scholarly journals The dorsal hippocampus is required for the formation of long‐term duration memories in rats

2021 ◽  
Author(s):  
Toshimichi Hata ◽  
Tatsuya Yamashita ◽  
Taisuke Kamada
Keyword(s):  
Dorsal Hippocampus

scholarly journals Prenatally traumatized mice reveal hippocampal methylation and expression changes of the stress-related genes Crhr1 and Fkbp5

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anne-Christine Plank ◽  
Stefan Frey ◽  
Lukas Andreas Basedow ◽  
Jalal Solati ◽  
Fabio Canneva ◽  
...  
Keyword(s):  
Stress Reactivity ◽  
Dorsal Hippocampus ◽  
Methylation Status ◽  
Stress Axis ◽  
Mrna Levels ◽  
Fk506 Binding Protein ◽  
Adult Mice ◽  
Stress Related Genes ◽  
Long Term Impact

AbstractIn our previous study, we found that prenatal trauma exposure leads to an anxiety phenotype in mouse pups, characterized by increased corticosterone levels and increased anxiety-like behavior. In order to understand the mechanisms by which aversive in utero experience leads to these long-lasting behavioral and neuroendocrine changes, we investigated stress reactivity of prenatally traumatized (PT) mice, as well as the expression and methylation levels of several key regulatory genes of the stress axis in the dorsal hippocampus (dHPC) of the PT embryo and adult mice. We detected increased corticotropin-releasing hormone receptor 1 (Crhr1) and decreased FK506 binding protein 5 (Fkbp5) mRNA levels in the left dHPC of adult PT mice. These alterations were accompanied by a decreased methylation status of the Crhr1 promoter and an increased methylation status of the Fkbp5 promoter, respectively. Interestingly, the changes in Fkbp5 and Crhr1 mRNA levels were not detected in the embryonic dHPC of PT mice. Together, our findings provide evidence that prenatal trauma has a long-term impact on stress axis function and anxiety phenotype associated with altered Crhr1 and Fkbp5 transcripts and promoter methylation.

Serotonin1A receptors in the dorsal hippocampus regulate working memory and long-term habituation in the hemiparkinsonian rats

2019 ◽  
Vol 376 ◽  
pp. 112207 ◽  
Author(s):  
Ye Liu ◽  
Jian Liu ◽  
Si Rui Jiao ◽  
Xin Liu ◽  
Yuan Guo ◽  
...  
Keyword(s):  
Working Memory ◽  
Dorsal Hippocampus

Posttraining activation of CB1 cannabinoid receptors in the CA1 region of the dorsal hippocampus impairs object recognition long-term memory

2008 ◽  
Vol 90 (2) ◽  
pp. 374-381 ◽  
Author(s):  
Julia R. Clarke ◽  
Janine I. Rossato ◽  
Siomara Monteiro ◽  
Lia R.M. Bevilaqua ◽  
Iván Izquierdo ◽  
...  
Keyword(s):  
Object Recognition ◽  
Cannabinoid Receptors ◽  
Dorsal Hippocampus ◽  
Long Term Memory ◽  
Term Memory ◽  
Ca1 Region

scholarly journals CREB overexpression in dorsal CA1 ameliorates long-term memory deficits in aged rats

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Xiao-Wen Yu ◽  
Daniel M Curlik ◽  
M Matthew Oh ◽  
Jerry CP Yin ◽  
John F Disterhoft
Keyword(s):  
Molecular Mechanisms ◽  
Pyramidal Neurons ◽  
Dorsal Hippocampus ◽  
Memory Deficits ◽  
Camp Response Element Binding ◽  
Intrinsic Excitability ◽  
Long Term Memory ◽  
Term Memory ◽  
Age Related

The molecular mechanisms underlying age-related cognitive deficits are not yet fully elucidated. In aged animals, a decrease in the intrinsic excitability of CA1 pyramidal neurons is believed to contribute to age-related cognitive impairments. Increasing activity of the transcription factor cAMP response element-binding protein (CREB) in young adult rodents facilitates cognition, and increases intrinsic excitability. However, it has yet to be tested if increasing CREB expression also ameliorates age-related behavioral and biophysical deficits. To test this hypothesis, we virally overexpressed CREB in CA1 of dorsal hippocampus. Rats received CREB or control virus, before undergoing water maze training. CREB overexpression in aged animals ameliorated the long-term memory deficits observed in control animals. Concurrently, cells overexpressing CREB in aged animals had reduced post-burst afterhyperpolarizations, indicative of increased intrinsic excitability. These results identify CREB modulation as a potential therapy to treat age-related cognitive decline.

scholarly journals Increased excitability in hippocampal neurons of synaptopodin-knockout mouse

2021 ◽  
Author(s):  
Etay Aloni ◽  
Serphima Verbitzky ◽  
Lilia kushnireva ◽  
Eduard Korkotian ◽  
Menahem Segal
Keyword(s):  
Endoplasmic Reticulum ◽  
Hippocampal Neurons ◽  
Dorsal Hippocampus ◽  
Long Term Potentiation ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Term Potentiation ◽  
Hippocampus Slice ◽  
Recorded Activity

Abstract Synaptopodin (SP) is localized within the spine apparatus, an enigmatic structure located in the neck of spines of central excitatory neurons. It serves as a link between the spine head, where the synapse is located, and the endoplasmic reticulum (ER) in the parent dendrite (Vlachos et al. 2009, Korkotian and Segal, 2011, Zhang et al. 2013). SP is also located in the axon initial segment, in association with the cisternal organelle, another structure related to endoplasmic reticulum. Extensive research using SP knockout (SPKO) mice suggests that SP has a pivotal role in structural and functional plasticity (Deller et al. 2003, Deller et al. 2007). Consequently, SPKO mice were shown to be deficient in cognitive functions, and in ability to undergo long term potentiation of reactivity to afferent stimulation (Deller et al. 2003). In contrast, neurons of SPKO mice appear to be more excitable than their wild type (wt) counterparts(Bas Orth et al, 2007). To address this discrepancy, we have now recorded activity of CA1 neurons in the mouse hippocampus slice, with both extracellular and patch recording methods. Electrophysiologically, SPKO cells in CA1 region of the dorsal hippocampus were more excitable than wt ones. In addition, exposure of mice to a complex environment caused a higher proportion of arc-expressing cells in SPKO than in wt mice hippocampus. These experiments indicate that higher excitability and higher expression of arc staining may reflect SP deficiency in the hippocampus of adult SPKO mice.

scholarly journals Long-Term Development of Selective Neuronal Loss and the Mechanism of Protection by 2-Amino-7-Phosphonoheptanoate in a Rat Model of Incomplete Forebrain Ischaemia

1988 ◽  
Vol 8 (1) ◽  
pp. 64-78 ◽  
Author(s):  
Jeanette H. Swan ◽  
Mary C. Evans ◽  
Brian S. Meldrum
Keyword(s):  
Nmda Receptor ◽  
Dorsal Hippocampus ◽  
Protective Action ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Significant Protection ◽  
Local Cerebral Blood Flow ◽  
Systemic Injection ◽  
Excitatory Neurotransmission

Excitatory neurotransmission at the N-methyl-D-aspartate (NMDA) receptor is selectively blocked by 2-amino-7-phosphonoheptanoate acid (2-APH). Acute focal microinjection of 2-APH into the rat hippocampus partially protects against cytopathology developing in selectively vulnerable neurons after 30 min of ischaemia and 2 h of reperfusion. We show that this protective action of 2-APH does not involve alterations in local cerebral blood flow (CBF). Intermediate cytopathology and long-term neuronal survival has been assessed in rats receiving focal injections of (±) 2-APH. 20 μg in 1 μl, into one dorsal hippocampus prior to and 4 and 10 h after a 10-min period of forebrain ischaemia. Cytopathology assessed 4 or 24 h after ischaemia shows no difference between the buffer and 2-APH–injected hippocampi. Assessment after 7 days survival shows a significant protection against neuronal loss in the CA1 zone of the 2-APH–injected hippocampus compared with the contralateral, buffer-injected hippocampus. Systemic injection of D(-)2-APH (675 mg/kg i.v. at 0 h, 4 h, and 10 h) affords significant protection to CA1 hippocampal neurones (as assessed after 7 days). These results suggest that maintained blockade of neurotransmission at the NMDA receptor in the postischaemic period can protect against delayed cell loss. The mechanism may be through antagonism of the excitotoxic action of an endogenous neurotransmitter acting in the postischaemic period.

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