Long-term consumption of virgin coconut (Cocos nucifera) oil diet impairs learning and memory in CD1 mice

: Neurological diseases bring great mental and physical torture to the patients, and have long-term and sustained negative effects on families and society. The attention to neurological diseases is increasing, and the improvement of the material level is accompanied by an increase in the demand for mental level. The p75 neurotrophin receptor (p75NTR) is a low-affinity neurotrophin receptor and involved in diverse and pleiotropic effects in the developmental and adult central nervous system (CNS). Since neurological diseases are usually accompanied by the regression of memory, the pathogenesis of p75NTR also activates and inhibits other signaling pathways, which has a serious impact on the learning and memory of patients. The results of studies shown that p75NTR is associated with LTP/LTD-induced synaptic enhancement and inhibition, suggest that p75NTR may be involved in the progression of synaptic plasticity. And its pro-apoptotic effect is associated with activation of proBDNF and inhibition of proNGF, and TrkA/p75NTR imbalance leads to pro-survival or pro-apoptotic phenomena. It can be inferred that p75NTR mediates apoptosis in the hippocampus and amygdale, which may affect learning and memory behavior. This article mainly discusses the relationship between p75NTR and learning memory and associated mechanisms, which may provide some new ideas for the treatment of neurological diseases.

Download Full-text

Arousing the LTP and learning debate

Behavioral and Brain Sciences ◽

10.1017/s0140525x97321591 ◽

1997 ◽

Vol 20 (4) ◽

pp. 622-623 ◽

Cited By ~ 1

Author(s):

Stephen Maren

Keyword(s):

Learning And Memory ◽

Long Term Potentiation ◽

Term Potentiation ◽

Arousal Mechanism

Shors & Matzel provide compelling arguments against a role for hippocampal long-term potentiation (LTP) in mammalian learning and memory. As an alternative, they suggest that LTP is an arousal mechanism. I will argue that this view is not a satisfactory alternative to current conceptions of LTP function.

Download Full-text

Long-term potentiation in the amygdala: a mechanism for emotional learning and memory

Trends in Neurosciences ◽

10.1016/s0166-2236(99)01465-4 ◽

1999 ◽

Vol 22 (12) ◽

pp. 561-567 ◽

Cited By ~ 237

Author(s):

Stephen Maren

Keyword(s):

Learning And Memory ◽

Long Term Potentiation ◽

Emotional Learning ◽

Term Potentiation

Download Full-text

Long-term effects of selective neonatal temporal lobe lesions on learning and memory in monkeys.

Behavioral Neuroscience ◽

10.1037/0735-7044.109.2.212 ◽

1995 ◽

Vol 109 (2) ◽

pp. 212-226 ◽

Cited By ~ 26

Author(s):

Ludiše Málková ◽

Mortimer Mishkin ◽

Jocelyne Bachevalier

Keyword(s):

Learning And Memory ◽

Temporal Lobe ◽

Long Term Effects ◽

Temporal Lobe Lesions

Download Full-text

Dopamine D-1/D-5 Receptor Activation Is Required for Long-Term Potentiation in the Rat Neostriatum In Vitro

Journal of Neurophysiology ◽

10.1152/jn.2001.85.1.117 ◽

2001 ◽

Vol 85 (1) ◽

pp. 117-124 ◽

Cited By ~ 221

Author(s):

J.N.D. Kerr ◽

J. R. Wickens

Keyword(s):

Receptor Antagonist ◽

Learning And Memory ◽

Sch 23390 ◽

Long Term Potentiation ◽

Receptor Activation ◽

Striatal Neurons ◽

Theoretical Understanding ◽

Endogenous Dopamine ◽

Term Potentiation

Dopamine and glutamate are key neurotransmitters involved in learning and memory mechanisms of the brain. These two neurotransmitter systems converge on nerve cells in the neostriatum. Dopamine modulation of activity-dependent plasticity at glutamatergic corticostriatal synapses has been proposed as a cellular mechanism for learning in the neostriatum. The present research investigated the role of specific subtypes of dopamine receptors in long-term potentiation (LTP) in the corticostriatal pathway, using intracellular recording from striatal neurons in a corticostriatal slice preparation. In agreement with previous reports, LTP could be induced reliably under Mg2+-free conditions. This Mg2+-free LTP was blocked by dopamine depletion and by the dopamine D-1/D-5 receptor antagonist SCH 23390 but was not blocked by the dopamine D-2 receptor antagonist remoxipride or the GABAA antagonist picrotoxin. In dopamine-depleted slices, the ability to induce LTP could be restored by bath application of the dopamine D-1/D-5 receptor agonist, SKF 38393. These results show that activation of dopamine D-1/D-5 receptors by either endogenous dopamine or exogenous dopamine agonists is a requirement for the induction of LTP in the corticostriatal pathway. These findings have significance for current understanding of learning and memory mechanisms of the neostriatum and for theoretical understanding of the mechanism of action of drugs used in the treatment of psychotic illnesses and Parkinson's disease.

Download Full-text

Dopaminergic Neuromodulation of Spike Timing Dependent Plasticity in Mature Adult Rodent and Human Cortical Neurons

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2021.668980 ◽

2021 ◽

Vol 15 ◽

Author(s):

Emma Louise Louth ◽

Rasmus Langelund Jørgensen ◽

Anders Rosendal Korshoej ◽

Jens Christian Hedemann Sørensen ◽

Marco Capogna

Keyword(s):

Learning And Memory ◽

Cortical Neurons ◽

Synaptic Depression ◽

Spike Timing ◽

Therapeutic Interventions ◽

Spike Timing Dependent Plasticity ◽

Mature Adult ◽

Dependent Plasticity ◽

Cortical Synapses

Synapses in the cerebral cortex constantly change and this dynamic property regulated by the action of neuromodulators such as dopamine (DA), is essential for reward learning and memory. DA modulates spike-timing-dependent plasticity (STDP), a cellular model of learning and memory, in juvenile rodent cortical neurons. However, it is unknown whether this neuromodulation also occurs at excitatory synapses of cortical neurons in mature adult mice or in humans. Cortical layer V pyramidal neurons were recorded with whole cell patch clamp electrophysiology and an extracellular stimulating electrode was used to induce STDP. DA was either bath-applied or optogenetically released in slices from mice. Classical STDP induction protocols triggered non-hebbian excitatory synaptic depression in the mouse or no plasticity at human cortical synapses. DA reverted long term synaptic depression to baseline in mouse via dopamine 2 type receptors or elicited long term synaptic potentiation in human cortical synapses. Furthermore, when DA was applied during an STDP protocol it depressed presynaptic inhibition in the mouse but not in the human cortex. Thus, DA modulates excitatory synaptic plasticity differently in human vs. mouse cortex. The data strengthens the importance of DA in gating cognition in humans, and may inform on therapeutic interventions to recover brain function from diseases.

Download Full-text

A Long-Term Enriched Environment Ameliorates the Accelerated Age-Related Memory Impairment Induced by Gestational Administration of Lipopolysaccharide: Role of Plastic Mitochondrial Quality Control

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2020.559182 ◽

2021 ◽

Vol 14 ◽

Author(s):

Zhan-Qiang Zhuang ◽

Zhe-Zhe Zhang ◽

Yue-Ming Zhang ◽

He-Hua Ge ◽

Shi-Yu Sun ◽

...

Keyword(s):

Learning And Memory ◽

Spatial Learning ◽

Memory Impairment ◽

Spatial Learning And Memory ◽

Mitochondrial Quality Control ◽

Protein Levels ◽

Age Related ◽

Old Mice ◽

Lps Treatment

Studies have shown that gestational inflammation accelerates age-related memory impairment in mother mice. An enriched environment (EE) can improve age-related memory impairment, whereas mitochondrial dysfunction has been implicated in the pathogenesis of brain aging. However, it is unclear whether an EE can counteract the accelerated age-related memory impairment induced by gestational inflammation and whether this process is associated with the disruption of mitochondrial quality control (MQC) processes. In this study, CD-1 mice received daily intraperitoneal injections of lipopolysaccharide (LPS, 50 μg/kg) or normal saline (CON group) during gestational days 15–17 and were separated from their offspring at the end of normal lactation. The mothers that received LPS were divided into LPS group and LPS plus EE (LPS-E) treatment groups based on whether the mice were exposed to an EE until the end of the experiment. At 6 and 18 months of age, the Morris water maze test was used to evaluate spatial learning and memory abilities. Quantitative reverse transcription polymerase chain reaction and Western blot were used to measure the messenber RNA (mRNA) and protein levels of MQC-related genes in the hippocampus, respectively. The results showed that all the aged (18 months old) mice underwent a striking decline in spatial learning and memory performances and decreased mRNA/protein levels related to mitochondrial dynamics (Mfn1/Mfn2, OPA1, and Drp1), biogenesis (PGC-1α), and mitophagy (PINK1/parkin) in the hippocampi compared with the young (6 months old) mice. LPS treatment exacerbated the decline in age-related spatial learning and memory and enhanced the reduction in the mRNA and protein levels of MQC-related genes but increased the levels of PGC-1α in young mice. Exposure to an EE could alleviate the accelerated decline in age-related spatial learning and memory abilities and the accelerated changes in MQC-related mRNA or protein levels resulting from LPS treatment, especially in aged mice. In conclusion, long-term exposure to an EE can counteract the accelerated age-related spatial cognition impairment modulated by MQC in CD-1 mother mice that experience inflammation during pregnancy.

Download Full-text