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

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...
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...
Disorders of the Nervous Tissue01:28

Disorders of the Nervous Tissue

Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises from the...
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...

You might also read

Related Articles

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

Sort by
Same author

DPP6 Loss Causes Age-Dependent Sleep Dysregulation and Depression-like Phenotypes Linked to Neurodegeneration.

International journal of molecular sciences·2026
Same author

Activity-dependent degradation of Kv4.2 contributes to synaptic plasticity and behavior in Angelman syndrome model mice.

Cell reports·2025
Same author

Future scientific innovation requires the transformative power of philanthropy.

Proceedings of the National Academy of Sciences of the United States of America·2024
Same author

Identification of Kv4.2 protein complex and modifications by tandem affinity purification-mass spectrometry in primary neurons.

Frontiers in cellular neuroscience·2022
Same author

Transcriptomic analysis of isolated and pooled human postmortem cerebellar Purkinje cells in autism spectrum disorders.

Frontiers in genetics·2022
Same author

Transport between im/mobile fractions shapes the speed and profile of cargo distribution in neurons.

Biophysical reports·2022

Related Experiment Video

Updated: May 22, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons
11:48

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Published on: July 13, 2011

Aberrant dendritic excitability: a common pathophysiology in CNS disorders affecting memory?

Michael W Nestor1, Dax A Hoffman

  • 1Molecular Neurophysiology and Biophysics Unit, NICHD, NIH, Porter Neuroscience Research Center, Bethesda, MD 20892-4995, USA. mnestor@nyscf.org

Molecular Neurobiology
|April 25, 2012
PubMed
Summary

Many central nervous system (CNS) disorders share common memory dysfunctions. This review proposes abnormal dendritic integration of synaptic signals as a potential unifying cause for CNS disorders and their impact on memory.

More Related Videos

Automated Sholl Analysis of Digitized Neuronal Morphology at Multiple Scales
11:41

Automated Sholl Analysis of Digitized Neuronal Morphology at Multiple Scales

Published on: November 14, 2010

Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software
07:45

Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software

Published on: September 27, 2024

Related Experiment Videos

Last Updated: May 22, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons
11:48

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Published on: July 13, 2011

Automated Sholl Analysis of Digitized Neuronal Morphology at Multiple Scales
11:41

Automated Sholl Analysis of Digitized Neuronal Morphology at Multiple Scales

Published on: November 14, 2010

Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software
07:45

Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software

Published on: September 27, 2024

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Central nervous system (CNS) disorders often present with complex etiologies involving genetics, epigenetics, and environmental factors.
  • Despite diverse causes, many CNS disorders exhibit converging deficits in memory function.
  • Advances in genomics reveal significant genetic heterogeneity contributing to neuronal pathologies in CNS disorders.

Purpose of the Study:

  • To propose a unifying mechanism for the development of various CNS disorders.
  • To explore the role of abnormal dendritic integration of synaptic signals in CNS pathophysiology.
  • To link molecular genetics and cellular neurophysiology to network-level dysfunctions and memory impairments.

Main Methods:

  • This is a review article, synthesizing existing research.
  • It focuses on the integration of molecular genetics, dendritic computation, and network abnormalities.
  • The review examines how synaptic signal integration impacts neuronal function and behavior.

Main Results:

  • The review posits that abnormal dendritic integration is a common pathway in CNS disorders.
  • This cellular-level dysfunction may underlie higher-order circuit and network abnormalities.
  • Understanding this link can illuminate the basis of memory deficits in CNS disorders.

Conclusions:

  • Abnormal dendritic integration of synaptic signals is proposed as a fundamental mechanism in many CNS disorders.
  • Future research should focus on the interplay between molecular genetics and dendritic computation.
  • This approach may reveal critical links between cellular neurophysiology and CNS disorder manifestations, particularly memory dysfunction.