AIDS-related dementia complex... - Glucocorticoids and central nervous system inflammationKlaus Dinkel
Department of Biological Sciences, Stanford University, Stanford, California, USA
J Neurovirol 8:513-28. 2002..This article provides a review of the current literature, showing that under certain circumstances GCs might fail to have anti-inflammatory effects and sometimes even enhance inflammation... - Is impaired neurogenesis relevant to the affective symptoms of depression?Robert M Sapolsky
Gilbert Laboratory, Department of Biological Sciences, Stanford, CA 94305 5020, USA
Biol Psychiatry 56:137-9. 2004 - Conditions of protection by hypothermia and effects on apoptotic pathways in a rat model of permanent middle cerebral artery occlusionHeng Zhao
Department of Neurosurgery, Stanford University, Stanford, California 94305 5327, USA
J Neurosurg 107:636-41. 2007..This models a scenario in which the MCA remains occluded but partial reperfusion occurs through collateral vessels. The authors also determined whether hypothermia mediates ischemic damage by blocking apoptotic pathways... - Disruptive effects of glucocorticoids on glutathione peroxidase biochemistry in hippocampal culturesRavi Patel
Gilbert Laboratory, Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA
J Neurochem 82:118-25. 2002..Thus, GCs have various effects, both energetic and non-energetic in nature, upon steps in GSPx biochemistry that, collectively, may impair hippocampal antioxidant capacity... - Mineralocorticoid receptor overexpression differentially modulates specific phases of spatial and nonspatial memoryDeveroux Ferguson
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA
J Neurosci 27:8046-52. 2007..Thus, this study illustrates the critical role of MR in mediating the retrieval and consolidation of nonspatial memory... - Hippocampal-dependent learning requires a functional circadian systemNorman F Ruby
Department of Biology, Stanford University, Stanford, CA 94305 5020, USA
Proc Natl Acad Sci U S A 105:15593-8. 2008..Arrhythmic hamsters may have failed to perform this task because of chronic inhibitory signaling from the SCN that interfered with the plastic mechanisms that encode learning in the hippocampus... - Hypothermia blocks beta-catenin degradation after focal ischemia in ratsHanfeng Zhang
Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305 5327, USA
Brain Res 1198:182-7. 2008..In conclusion, moderate hypothermia can stabilize beta-catenin, which may contribute to the protective effect of moderate hypothermia... - Stress and depression: possible links to neuron death in the hippocampusAngela L Lee
Department of Biological Sciences, Stanford University, CA 94305-5020, USA
Bipolar Disord 4:117-28. 2002..Thus glucocorticoids may play a contributing role toward neuron death. We further discuss how glucocorticoids cause or exacerbate cellular changes associated with hippocampal neuron loss in the context of the events listed above... - Predator cat odors activate sexual arousal pathways in brains of Toxoplasma gondii infected ratsPatrick K House
Program in Neuroscience, Stanford University, Stanford, California, United States of America
PLoS ONE 6:e23277. 2011.... - Transient gastric irritation in the neonatal rats leads to changes in hypothalamic CRF expression, depression- and anxiety-like behavior as adultsLiansheng Liu
Division of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, California, United States of America
PLoS ONE 6:e19498. 2011..We hypothesized that psychological morbidity in these conditions may result from gastrointestinal problems, rather than causing them... - Male orangutan subadulthood: a new twist on the relationship between chronic stress and developmental arrestAnne N Maggioncalda
Department of Anthropological Sciences, Stanford University, California 94305 2117, USA
Am J Phys Anthropol 118:25-32. 2002..1999], [2000]... - Akt contributes to neuroprotection by hypothermia against cerebral ischemia in ratsHeng Zhao
Department of Neurosurgery, Stanford University, Stanford, California 94305, USA
J Neurosci 25:9794-806. 2005..Hypothermia may protect from ischemic damage in part by preserving Akt activity and attenuating the apoptotic effects of PTEN, PDK1, and FKHR... - Structural consequences of Kcna1 gene deletion and transfer in the mouse hippocampusH Jurgen Wenzel
Department of Neurological Surgery, School of Medicine, University of California Davis, 1515 Newton Court, Davis, CA 95618, USA
Epilepsia 48:2023-46. 2007..We examined the neuropathological consequences of seizure activity in the Kv1.1(-/-) (knock-out) mouse, and explored the effects of injecting a viral vector carrying the deleted Kcna1 gene into hippocampal neurons... - Mothering style and methylationRobert M Sapolsky
Nat Neurosci 7:791-2. 2004 - Environmental enrichment reduces Abeta levels and amyloid deposition in transgenic miceOrly Lazarov
Department of Neurobiology, Pharmacology, and Physiology, University of Chicago, Chicago, IL 60637, USA
Cell 120:701-13. 2005.... - Physiologic manifestations of stress from capture and restraint of free-ranging male African green monkeys (Cercopithecus aethiops)Mbaruk A Suleman
Institute of Primate Research, P.O. Box 24481, Karen, Nairobi, Kenya
J Zoo Wildl Med 35:20-4. 2004..Mean prolactin concentration was significantly lower in the wild-caught monkeys on day 2 after capture, and the levels increased gradually to 45 days in captivity and was highest in monkeys that had been captive for 7 mo... - Sleep restriction suppresses neurogenesis induced by hippocampus-dependent learningIlana S Hairston
Psychology Department, University of California, Berkeley, 94720, USA
J Neurophysiol 94:4224-33. 2005..These findings suggest that sleep loss altered behavioral strategies to those that do not depend on the hippocampus, concomitantly reversing the neurogenic effects of hippocampus-dependent learning... - Chronic unpredictable stress exacerbates lipopolysaccharide-induced activation of nuclear factor-kappaB in the frontal cortex and hippocampus via glucocorticoid secretionCarolina Demarchi Munhoz
Department of Pharmacology, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, 05508 900, Brazil
J Neurosci 26:3813-20. 2006..Our results indicate that stress, via GC secretion, can increase LPS-induced NF-kappaB activation in the frontal cortex and hippocampus, agreeing with a growing literature demonstrating proinflammatory effects of GCs... - Effects of food availability on serum insulin and lipid concentrations in free-ranging baboonsJoseph W Kemnitz
Wisconsin Regional Primate Research Center and Department of Physiology, University of Wisconsin Madison, Madison, Wisconsin 53715 1299, USA
Am J Primatol 57:13-9. 2002..The present results suggest potentially deleterious effects of a highly accessible, calorically dense food source, and associated reduction of physical activity for baboons living in an otherwise natural environment... - Biological stress response terminology: Integrating the concepts of adaptive response and preconditioning stress within a hormetic dose-response frameworkEdward J Calabrese
School of Public Health, Morrill I, N344, University of Massachusetts, Amherst, MA 01003, USA
Toxicol Appl Pharmacol 222:122-8. 2007.... - Chickens, eggs and hippocampal atrophyRobert M Sapolsky
Nat Neurosci 5:1111-3. 2002 - Serum leptin levels as a marker for a syndrome X-like condition in wild baboonsWilliam A Banks
Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center St Louis, St Louis, Missouri 63106, USA
J Clin Endocrinol Metab 88:1234-40. 2003..The differences were not explained by age or social status. These results show that a subgroup of wild baboons is susceptible to developing obesity and insulin resistance and that this susceptibility is not related to age or social rank...
Research Grants
- Parasite/Host Interactions and the Neurobiology of FearRobert Sapolsky; Fiscal Year: 2006..In Specific Aim 3, we will examine the effects of Toxoplasma infection on cell number and volume, and on dendritic morphology in brain regions implicated in the prior two Specific Aims in the effects of Toxo. ..
- Pro-inflammatory glucocorticoid effects in the CNSRobert Sapolsky; Fiscal Year: 2009..The proposal begins to dissect the molecular mechanisms underlying these unexpected and damaging pro-inflammatory GC effects. ..
- Gene Therapy, Stress and Hippocampal FunctionRobert Sapolsky; Fiscal Year: 2007..We will then determine whether these vectors can protect neurogenesis from the inhibitory effects of GCs and, in the case of the chimeric vector, harness this to produce stimulatory estrogenic effects. ..
- Parasite / host interaction and the neurobiology of fearRobert Sapolsky; Fiscal Year: 2009..Pathological fear is central to several psychiatric disorders. Understanding how Toxoplasma abolishes fear will shed light on how fear is generated in the first place and how we can manage pathological fear. ..
- Parasite / host interaction and the neurobiology of fearRobert M Sapolsky; Fiscal Year: 2010..Pathological fear is central to several psychiatric disorders. Understanding how Toxoplasma abolishes fear will shed light on how fear is generated in the first place and how we can manage pathological fear. ..
- Gene therapy against conditioned fearRobert Sapolsky; Fiscal Year: 2005....
- DO GLUCOCORTICOIDS EXACERBATE GP120 NEUROENDANGERMENTRobert Sapolsky; Fiscal Year: 2002..That, coupled with the possible implications of the stressfulness of HIV infection prompt the proposed studies. ..
- Pro-inflammatory glucocorticoid effects in the CNSRobert M Sapolsky; Fiscal Year: 2010..The proposal begins to dissect the molecular mechanisms underlying these unexpected and damaging pro-inflammatory GC effects. ..