scholarly journals The Hebb Synapse Before Hebb: Theories of Synaptic Function in Learning and Memory Before Hebb (1949), With a Discussion of the Long-Lost Synaptic Theory of William McDougall

2021 ◽  
Vol 15 ◽  
Author(s):  
Richard E. Brown ◽  
Thaddeus W. B. Bligh ◽  
Jessica F. Garden
Keyword(s):  
Learning And Memory ◽  
Synaptic Function ◽  
Cell Assembly ◽  
Short Discussion ◽  
Neural Basis ◽  
Synaptic Change ◽  
The Brain

Since the work of Semon was rediscovered by Schacter in 1978, there has been a renewed interest is searching for the “engram” as the locus of memory in the brain and Hebb’s cell assembly has been equated with Semon’s engram. There have been many theories of memory involving some concept of synaptic change, culminating in the “Hebb Synapse” theory in 1949. However, Hebb said that the idea that any two cells or systems of cells that are repeatedly active at the same time will tend to become “associated,” was not his idea, but an old one. In this manuscript we give an overview of some of the theories of the neural basis of learning and memory before Hebb and describe the synaptic theory of William McDougall, which appears to have been an idea ahead of its time; so far ahead of its time that it was completely ignored by his contemporaries. We conclude by examining some critiques of McDougall’s theory of inhibition and with a short discussion on the fate of neuroscientists whose ideas were neglected when first presented but were accepted as important many decades later.

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 Traumatic Brain Injury Accelerates the Onset of Cognitive Dysfunction and Aggravates Alzheimer’s-like Pathology in the Hippocampus by Altering the Phenotype of Microglia in APP/PS1 Mouse Model

2020 ◽  
Author(s):  
Di Wu ◽  
Jay Prakash Prasad Kumal ◽  
Xiaodi Lu ◽  
Yixuan Li ◽  
Dongsheng Mao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Learning And Memory ◽  
Cell Density ◽  
Cognitive Dysfunction ◽  
Memory Function ◽  
Synaptic Function ◽  
Histopathological Study ◽  
The Brain

Abstract Background: There are increasing studies suggest that Traumatic Brain Injury(TBI) might be the cause of some neurodegenerative diseases, including Alzheimer’s Disease(AD). The mechanism of AD induced by TBI has also been elucidated from sorts of aspects. However, there are also researches which opponent to the viewpoint that TBI is the reason of AD. In this study, we investigate whether and how could TBI accelerated the Alzheimer’s-like pathology and cognitive dysfunction in APP/PS1 mice.Method: The traumatic brain injury model was established in adult male APP/PS1 and C57BL/6 mice. At the 29th and 30th day post-TBI, Novel object and novel position recognition test were performed to test the learning and memory function. After cognitive function test, all the mice were sacrificed with PBS perfusion to anatomize the brain for histopathological study. To determine whether the Alzheimer’s-like pathology and the synaptic function decline can be accelerated by TBI, HE staining, IF staining and IHC staining were performed to detect the cell density in the brain, the degree of Aβ-plaques deposition in the brain, and SYP expression in the brain. We also examined the activity and the phenotype of microglia by IF staining and western-blotting the after the 1st, 2nd, 3rd and 4th week of TBI.Result: In current study, we showed that, on the one hand, TBI impaired the hippocampal-dependent learning and memory, decreased the cell density in the brain, disturbed the synaptic function in the brain, aggravated Aβ-plaques deposition in the hippocampus. On the other hand, TBI also quickly activated microglia in the CNS and altered the phenotype of microglia polarizing to a pro-inflammatory direction. The duration of activation of microglia post-TBI can be at least 3 weeks. We also found that microglia activity was related to the deposition of Aβ-plaques in the specific region of hippocampus. Conclusion: Our experiment suggested that TBI accelerate the onset of cognitive dysfunction and Alzheimer’s-like pathology in APP/PS1 mouse model by altering microglia polarizing direction to mostly exhibiting pro-inflammatory phenotype.

Effects of High BMI on Synaptic Function and Metabolic Connectivity in the Brain—Evidence of Gender Difference

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 363-OR ◽  
Author(s):  
ARIANNA SALA ◽  
MAURA MALPETTI ◽  
ANNA FERRULLI ◽  
LUIGI GIANOLLI ◽  
LIVIO LUZI ◽  
...  
Keyword(s):  
Gender Difference ◽  
Synaptic Function ◽  
Metabolic Connectivity ◽  
The Brain ◽  
High Bmi

Dendrobium officinalis Flower Improves Learning and Reduces Memory Impairment by Mediating Antioxidant Effect and Balancing the Release of Neurotransmitters in Senescent Rats

2020 ◽  
Vol 23 (5) ◽  
pp. 402-410 ◽  
Author(s):  
Lin-Zi Li ◽  
Shan-Shan Lei ◽  
Bo Li ◽  
Fu-Chen Zhou ◽  
Ye-Hui Chen ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Brain Aging ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Histopathological Analysis ◽  
Hippocampal Damage ◽  
Common Belief ◽  
Mao B ◽  
Positive Effects ◽  
The Brain

Aim and Objective: The Dendrobium officinalis flower (DOF) is popular in China due to common belief in its anti-aging properties and positive effects on “nourish yin”. However, there have been relatively few confirmatory pharmacological experiments conducted to date. The aim of this work was to evaluate whether DOF has beneficial effects on learning and memory in senescent rats, and, if so, to determine its potential mechanism of effect. Materials and Methods: SD rats were administrated orally DOF at a dose of 1.38, or 0.46 g/kg once a day for 8 weeks. Two other groups included a healthy untreated control group and a senescent control group. During the 7th week, a Morris water maze test was performed to assess learning and memory. At the end of the experiment, serum and brain samples were collected to measure concentrations of antioxidant enzymes, including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GSH-Px) in serum, and the neurotransmitters, including γ-aminobutyric acid (γ-GABA), Glutamic (Glu), and monoamine oxidase B (MAO-B) in the brain. Histopathology of the hippocampus was assessed using hematoxylin-eosin (H&E) staining. Results: The results suggested that treatment with DOF improved learning as measured by escape latency, total distance, and target quadrant time, and also increased levels of γ-GABA in the brain. In addition, DOF decreased the levels of MDA, Glu, and MAO-B, and improved SOD and GSHPx. Histopathological analysis showed that DOF also significantly reduced structural lesions and neurodegeneration in the hippocampus relative to untreated senescent rats. Conclusion: DOF alleviated brain aging and improved the spatial learning abilities in senescent rats, potentially by attenuating oxidative stress and thus reducing hippocampal damage and balancing the release of neurotransmitters.

scholarly journals Genistein reduced the neural apoptosis in the brain of ovariectomised rats by modulating mitochondrial oxidative stress

2010 ◽  
Vol 104 (9) ◽  
pp. 1297-1303 ◽  
Author(s):  
Yan-Hong Huang ◽  
Qing-Hong Zhang
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Caspase 3 ◽  
Visual Learning ◽  
Morris Water Maze Test ◽  
High Dose ◽  
Dependent Manner ◽  
Ovx Rats ◽  
Neural Apoptosis ◽  
The Brain

The present study was undertaken to investigate the antioxidant effect of chronic ingestion of genistein (Gen) against neural death in the brain of ovariectomised (Ovx) rats. The rats were randomly divided into five groups, i.e. sham-operated (sham), Ovx-only, Ovx with 17β-oestradiol, Ovx with low (15 mg/kg) and high (30 mg/kg) doses of Gen (Gen-L and Gen-H), and were orally administered daily with drugs or vehicle for 6 weeks. The learning and memory abilities were measured by Morris water maze test. Oxidative damages in the brain were evaluated by the level of superoxide dismutase (SOD), malondialdehyde (MDA) and monoamine oxidase (MAO) activities. Neural apoptosis was shown by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining and caspase-3 activity. In the visual learning and memory test, there were no significant differences among the population means of the five groups. While in the probe trial test, the Gen-L group instead of the Gen-H group exhibited reduced escape latency and increased memory frequency than the Ovx group. Although both doses of Gen could reduce acetylcholinesterase activity, only a low dose of Gen could diminish MDA activity significantly in frontal cortex and enhance SOD content in the hippocampus. In contrast, MAO content was decreased in the cortex by either dose of Gen, while in the hippocampus, only a high dose of Gen appeared to be effective. Interestingly, Gen at both the doses could attenuate the increased number of TUNEL-positive neurons and caspase-3 activity in Ovx rats. These results suggest that Gen confers protection against Ovx-induced neurodegeneration by attenuating oxidative stress, lipid peroxidation and the mitochondria-mediated apoptotic pathway in a region- and dose-dependent manner.

Conditioned medium from overly excitatory primary astrocytes induced by La3+ increases apoptosis in primary neurons via upregulating the expression of NMDA receptors

Metallomics ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 1016-1028 ◽  
Author(s):  
Yaling Sun ◽  
Jinghua Yang ◽  
Xiaoyu Hu ◽  
Xiang Gao ◽  
Yingqi Li ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Conditioned Medium ◽  
Learning And Memory ◽  
Primary Neurons ◽  
Primary Astrocytes ◽  
The Brain

Lanthanum (La) can accumulate in the brain and impair learning and memory.

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 The brain-tumor related protein podoplanin regulates synaptic plasticity and hippocampus-dependent learning and memory

2016 ◽  
Vol 48 (8) ◽  
pp. 652-668 ◽  
Author(s):  
Ana Cicvaric ◽  
Jiaye Yang ◽  
Sigurd Krieger ◽  
Deeba Khan ◽  
Eun-Jung Kim ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Related Protein ◽  
Dependent Learning ◽  
The Brain

Dream science 2000: A response to commentaries on Dreaming and the brain

2000 ◽  
Vol 23 (6) ◽  
pp. 1019-1035 ◽  
Author(s):  
J. Allan Hobson ◽  
Edward F. Pace-Schott ◽  
Robert Stickgold
Keyword(s):  
Learning And Memory ◽  
Emerging Technologies ◽  
Mental Activity ◽  
Control Mechanisms ◽  
Dream Research ◽  
The Brain ◽  
Formal Features

Definitions of dreaming are not required to map formal features of mental activity onto brain measures. While dreaming occurs during all stages of sleep, intense dreaming is largely confined to REM. Forebrain structures and many neurotransmitters can contribute to sleep and dreaming without negating brainstem and aminergic-cholinergic control mechanisms. Reductionism is essential to science and AIM has considerable heuristic value. Recent findings support sleep's role in learning and memory. Emerging technologies may address long-standing issues in sleep and dream research.

Ex Vivo Brain Preparation to Analyze Vocal Pathways of Xenopus Frogs

2021 ◽  
Vol 2021 (9) ◽  
pp. pdb.prot106872
Author(s):  
Ayako Yamaguchi
Keyword(s):  
Neural Activity ◽  
Ex Vivo ◽  
Neural Circuitry ◽  
Neural Basis ◽  
Vocal Production ◽  
Basic Principles ◽  
Electrophysiological Recordings ◽  
The Brain

Understanding the neural basis of behavior is a challenging task for technical reasons. Most methods of recording neural activity require animals to be immobilized, but neural activity associated with most behavior cannot be recorded from an anesthetized, immobilized animal. Using amphibians, however, there has been some success in developing in vitro brain preparations that can be used for electrophysiological and anatomical studies. Here, we describe an ex vivo frog brain preparation from which fictive vocalizations (the neural activity that would have produced vocalizations had the brain been attached to the muscle) can be elicited repeatedly. When serotonin is applied to the isolated brains of male and female African clawed frogs, Xenopus laevis, laryngeal nerve activity that is a facsimile of those that underlie sex-specific vocalizations in vivo can be readily recorded. Recently, this preparation was successfully used in other species within the genus including Xenopus tropicalis and Xenopus victorianus. This preparation allows a variety of techniques to be applied including extracellular and intracellular electrophysiological recordings and calcium imaging during vocal production, surgical and pharmacological manipulation of neurons to evaluate their impact on motor output, and tract tracing of the neural circuitry. Thus, the preparation is a powerful tool with which to understand the basic principles that govern the production of coherent and robust motor programs in vertebrates.

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