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Related Concept Videos

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...
The Synapse02:47

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Neurons communicate with one another by passing on their electrical signals to other neurons. A synapse is the location where two neurons meet to exchange signals. At the synapse, the neuron that sends the signal is called the presynaptic cell, while the neuron that receives the message is called the postsynaptic cell. Note that most neurons can be both presynaptic and postsynaptic, as they both transmit and receive information.
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...
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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.
Synaptic Signaling01:09

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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...

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Cytoplasmic ATM in neurons modulates synaptic function.

Jiali Li1, Yu R Han, Mark R Plummer

  • 1Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, USA.

Current Biology : CB
|December 8, 2009
PubMed
Summary
This summary is machine-generated.

Ataxia-telangiectasia (A-T) neurological symptoms may stem from non-DNA repair roles of ATM protein in neurons. This study reveals ATM

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Ataxia-telangiectasia (A-T) is a genetic disorder linked to ATM deficiency, primarily known for DNA damage repair defects.
  • A-T patients exhibit neurological symptoms like ataxia and speech defects, which are not fully explained by DNA repair deficiencies alone.
  • Mouse models with Atm mutations show impaired DNA repair but only mild neurological issues, suggesting non-DNA repair functions of ATM are crucial for neuronal health.

Purpose of the Study:

  • To investigate the non-DNA repair functions of ATM protein in neurons.
  • To explore the role of cytoplasmic ATM in neuronal function and its potential link to A-T neurological phenotypes.

Main Methods:

  • Examined the subcellular localization of ATM protein in neurons.
  • Assessed hippocampal long-term potentiation and spontaneous vesicular dye release in Atm mutant mice.
  • Investigated the interaction of cytoplasmic ATM with synaptic vesicle proteins (VAMP2, synapsin-I) and ATR.

Main Results:

  • ATM protein exhibits significant cytoplasmic distribution in neurons.
  • Atm mutant mice showed reduced hippocampal long-term potentiation and impaired spontaneous vesicular dye release.
  • Cytoplasmic ATM forms complexes with phosphorylated VAMP2 and synapsin-I, and associates with ATR.

Conclusions:

  • The neurological symptoms of A-T may arise from impaired non-DNA repair functions of ATM in the neuronal cytoplasm.
  • Cytoplasmic ATM plays a critical role in synaptic function, independent of its DNA repair role.
  • These findings suggest novel therapeutic targets for the neurological aspects of ataxia-telangiectasia.