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Related Concept Videos

Integration of Synaptic Events01:28

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
Synaptic Signaling01:09

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is critical for...

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Related Experiment Video

Updated: Jun 10, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

SIRT1 is essential for normal cognitive function and synaptic plasticity.

Shaday Michán1, Ying Li, Maggie Meng-Hsiu Chou

  • 1Paul F. Glenn Laboratories, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|July 28, 2010
PubMed
Summary
This summary is machine-generated.

The nicotinamide-adenine dinucleotide-dependent deacetylase SIRT1 is essential for normal learning and memory in mice. Its absence impairs cognitive functions and synaptic plasticity in the hippocampus.

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Published on: March 23, 2011

Related Experiment Videos

Last Updated: Jun 10, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Area of Science:

  • Neuroscience
  • Molecular Biology

Background:

  • Normal cognitive function depends on cellular and molecular processes in the nervous system.
  • SIRT1, a deacetylase, influences brain integrity through chromatin remodeling, DNA repair, cell survival, and neurogenesis.

Purpose of the Study:

  • To investigate the role of SIRT1 in learning, memory, and synaptic plasticity in the mouse hippocampus.
  • To analyze the effects of SIRT1 deficiency and overexpression on cognitive functions and neuronal structure.

Main Methods:

  • Behavioral tests (immediate memory, classical conditioning, spatial learning) and electrophysiological paradigms were used.
  • Analysis of SIRT1 knock-out (KO) and high-expression mice.
  • Assessment of synaptic plasticity, basal synaptic transmission, NMDA receptor function, and dendritic morphology.

Main Results:

  • SIRT1 deficiency impaired learning and memory, associated with defects in synaptic plasticity.
  • Cognitive deficits in KO mice were linked to decreased dendritic branching, reduced ERK1/2 phosphorylation, and altered hippocampal gene expression.
  • Normal synaptic plasticity and memory were observed in mice with high SIRT1 expression.

Conclusions:

  • SIRT1 is crucial for maintaining normal learning, memory, and synaptic plasticity.
  • SIRT1 deficiency leads to specific molecular and structural changes in hippocampal neurons, impacting cognitive function.