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Related Concept Videos

Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Catenins01:23

Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...

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Aversive Associative Learning and Memory Formation by Pairing Two Chemicals in Caenorhabditis elegans
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Aversive Associative Learning and Memory Formation by Pairing Two Chemicals in Caenorhabditis elegans

Published on: June 23, 2022

Bidirectional synaptic plasticity and spatial memory flexibility require Ca2+-stimulated adenylyl cyclases.

Ming Zhang1, Daniel R Storm, Hongbing Wang

  • 1Department of Physiology, Neuroscience Program, Michigan State University, East Lansing, Michigan 48824, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|July 15, 2011
PubMed
Summary
This summary is machine-generated.

Calcium-stimulated adenylyl cyclase (AC) activity is crucial for suppressing old memories and forming new ones. This study shows impaired memory suppression and formation in mice lacking specific ACs, highlighting their role in synaptic plasticity.

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Molecular Biology

Background:

  • Synaptic plasticity underlies learning and memory.
  • Effective memory suppression is vital for adaptation to environmental changes.
  • Adenylyl cyclases (ACs) mediate cAMP signaling, crucial for cellular processes.

Purpose of the Study:

  • Investigate the role of Ca(2+)-stimulated AC activity in synaptic plasticity and spatial memory.
  • Examine the function of AC1 and AC8 in memory suppression and formation.

Main Methods:

  • Utilized double knock-out (DKO) mice lacking AC1 and AC8.
  • Assessed long-term potentiation (LTP) using high-frequency stimulation (HFS).
  • Evaluated spatial memory and reversal learning in the Morris water maze and reversal platform tests.

Main Results:

  • DKO mice exhibited defective LTP under specific HFS paradigms.
  • Impaired reversal of synaptic potentiation and de novo synaptic depression observed in DKO mice.
  • DKO mice showed deficits in spatial memory acquisition, retention, and suppression of old memories.

Conclusions:

  • Ca(2+)-stimulated AC activity is essential for both establishing new memories and suppressing obsolete ones.
  • AC1 and AC8 play critical roles in regulating bidirectional synaptic plasticity.
  • Disruption of AC signaling impairs adaptive behavioral responses requiring memory flexibility.