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

Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

2.0K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
2.0K
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

479
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.
479
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

1.5K
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
1.5K
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

12.4K
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...
12.4K
CNS Stimulants: Psychedelic Agents01:22

CNS Stimulants: Psychedelic Agents

607
Hallucinogens, also known as psychedelic drugs, are a class of substances known for their ability to alter perception, cognition, and emotions. Despite their profound effects on the mind, these drugs are non-addictive, setting them apart from many other abused substances. The mechanism of action of these drugs lies in their impact on the 5-HT2A receptor in the brain. Upon activation, this receptor couples to Gq-type G proteins, triggering a cascade that releases intracellular calcium. This...
607
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

2.3K
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...
2.3K

You might also read

Related Articles

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

Sort by
Same author

Genesis of a functional astrocyte syncytium in the developing mouse hippocampus.

Glia·2023
Same author

Microglia maintain the normal structure and function of the hippocampal astrocyte network.

Glia·2022
Same author

Clinicopathologic features of scrotal leiomyosarcoma: single institutional experience of ten cases.

Human pathology·2022
Same author

Ultrastructural view of astrocyte arborization, astrocyte-astrocyte and astrocyte-synapse contacts, intracellular vesicle-like structures, and mitochondrial network.

Progress in neurobiology·2022
Same author

On the electrical passivity of astrocyte potassium conductance.

Journal of neurophysiology·2021
Same author

Epileptiform Neuronal Discharges Impair Astrocyte Syncytial Isopotentiality in Acute Hippocampal Slices.

Brain sciences·2020

Related Experiment Video

Updated: Jan 3, 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

11.7K

TREK-1 Null Impairs Neuronal Excitability, Synaptic Plasticity, and Cognitive Function.

Wei Wang1,2, Conrad M Kiyoshi1, Yixing Du1

  • 1Department of Neuroscience, Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA.

Molecular Neurobiology
|November 16, 2019
PubMed
Summary

TREK-1 deficiency in mice enhances neuronal structure and excitability, impairing recognition memory. This suggests TREK-1 channels regulate cognitive function by controlling neuronal morphology and synaptic plasticity.

Keywords:
Cognitive impairmentHippocampusSynaptic plasticitySynaptic transmissionTREK-1 (tandem of pore domain in a weak inwardly rectifying K+ channel (Twik)-related K+ channels)

More Related Videos

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

95.0K
Barnes Maze Testing Strategies with Small and Large Rodent Models
12:59

Barnes Maze Testing Strategies with Small and Large Rodent Models

Published on: February 26, 2014

43.3K

Related Experiment Videos

Last Updated: Jan 3, 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

11.7K
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

95.0K
Barnes Maze Testing Strategies with Small and Large Rodent Models
12:59

Barnes Maze Testing Strategies with Small and Large Rodent Models

Published on: February 26, 2014

43.3K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Channelopathy

Background:

  • TREK-1 (a two-pore-domain K+ channel) is highly expressed in the central nervous system.
  • Aberrant TREK-1 expression is linked to cognitive impairment, but its mechanisms are unclear.

Purpose of the Study:

  • To investigate the role of TREK-1 in neuronal morphology, excitability, synaptic plasticity, and cognitive function using TREK-1 knockout mice.

Main Methods:

  • TREK-1 immunostaining in mouse hippocampus.
  • Analysis of dendritic morphology and spine density in TREK-1 knockout (KO) mice.
  • Electrophysiological recordings to assess neuronal excitability and synaptic currents (EPSCs, IPSCs).
  • Evaluation of long-term potentiation (LTP) and paired-pulse ratio.
  • Assessment of cognitive function, specifically recognition memory.

Main Results:

  • TREK-1 KO increased dendritic sprouting and immature spines in hippocampal CA1 pyramidal neurons.
  • TREK-1 KO enhanced neuronal excitability and both excitatory and inhibitory postsynaptic currents.
  • Increased presynaptic glutamate release probability and postsynaptic AMPA receptor expression contributed to enhanced EPSCs.
  • TREK-1 KO decreased paired-pulse ratio and occluded LTP, indicating altered synaptic plasticity.
  • TREK-1 KO mice exhibited deficits in recognition memory.
  • TREK-1 KO did not affect astrocyte function.

Conclusions:

  • TREK-1 deficiency profoundly impacts hippocampal pyramidal neuron structure and function.
  • Impaired cognitive function in diseases with aberrant TREK-1 expression may stem from this channel's failure to regulate neuronal morphology, excitability, synaptic transmission, and plasticity.