Prandial increase of leptin in the brain activates spatial learning and memory

2010 ◽  
Vol 17 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Yutaka Oomura ◽  
Shuji Aou ◽  
Kouji Fukunaga
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Spatial Learning And Memory ◽  
The Brain

scholarly journals Reappearance of Hippocampal CA1 Neurons after Ischemia is Associated with Recovery of Learning and Memory

2005 ◽  
Vol 25 (12) ◽  
pp. 1586-1595 ◽  
Author(s):  
Olof Bendel ◽  
Tjerk Bueters ◽  
Mia von Euler ◽  
Sven Ove Ögren ◽  
Johan Sandin ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Cognitive Functions ◽  
Spatial Learning And Memory ◽  
Neuronal Marker ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Hippocampal Ca1 ◽  
The Brain

The pyramidal neurons of the hippocampal CA1 region are essential for cognitive functions such as spatial learning and memory, and are selectively destroyed after cerebral ischemia. To analyze whether degenerated CA1 neurons are replaced by new neurons and whether such regeneration is associated with amelioration in learning and memory deficits, we have used a rat global ischemia model that provides an almost complete disappearance (to approximately 3% of control) of CA1 neurons associated with a robust impairment in spatial learning and memory at two weeks after ischemia. We found that transient cerebral ischemia can evoke a massive formation of new neurons in the CA1 region, reaching approximately 40% of the original number of neurons at 90 days after ischemia (DAI). Co-localization of the mature neuronal marker neuronal nuclei with 5-bromo-2'-deoxyuridine in CA1 confirmed that neurogenesis indeed had occurred after the ischemic insult. Furthermore, we found increased numbers of cells expressing the immature neuron marker polysialic acid neuronal cell adhesion molecule in the adjacent lateral periventricular region, suggesting that the newly formed neurons derive from this region. The reappearance of CA1 neurons was associated with a recovery of ischemia-induced impairments in spatial learning and memory at 90 DAI, suggesting that the newly formed CA1 neurons restore hippocampal CA1 function. In conclusion, these results show that the brain has an endogenous capacity to form new nerve cells after injury, which correlates with a restoration of cognitive functions of the brain.

scholarly journals Insulin signaling in the hippocampus and amygdala regulates metabolism and neurobehavior

2019 ◽  
Vol 116 (13) ◽  
pp. 6379-6384 ◽  
Author(s):  
Marion Soto ◽  
Weikang Cai ◽  
Masahiro Konishi ◽  
C. Ronald Kahn
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Insulin Receptors ◽  
Synaptic Function ◽  
Spatial Learning And Memory ◽  
Central Amygdala ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
The Brain ◽  
Behavior And Cognition

Previous studies have shown that insulin and IGF-1 signaling in the brain, especially the hypothalamus, is important for regulation of systemic metabolism. Here, we develop mice in which we have specifically inactivated both insulin receptors (IRs) and IGF-1 receptors (IGF1Rs) in the hippocampus (Hippo-DKO) or central amygdala (CeA-DKO) by stereotaxic delivery of AAV-Cre into IRlox/lox/IGF1Rlox/loxmice. Consequently, both Hippo-DKO and CeA-DKO mice have decreased levels of the GluA1 subunit of glutamate AMPA receptor and display increased anxiety-like behavior, impaired cognition, and metabolic abnormalities, including glucose intolerance. Hippo-DKO mice also display abnormal spatial learning and memory whereas CeA-DKO mice have impaired cold-induced thermogenesis. Thus, insulin/IGF-1 signaling has common roles in the hippocampus and central amygdala, affecting synaptic function, systemic glucose homeostasis, behavior, and cognition. In addition, in the hippocampus, insulin/IGF-1 signaling is important for spatial learning and memory whereas insulin/IGF-1 signaling in the central amygdala controls thermogenesis via regulation of neural circuits innervating interscapular brown adipose tissue.

scholarly journals Tumor Necrosis Factor (TNF) Is Required for Spatial Learning and Memory in Male Mice under Physiological, but Not Immune-Challenged Conditions

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 608
Author(s):  
Leda Mygind ◽  
Marianne Skov-Skov Bergh ◽  
Vivien Tejsi ◽  
Ramanan Vaitheeswaran ◽  
Kate L. Lambertsen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Tumor Necrosis ◽  
Spatial Learning And Memory ◽  
Male Mice ◽  
Inflammatory Conditions ◽  
Baseline Conditions ◽  
The Brain ◽  
Necrosis Factor

Increasing evidence demonstrates that inflammatory cytokines—such as tumor necrosis factor (TNF)—are produced at low levels in the brain under physiological conditions and may be crucial for synaptic plasticity, neurogenesis, learning and memory. Here, we examined the effects of developmental TNF deletion on spatial learning and memory using 11–13-month-old TNF knockout (KO) and C57BL6/J wild-type (WT) mice. The animals were tested in the Barnes maze (BM) arena under baseline conditions and 48 h following an injection of the endotoxin lipopolysaccharide (LPS), which was administered at a dose of 0.5 mg/kg. Vehicle-treated KO mice were impaired compared to WT mice during the acquisition and memory-probing phases of the BM test. No behavioral differences were observed between WT and TNF-KO mice after LPS treatment. Moreover, there were no differences in the hippocampal content of glutamate and noradrenaline between groups. The effects of TNF deletion on spatial learning and memory were observed in male, but not female mice, which were not different compared to WT mice under baseline conditions. These results indicate that TNF is required for spatial learning and memory in male mice under physiological, non-inflammatory conditions, however not following the administration of LPS. Inflammatory signalling can thereby modulate spatial cognition in male subjects, highlighting the importance of sex- and probably age-stratified analysis when examining the role of TNF in the brain.

scholarly journals Effect of Dehydroepiandrosterone Sulfate on the Modulation of Memory and Learning in Sprague-Dawley Rat Hippocampus

2019 ◽  
Vol 2 ◽  
pp. 291-295
Author(s):  
Asma Ulhusna Shaimi ◽  
Hasmah Abdullah ◽  
Zalina Ismail ◽  
Wan Amir Nizam Wan Ahmad
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Spatial Learning ◽  
Water Maze ◽  
Rat Hippocampus ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Sprague Dawley ◽  
Swimming Pattern ◽  
The Brain

Dehydroepiandrosterone sulphate (DHEAS) is a neurosteroid that is found in greater concentration within the brain rather than in any other body organ (Corpechot et al., 1981) and studies have shown that in the brain, DHEAS has a role in enhancing both learning and memory (Markowski et.al., 2001). This present study investigated the relationship between DHEAS and spatial learning and memory in the rat hippocampus. Male Sprague-Dawley rats were divided into two groups and their spatial learning behaviour was evaluated with the Morris Water Maze. The intensity of DHEAS was simultaneously recorded in real time via the Fiber Fluorescence Microscopy (FFM) S-650 probe of the Cellvisio system. There were significant changes in the swimming pattern of the experimental groups obtained via the Morris Water Maze from day 1 until day 5 and day 6 for the probe test. Meanwhile, it was also seen that the intensity of DHEAS fluorescence increased in parallel to the swimming pattern of the experimental rats in comparison to the control group. The findings suggest that the changes in DHEAS fluorescence has a strong link to both spatial learning and memory.

scholarly journals Targeted Reducing of Tauopathy Alleviates Epileptic Seizures and Spatial Memory Impairment in an Optogenetically Inducible Mouse Model of Epilepsy

2021 ◽  
Vol 8 ◽  
Author(s):  
Yang Gao ◽  
Jie Zheng ◽  
Tao Jiang ◽  
Guilin Pi ◽  
Fei Sun ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Epileptic Seizures ◽  
Neuronal Firing ◽  
Spatial Learning And Memory ◽  
Memory Impairments ◽  
Optogenetic Stimulation ◽  
Hippocampal Ca1 ◽  
The Brain

Intracellular deposition of hyperphosphorylated tau has been reported in the brain of epilepsy patients, but its contribution to epileptic seizures and the association with spatial cognitive functions remain unclear. Here, we found that repeated optogenetic stimulation of the excitatory neurons in ventral hippocampal CA1 subset could induce a controllable epileptic seizure in mice. Simultaneously, the mice showed spatial learning and memory deficits with a prominently elevated total tau and phospho-tau levels in the brain. Importantly, selective facilitating tau degradation by using a novel designed proteolysis-targeting chimera named C4 could effectively ameliorate the epileptic seizures with remarkable restoration of neuronal firing activities and improvement of spatial learning and memory functions. These results confirm that abnormal tau accumulation plays a pivotal role in the epileptic seizures and the epilepsy-associated spatial memory impairments, which provides new molecular target for the therapeutics.

scholarly journals Prandial Increases of Leptin and Orexin in the Brain Modulate Spatial Learning and Memory

2011 ◽  
Vol 41 (3) ◽  
pp. 233-242 ◽  
Author(s):  
Y. Oomura ◽  
S. Aou ◽  
K. Fukunaga ◽  
S. Moriguchi ◽  
K. Sasaki
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Spatial Learning And Memory ◽  
The Brain

scholarly journals Neurobehavioral Changes Resulting from Recombinase Activation Gene 1 Deletion

2003 ◽  
Vol 10 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Jesse Cushman ◽  
Jeannette Lo ◽  
Zhi Huang ◽  
Clive Wasserfall ◽  
John M. Petitto
Keyword(s):  
Immune System ◽  
Locomotor Activity ◽  
Learning And Memory ◽  
Open Field ◽  
Spatial Learning ◽  
Knockout Mice ◽  
Spatial Learning And Memory ◽  
Rag 1 ◽  
And Control ◽  
The Brain

ABSTRACT Recombinase activation gene 1 (RAG-1) function is essential for V(D)J recombination in T-cell-receptor and immunoglobulin rearrangements whereby the immune system may encode memories of a vast array of antigens. The RAG-1 gene is also localized to neurons in the hippocampal formation and related limbic regions that are involved in spatial learning and memory as well as other parameters of neurobehavioral performance. Since the unique ability to encode memory is shared by the immune system and the brain, we tested the hypothesis that loss of the RAG-1 gene in the brain would influence learning and memory performance and examined several different domains of behavior in RAG-1-knockout and control mice. Compared to control mice, RAG-1-knockout mice exhibited increased locomotor activity in an open field under both dim and bright lighting conditions and decreased habituation (reduction in the expected decline in locomotor activity with increasing familiarity with the novel environment in a 1-h test session) in bright lighting. RAG-1-knockout mice also showed reduced levels of fearfulness for some measures of fear-motivated behavior in both the open-field behavior test and elevated-plus maze test. Contrary to our hypothesis, no differences in spatial learning and memory were found between the groups, although modest differences were observed visible-platform testing in the Morris water maze. Neither prepulse inhibition, a measure of sensorimotor gating, nor reflexive acoustic startle responses differed between the RAG-1-knockout and control mice. It remains to be determined if these changes are due to the loss of RAG-1 gene expression in the brain, are due to the absence of the gene in the immune system (e.g., the loss of cytokines with neuromodulatory activities), or are due to some combination of both effects. Study of the neurobiological actions of RAG-1 in the brain may provide new insights into important processes involved in normal brain function and disease.

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