Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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.
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Incise parallel, section perpendicular to the dermatoglyphs for diagnosis of acral melanocytic lesions-A comment on Thakker et al.

Journal of the American Academy of Dermatology·2026
Same author

A 25-year evolution of systemic mastocytosis to mast cell leukemia: Cutaneous clues.

JAAD case reports·2026
Same author

Maternal separation increases anxiety-like phenotypes, fear responses, and alters <i>Bdnf</i> methylation in a predator odor exposure model of early life adversity.

Neurobiology of stress·2026
Same author

Photo Quiz: Persistent eyelash debris in a 10-year-old female.

Journal of clinical microbiology·2026
Same author

Hypertrophic Lichen Sclerosus: A Form of "Atypical" Lichen Sclerosus in the Pathway to HPV-Independent Squamous Cell Carcinoma of the Vulva.

The American journal of surgical pathology·2026
Same author

Case Study of Fulminant Pyoderma Gangrenosum: Conservative Therapy-Cornerstone of Management.

International medical case reports journal·2026

Related Experiment Video

Updated: Jul 18, 2026

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

Signal transduction mechanisms in memory disorders.

Sara C Shalin1, Regula Egli, Shari G Birnbaum

  • 1Department of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Progress in Brain Research
|December 16, 2006
PubMed
Summary

This chapter examines molecular mechanisms of memory formation and how their disruption leads to intellectual disabilities. It discusses Angelman syndrome, Neurofibromatosis 1, Coffin-Lowry, Rubinstein-Taybi, and Rett syndromes.

More Related Videos

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
11:29

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain
09:25

Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain

Published on: May 21, 2019

Related Experiment Videos

Last Updated: Jul 18, 2026

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
11:29

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain
09:25

Quantifying Subcellular Ubiquitin-proteasome Activity in the Rodent Brain

Published on: May 21, 2019

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Memory formation relies on complex molecular signaling pathways, particularly within the hippocampus.
  • Disruptions in these molecular events can lead to cognitive impairments and intellectual disabilities.
  • Several human genetic syndromes are associated with malfunctioning molecular pathways crucial for memory.

Purpose of the Study:

  • To explore the molecular mechanisms underlying memory formation.
  • To investigate how the malfunction of these molecular events contributes to memory disturbances.
  • To examine specific human intellectual disability syndromes linked to these disrupted processes.

Main Methods:

  • Review of molecular signaling pathways in the hippocampus.
  • Analysis of genetic and molecular underpinnings of intellectual disability syndromes.
  • Integration of findings from neuroscience and genetics research.

Main Results:

  • Identified key molecular events critical for hippocampal memory formation.
  • Established links between specific molecular pathway disruptions and cognitive deficits.
  • Detailed the characteristics of Angelman syndrome, NF1-associated disorders, CLS, RTS, and RTT in relation to molecular malfunctions.

Conclusions:

  • Molecular signaling in the hippocampus is fundamental for memory.
  • Malfunctions in these pathways are directly implicated in various intellectual disability syndromes.
  • Understanding these molecular links is crucial for potential therapeutic strategies.