Long-term Depression
Long-term Depression - Related Videos
01:05
Long-term Depression
0 Views •
2019
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...
01:03
Long-term Depression
0 Views •
2023
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...
02:47
Optogenetic Induction of Long-Term Depression for Suppressing Narcotic-Seeking Behavior in Rats
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2025
Source: Rich, M. T., et al. Using Optogenetics to Reverse Neuroplasticity and Inhibit Cocaine Seeking in Rats. J. Vis. Exp. (2021)This video demonstrates the use of optogenetics to induce long-term depression (LTD) at medial geniculate nucleus to lateral amygdala (MGN-LA) synapses, weakening cue-induced narcotic-seeking behavior in a rat model. The rat, surgically implanted with optical fibers and virally transduced to express light-sensitive ion channels, undergoes optogenetic stimulation with...
02:24
Induction of Long-Term Depression in Cerebellar Purkinje Neurons in a Mouse Brain Slice
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2025
In this video, a mouse cerebellar brain slice was used to investigate synaptic interactions between parallel fibers, climbing fibers, and Purkinje cells, which are essential for motor control. Stimulation of climbing fibers induced long-term depression (LTD) in Purkinje cells, weakening synaptic strength and resulting in reduced response to parallel fiber stimulation.
09:30
Assessment of Long-term Depression Induction in Adult Cerebellar Slices
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2019
In some gene-manipulated animals, using a single protocol may fail to induce LTD in cerebellar Purkinje cells, and there may be a discrepancy between LTD and motor learning. Multiple protocols are necessary to assess LTD-induction in gene-manipulated animals. Standard protocols are shown.
FAQs
Prolonged low-frequency stimulation produces a modest influx of calcium through NMDA receptors rather than the stronger calcium signal associated with strengthening. This calcium entry activates intracellular signaling pathways that promote removal of AMPA receptors from the postsynaptic membrane. Fewer AMPA receptors reduce the postsynaptic response to excitatory transmission, providing a cellular mechanism for weakening synaptic communication.
AMPA receptors help postsynaptic neurons respond to excitatory signals. When signaling pathways remove these receptors from the postsynaptic membrane, the receiving cell becomes less responsive to incoming transmission at that synapse. This change links molecular trafficking to altered circuit behavior, allowing neural connections to reduce their influence instead of maintaining a fixed level of excitatory communication.
Long-term Depression and long-term potentiation provide opposing adjustments in synaptic strength. Whereas potentiation supports stronger transmission, depression reduces transmission efficiency through AMPA receptor removal. Their balance allows neural circuits to refine responses rather than shift only toward greater excitation. This complementary plasticity is important for maintaining adaptable signaling as circuits change with activity and experience.
A common experimental approach uses prolonged low-frequency stimulation to evoke the calcium-dependent signaling changes associated with synaptic weakening. Investigators can then examine how excitatory transmission changes after stimulation, often focusing on the postsynaptic response and receptor distribution. This paradigm connects a controlled activity pattern with the cellular mechanisms that alter synaptic strength over time.
Studies of Long-term Depression commonly examine the hippocampus and cerebellum. These regions provide important biological contexts for investigating how synapses adjust their effectiveness in response to activity. Comparing them helps researchers consider how related plasticity mechanisms contribute to circuit refinement, learning, memory, and the specialized processing performed by different neural networks.
By reducing the influence of selected synapses, this process can help refine developing neural circuits and adjust how information flows through established networks. In the hippocampus and cerebellum, such activity-dependent changes are relevant to learning and memory. Its interaction with synaptic strengthening also allows circuits to encode experience through coordinated increases and decreases in transmission.
The mechanisms underlying Long-term Depression offer a way to investigate how disrupted synaptic plasticity might affect neural circuit function. Altered calcium-dependent signaling or AMPA receptor regulation could change how synapses adapt to activity. Studying these processes therefore helps connect cellular changes in synaptic strength with broader questions about neurological and neurodevelopmental dysfunction.