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Medial temporal lobe volumes in late-life depression: effects of age and vascular risk factors.
Taylor WD, Deng Y, Boyd BD, Donahue MJ, Albert K, McHugo M, Gandelman JA, Landman BA
(2020) Brain Imaging Behav 14: 19-29
MeSH Terms: Age Factors, Aged, Aged, 80 and over, Atrophy, Cerebral Cortex, Cerebrovascular Circulation, Depression, Depressive Disorder, Major, Female, Hippocampus, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Risk Factors, Temporal Lobe
Show Abstract · Added March 26, 2019
Substantial work associates late-life depression with hippocampal pathology. However, there is less information about differences in hippocampal subfields and other connected temporal lobe regions and how these regions may be influenced by vascular factors. Individuals aged 60 years or older with and without a DSM-IV diagnosis of Major Depressive Disorder completed clinical assessments and 3 T cranial MRI using a protocol allowing for automated measurement of medial temporal lobe subfield volumes. A subset also completed pseudo-continuous arterial spin labeling, allowing for the measurement of hippocampal cerebral blood flow. In 59 depressed and 21 never-depressed elders (mean age = 66.4 years, SD = 5.8y, range 60-86y), the depressed group did not exhibit statistically significant volumetric differences for the total hippocampus or hippocampal subfields but did exhibit significantly smaller volumes of the perirhinal cortex, specifically in the BA36 region. Additionally, age had a greater effect in the depressed group on volumes of the cornu ammonis, entorhinal cortex, and BA36 region. Finally, both clinical and radiological markers of vascular risk were associated with smaller BA36 volumes, while reduced hippocampal blood flow was associated with smaller hippocampal and cornu ammonis volumes. In conclusion, while we did not observe group differences in hippocampal regions, we observed group differences and an effect of vascular pathology on the BA36 region, part of the perirhinal cortex. This is a critical region exhibiting atrophy in prodromal Alzheimer's disease. Moreover, the observed greater effect of age in the depressed groups is concordant with past longitudinal studies reporting greater hippocampal atrophy in late-life depression.
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17 MeSH Terms
Axonal organization defects in the hippocampus of adult conditional BACE1 knockout mice.
Ou-Yang MH, Kurz JE, Nomura T, Popovic J, Rajapaksha TW, Dong H, Contractor A, Chetkovich DM, Tourtellotte WG, Vassar R
(2018) Sci Transl Med 10:
MeSH Terms: Aging, Amyloid Precursor Protein Secretases, Animals, Animals, Newborn, Apoptosis, Aspartic Acid Endopeptidases, Axons, Cognition, Epilepsy, Gene Deletion, Hippocampus, Long-Term Potentiation, Memory Disorders, Mice, Inbred C57BL, Mice, Knockout, Myelin Sheath, Neurogenesis, Phenotype, Substrate Specificity
Show Abstract · Added April 2, 2019
β-Site APP (amyloid precursor protein) cleaving enzyme 1 (BACE1) is the β-secretase enzyme that initiates production of the toxic amyloid-β peptide that accumulates in the brains of patients with Alzheimer's disease (AD). Hence, BACE1 is a prime therapeutic target, and several BACE1 inhibitor drugs are currently being tested in clinical trials for AD. However, the safety of BACE1 inhibition is unclear. Germline BACE1 knockout mice have multiple neurological phenotypes, although these could arise from BACE1 deficiency during development. To address this question, we report that tamoxifen-inducible conditional BACE1 knockout mice in which the gene was ablated in the adult largely lacked the phenotypes observed in germline BACE1 knockout mice. However, one BACE1-null phenotype was induced after gene deletion in the adult mouse brain. This phenotype showed reduced length and disorganization of the hippocampal mossy fiber infrapyramidal bundle, the axonal pathway of dentate gyrus granule cells that is maintained by neurogenesis in the mouse brain. This defect in axonal organization correlated with reduced BACE1-mediated cleavage of the neural cell adhesion protein close homolog of L1 (CHL1), which has previously been associated with axon guidance. Although our results indicate that BACE1 inhibition in the adult mouse brain may avoid phenotypes associated with BACE1 deficiency during embryonic and postnatal development, they also suggest that BACE1 inhibitor drugs developed for treating AD may disrupt the organization of an axonal pathway in the hippocampus, an important structure for learning and memory.
Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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19 MeSH Terms
Alteration of BDNF in the medial prefrontal cortex and the ventral hippocampus impairs extinction of avoidance.
Rosas-Vidal LE, Lozada-Miranda V, Cantres-Rosario Y, Vega-Medina A, Melendez L, Quirk GJ
(2018) Neuropsychopharmacology 43: 2636-2644
MeSH Terms: Animals, Avoidance Learning, Brain-Derived Neurotrophic Factor, CRISPR-Cas Systems, Cell Line, Tumor, Extinction, Psychological, Hippocampus, Male, Neural Pathways, Neuronal Plasticity, Prefrontal Cortex, Rats, Rats, Sprague-Dawley
Show Abstract · Added March 3, 2020
Brain-derived neurotrophic factor (BDNF) is critical for establishing activity-related neural plasticity. There is increasing interest in the mechanisms of active avoidance and its extinction, but little is known about the role of BDNF in these processes. Using the platform-mediated avoidance task combined with local infusions of an antibody against BDNF, we show that blocking BDNF in either prelimbic (PL) or infralimbic (IL) medial prefrontal cortex during extinction training impairs subsequent recall of extinction of avoidance, differing from extinction of conditioned freezing. By combining retrograde tracers with BDNF immunohistochemistry, we show that extinction of avoidance increases BDNF expression in ventral hippocampal (vHPC) neurons, but not amygdala neurons, projecting to PL and IL. Using the CRISPR/Cas9 system, we further show that reducing BDNF production in vHPC neurons impairs recall of avoidance extinction. Thus, the vHPC may mediate behavioral flexibility in avoidance by driving extinction-related plasticity via BDNFergic projections to both PL and IL. These findings add to the growing body of knowledge implicating the hippocampal-prefrontal pathway in anxiety-related disorders and extinction-based therapies.
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HCN channels in the hippocampus regulate active coping behavior.
Fisher DW, Han Y, Lyman KA, Heuermann RJ, Bean LA, Ybarra N, Foote KM, Dong H, Nicholson DA, Chetkovich DM
(2018) J Neurochem 146: 753-766
MeSH Terms: Adaptation, Psychological, Animals, Avoidance Learning, Depression, Disease Models, Animal, Exploratory Behavior, Hippocampus, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Male, Maze Learning, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Peroxins, Pyramidal Cells, Swimming
Show Abstract · Added April 2, 2019
Active coping is an adaptive stress response that improves outcomes in medical and neuropsychiatric diseases. To date, most research into coping style has focused on neurotransmitter activity and little is known about the intrinsic excitability of neurons in the associated brain regions that facilitate coping. Previous studies have shown that HCN channels regulate neuronal excitability in pyramidal cells and that HCN channel current (I ) in the CA1 area increases with chronic mild stress. Reduction of I in the CA1 area leads to antidepressant-like behavior, and this region has been implicated in the regulation of coping style. We hypothesized that the antidepressant-like behavior achieved with CA1 knockdown of I is accompanied by increases in active coping. In this report, we found that global loss of TRIP8b, a necessary subunit for proper HCN channel localization in pyramidal cells, led to active coping behavior in numerous assays specific to coping style. We next employed a viral strategy using a dominant negative TRIP8b isoform to alter coping behavior by reducing HCN channel expression. This approach led to a robust reduction in I in CA1 pyramidal neurons and an increase in active coping. Together, these results establish that changes in HCN channel function in CA1 influences coping style.
© 2018 International Society for Neurochemistry.
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18 MeSH Terms
A person-centered approach to the assessment of early life stress: Associations with the volume of stress-sensitive brain regions in early adolescence.
King LS, Humphreys KL, Camacho MC, Gotlib IH
(2019) Dev Psychopathol 31: 643-655
MeSH Terms: Adolescent, Amygdala, Brain, Child, Female, Hippocampus, Humans, Magnetic Resonance Imaging, Male, Organ Size, Stress, Psychological, Temporal Lobe
Show Abstract · Added March 3, 2020
Researchers are becoming increasingly interested in linking specific forms of early life stress (ELS) to specific neurobiological markers, including alterations in the morphology of stress-sensitive brain regions. We used a person-centered, multi-informant approach to investigate the associations of specific constellations of ELS with hippocampal and amygdala volume in a community sample of 211 9- to 13-year-old early adolescents. Further, we compared this approach to a cumulative risk model of ELS, in which ELS was quantified by the total number of stressors reported. Using latent class analysis, we identified three classes of ELS (labeled typical/low, family instability, and direct victimization) that were distinguished by experiences of family instability and victimization. Adolescents in the direct victimization class had significantly smaller hippocampal volume than did adolescents in the typical/low class; ELS classes were not significantly associated with amygdala volume. The cumulative risk model of ELS had a poorer fit than did the person-centered model; moreover, cumulative ELS was not significantly associated with hippocampal or amygdala volume. Our results underscore the utility of taking a person-centered approach to identify alterations in stress-sensitive brain regions based on constellations of ELS, and suggest victimization is specifically associated with hippocampal hypotrophy observed in early adolescence.
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Hippocampal Network Modularity Is Associated With Relational Memory Dysfunction in Schizophrenia.
Avery SN, Rogers BP, Heckers S
(2018) Biol Psychiatry Cogn Neurosci Neuroimaging 3: 423-432
MeSH Terms: Adult, Brain Mapping, Female, Hippocampus, Humans, Magnetic Resonance Imaging, Male, Memory Disorders, Memory, Episodic, Middle Aged, Neural Pathways, Prefrontal Cortex, Schizophrenia, Temporal Lobe
Show Abstract · Added March 26, 2019
BACKGROUND - Functional dysconnectivity has been proposed as a major pathophysiological mechanism for cognitive dysfunction in schizophrenia. The hippocampus is a focal point of dysconnectivity in schizophrenia, with decreased hippocampal functional connectivity contributing to the marked memory deficits observed in patients. Normal memory function relies on the interaction of complex corticohippocampal networks. However, only recent technological advances have enabled the large-scale exploration of functional networks with accuracy and precision.
METHODS - We investigated the modularity of hippocampal resting-state functional networks in a sample of 45 patients with schizophrenia spectrum disorders and 38 healthy control subjects. Modularity was calculated for two distinct functional networks: a core hippocampal-medial temporal lobe cortex network and an extended hippocampal-cortical network. As hippocampal function differs along its longitudinal axis, follow-up analyses examined anterior and posterior networks separately. To explore effects of resting network function on behavior, we tested associations between modularity and relational memory ability. Age, sex, handedness, and parental education were similar between groups.
RESULTS - Network modularity was lower in schizophrenia patients, especially in the posterior hippocampal network. Schizophrenia patients also showed markedly lower relational memory ability compared with control subjects. We found a distinct brain-behavior relationship in schizophrenia that differed from control subjects by network and anterior/posterior division-while relational memory in control subjects was associated with anterior hippocampal-cortical modularity, schizophrenia patients showed an association with posterior hippocampal-medial temporal lobe cortex network modularity.
CONCLUSIONS - Our findings support a model of abnormal resting-state corticohippocampal network coherence in schizophrenia, which may contribute to relational memory deficits.
Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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14 MeSH Terms
Neuroinflammation Alters Integrative Properties of Rat Hippocampal Pyramidal Cells.
Frigerio F, Flynn C, Han Y, Lyman K, Lugo JN, Ravizza T, Ghestem A, Pitsch J, Becker A, Anderson AE, Vezzani A, Chetkovich D, Bernard C
(2018) Mol Neurobiol 55: 7500-7511
MeSH Terms: Animals, Dendrites, Down-Regulation, Hippocampus, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Inflammation, Lipopolysaccharides, Male, Membrane Proteins, Microglia, Potassium Channels, Pyramidal Cells, Rats, Sprague-Dawley, Time Factors, Toll-Like Receptor 4
Show Abstract · Added April 2, 2019
Neuroinflammation is consistently found in many neurological disorders, but whether or not the inflammatory response independently affects neuronal network properties is poorly understood. Here, we report that intracerebroventricular injection of the prototypical inflammatory molecule lipopolysaccharide (LPS) in rats triggered a strong and long-lasting inflammatory response in hippocampal microglia associated with a concomitant upregulation of Toll-like receptor (TLR4) in pyramidal and hilar neurons. This, in turn, was associated with a significant reduction of the dendritic hyperpolarization-activated cyclic AMP-gated channel type 1 (HCN1) protein level while Kv4.2 channels were unaltered as assessed by western blot. Immunohistochemistry confirmed the HCN1 decrease in CA1 pyramidal neurons and showed that these changes were associated with a reduction of TRIP8b, an auxiliary subunit for HCN channels implicated in channel subcellular localization and trafficking. At the physiological level, this effect translated into a 50% decrease in HCN1-mediated currents (I) measured in the distal dendrites of hippocampal CA1 pyramidal cells. At the functional level, the band-pass-filtering properties of dendrites in the theta frequency range (4-12 Hz) and their temporal summation properties were compromised. We conclude that neuroinflammation can independently trigger an acquired channelopathy in CA1 pyramidal cell dendrites that alters their integrative properties. By directly changing cellular function, this phenomenon may participate in the phenotypic expression of various brain diseases.
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Memory decline from hippocampal electrodes? Let's not forget statistics and study design.
Englot DJ, Rolston JD
(2018) Epilepsia 59: 502-503
MeSH Terms: Electrodes, Hippocampus, Memory, Research Design, Temporal Lobe
Added September 25, 2018
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5 MeSH Terms
Time-varying effects of income on hippocampal volume trajectories in adolescent girls.
Ellwood-Lowe ME, Humphreys KL, Ordaz SJ, Camacho MC, Sacchet MD, Gotlib IH
(2018) Dev Cogn Neurosci 30: 41-50
MeSH Terms: Adolescent, Adolescent Development, Adult, Child, Depressive Disorder, Major, Female, Hippocampus, Humans, Income, Longitudinal Studies, Male, Middle Aged, Mother-Child Relations, Organ Size, Parents, Time Factors, Young Adult
Show Abstract · Added March 3, 2020
Children from lower-SES families exhibit smaller hippocampal volume than do their higher-SES peers. Few studies, however, have compared hippocampal developmental trajectories as a function of SES. Thus, it is unclear whether initial rank-order stability is preserved, or whether volumes diverge/converge over the course of adolescence. In a sample of 101 girls ages 10-24 years, we examined the longitudinal association between family income and parental education, proxies for SES, and changes in hippocampal volume. Hippocampal volume was obtained using MRI; using mixed modeling, we examined the effects of income and education on hippocampal volume across age. As expected, changes in volume were non-linear across development. Further, trajectories diverged in mid-adolescence, with lower-income girls exhibiting reductions in hippocampal volume. Maximal income-related differences were observed at 18 years, and trajectories converged thereafter. This interaction remained significant when accounting for maternal hippocampal volume, suggesting a unique contribution of environment over potential heritable differences. In contrast, the association between parental education and offspring hippocampal volume appeared to be stable across adolescence, with higher levels of parental education predicting consistently larger hippocampal volume. These findings constitute preliminary evidence that girls from lower-income homes exhibit unique trajectories of hippocampal growth, with differences most evident in late adolescence.
Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.
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Contextual Fear Extinction Induces Hippocampal Metaplasticity Mediated by Metabotropic Glutamate Receptor 5.
Stansley BJ, Fisher NM, Gogliotti RG, Lindsley CW, Conn PJ, Niswender CM
(2018) Cereb Cortex 28: 4291-4304
MeSH Terms: Animals, Extinction, Psychological, Fear, Hippocampus, Long-Term Potentiation, Long-Term Synaptic Depression, Male, Methyl-CpG-Binding Protein 2, Mice, Inbred C57BL, Mice, Transgenic, Receptor, Cannabinoid, CB1, Receptors, Kainic Acid, Receptors, N-Methyl-D-Aspartate
Show Abstract · Added March 3, 2020
Dysregulated fear memory can lead to a broad spectrum of anxiety disorders. The brain systems underlying fear memory are manifold, with the hippocampus being prominently involved by housing fear-related spatial memories as engrams, which are created and stored through neural changes such as synaptic plasticity. Although metabotropic glutamate (mGlu) receptors contribute significantly to both fear behavior and hippocampal synaptic plasticity, the relationship between these two phenomena has not been fully elucidated. Here, we report that contextual fear extinction induces a novel form of metaplasticity mediated by mGlu5 at the hippocampal SC-CA1 synapse. Further, blockade of mGlu5 prevents both contextual fear extinction and expression of this metaplasticity. This form of metaplasticity was absent in a mouse model of MECP2-duplication syndrome, corresponding to a complete deficit in extinction learning. These findings suggest that mGlu5-dependent metaplasticity within the hippocampus may play a critical role in extinction of contextual fear.
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