Effects of Oestradiol on Hippocampal Circuitry

2008 ◽  
pp. 173-187 ◽  
Author(s):  
Catherine S. Woolley
Keyword(s):  
Hippocampal Circuitry

Is adult hippocampal neurogenesis really relevant for the treatment of psychiatric disorders?

2020 ◽  
Vol 18 ◽  
Author(s):  
Marco Carli ◽  
Stefano Aringhieri ◽  
Shivakumar Kolachalam ◽  
Biancamaria Longoni ◽  
Giovanna Grenno ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Emotional Processing ◽  
Imaging Techniques ◽  
Hippocampal Neurogenesis ◽  
Adult Brain ◽  
Adult Hippocampal Neurogenesis ◽  
Mood Stabilizers ◽  
Post Traumatic Stress ◽  
Newborn Neurons ◽  
Hippocampal Circuitry

: Adult neurogenesis consists in the generation of newborn neurons from neural stem cells taking place in the adult brain. In mammals, this process is limited to very few areas of the brain, and one of these neurogenic niches is the subgranular layer of the dentate gyrus (DG) of the hippocampus. Adult newborn neurons are generated from quiescent neural progenitors (QNPs), which differentiate through different steps into mature granule cells (GCs), to be finally integrated into the existing hippocampal circuitry. In animal models, adult hippocampal neurogenesis (AHN) is relevant for pattern discrimination, cognitive flexibility, emotional processing and resilience to stressful situations. Imaging techniques allow to visualize newborn neurons within the hippocampus through all their stages of development and differentiation. In humans, the evidence of AHN is more challenging, and, based on recent findings, it persists through the adulthood, even if it declines with age. Whether this process has an important role in human brain function and how it integrates into the existing hippocampal circuitry is still a matter of exciting debate. Importantly, AHN deficiency has been proposed to be relevant in many psychiatric disorders, including mood disorders, anxiety, post-traumatic stress disorder and schizophrenia. This review aims to investigate how AHN is altered in different psychiatric conditions and how pharmacological treatments can rescue this process. In fact, many psychoactive drugs, such as antidepressants, mood stabilizers and atypical antipsychotics (AAPs), can boost AHN with different results. In addition, some non-pharmacological approaches are discussed as well.

scholarly journals Regionally specific changes in the hippocampal circuitry accompany progression of cerebrospinal fluid biomarkers in preclinical Alzheimer's disease

2017 ◽  
Vol 39 (2) ◽  
pp. 971-984 ◽  
Author(s):  
Christine L. Tardif ◽  
Gabriel A. Devenyi ◽  
Robert S. C. Amaral ◽  
Sandra Pelleieux ◽  
Judes Poirier ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Preclinical Alzheimer’S Disease ◽  
Cerebrospinal Fluid Biomarkers ◽  
Hippocampal Circuitry

scholarly journals Early postnatal hyperthyroidism alters hippocampal circuitry and improves radial-maze learning in adult mice

1991 ◽  
Vol 11 (7) ◽  
pp. 2102-2106 ◽  
Author(s):  
H Schwegler ◽  
WE Crusio ◽  
HP Lipp ◽  
I Brust ◽  
GG Mueller
Keyword(s):  
Radial Maze ◽  
Maze Learning ◽  
Adult Mice ◽  
Hippocampal Circuitry

scholarly journals Hyperexcitable Parvalbumin Interneurons Render Hippocampal Circuitry Vulnerable to Amyloid Beta

iScience ◽  
2020 ◽  
Vol 23 (7) ◽  
pp. 101271 ◽  
Author(s):  
Sara Hijazi ◽  
Tim S. Heistek ◽  
Rolinka van der Loo ◽  
Huibert D. Mansvelder ◽  
August B. Smit ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Parvalbumin Interneurons ◽  
Hippocampal Circuitry

Chromogranins as markers of altered hippocampal circuitry in temporal lobe epilepsy

2001 ◽  
Vol 50 (2) ◽  
pp. 216-226 ◽  
Author(s):  
Susanne Pirker ◽  
Thomas Czech ◽  
Christoph Baumgartner ◽  
Hans Maier ◽  
Klaus Novak ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Circuitry

scholarly journals The Susceptibility of CA1 Pyramidal Cells to Cerebral Ischemia is Maintained after Neonatal, Lesion-Induced Reorganization of the Hippocampal Circuitry

1994 ◽  
Vol 14 (3) ◽  
pp. 391-396 ◽  
Author(s):  
Niels Tønder ◽  
Flemming F. Johansen ◽  
Jens Zimmer ◽  
Nils H. Diemer
Keyword(s):  
Cerebral Ischemia ◽  
Pyramidal Cell ◽  
Neuronal Degeneration ◽  
Pyramidal Cells ◽  
Cell Loss ◽  
Transient Cerebral Ischemia ◽  
Ca1 Pyramidal Cells ◽  
Neonatal Lesion ◽  
Neonatal Lesions ◽  
Hippocampal Circuitry

Acute lesions of hippocampal pathways have been shown previously to ameliorate CA1 pyramidal cell loss after subsequent transient cerebral ischemia. In this study, we examined the effect of chronic neonatal lesion with reorganization of hippocampal circuitry on adult postischemic neuron loss in the hippocampus. Newborn rats were subjected to unilateral knife-cut lesions at various positions along the trisynaptic entorhino-dentatohippocampal pathway. Seven months later, the rats were subjected to transient cerebral ischemia using the four-vessel occlusion technique. At the time of killing 4 days later, a Nissl stain was used to demonstrate neuronal degeneration, while connective reorganization resulting from the neonatal lesions was monitored by Timm staining. In one group of rats, neonatal lesions had caused severe depletion of entorhinal projections to the septodorsal fascia dentata and hippocampus (CA1 and CA3), without any direct damage to the dorsal hippocampus itself. Another group had extensive damage of the dorsal CA3, with removal of the Schaffer collaterals from these levels to CA1, and variable damage to the entorhinal afferents. In both groups, the extent and pattern of ischemia-induced degeneration of CA1 pyramidal cells were the same on the lesioned and nonlesioned sides of the brain, demonstrating that neonatal lesions and the subsequent connective reorganization did not have a sparing effect. Seen in relationship to previous observations in adult rats of the neuroprotective actions of acute, preischemic lesions of the trisynaptic hippocampal pathway, it is concluded that CA1 pyramidal cell loss requires the presence of intact excitatory afferents rather than an intact hippocampal circuitry.

scholarly journals An In Vitro Model of Hippocampal Sharp Waves: Regional Initiation and Intracellular Correlates

2005 ◽  
Vol 94 (1) ◽  
pp. 741-753 ◽  
Author(s):  
Chiping Wu ◽  
Marjan Nassiri Asl ◽  
Jesse Gillis ◽  
Frances K. Skinner ◽  
Liang Zhang
Keyword(s):  
Dentate Gyrus ◽  
Large Amplitude ◽  
Pyramidal Neurons ◽  
Slow Wave Sleep ◽  
Hippocampal Slices ◽  
Field Potentials ◽  
Sharp Wave ◽  
Sharp Waves ◽  
Hippocampal Circuitry

During slow wave sleep and consummatory behaviors, electroencephalographic recordings from the rodent hippocampus reveal large amplitude potentials called sharp waves. The sharp waves originate from the CA3 circuitry and their generation is correlated with coherent discharges of CA3 pyramidal neurons and dependent on activities mediated by AMPA glutamate receptors. To model sharp waves in a relatively large hippocampal circuitry in vitro, we developed thick (1 mm) mouse hippocampal slices by separating the dentate gyrus from the CA2/CA1 areas while keeping the functional dentate gyrus-CA3-CA1 connections. We found that large amplitude (0.3–3 mV) sharp wave-like field potentials occurred spontaneously in the thick slices without extra ionic or pharmacological manipulation and they resemble closely electroencephalographic sharp waves with respect to waveform, regional initiation, pharmacological manipulations, and intracellular correlates. Through measuring tissue O2, K+, and synaptic and single cell activities, we verified that the sharp wave-like potentials are not a consequence of anoxia, nonspecific elevation of extracellular K+ and dissection-related tissue damage. Our data suggest that a subtle but crucial increase in the CA3 glutamatergic activity effectively recruits a population of neurons thus responsible for the generation of the sharp wave-like spontaneous field potentials in isolated hippocampal circuitry.

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