Long-term depression

Definition

Long-term depression (LTD) is a lasting decrease in the strength of synaptic transmission that occurs after certain patterns of activity between neurons. It plays a crucial role in synaptic plasticity, which allows for the adjustment of synaptic strength in response to experience. LTD is essential for processes such as learning and memory, as it helps to refine neural circuits by weakening less important connections.

5 Must Know Facts For Your Next Test

1. Long-term depression can be induced by low-frequency stimulation of neurons, leading to a gradual decrease in the efficacy of synaptic transmission.
2. The molecular mechanisms behind LTD often involve the activation of NMDA receptors and subsequent changes in intracellular calcium levels.
3. LTD is believed to be crucial for the removal of redundant synapses and the fine-tuning of neural circuits during development and learning.
4. Dysfunction in LTD has been linked to various neurological disorders, including Alzheimer's disease and schizophrenia, highlighting its importance in healthy cognitive function.
5. Research suggests that LTD may also contribute to homeostatic plasticity, where neurons adjust their overall activity to maintain stable network function.

Review Questions

• How does long-term depression differ from long-term potentiation in terms of synaptic strength and neuronal activity?
  • Long-term depression (LTD) and long-term potentiation (LTP) are opposites in terms of their effects on synaptic strength. LTD results in a lasting decrease in synaptic efficacy following low-frequency stimulation, while LTP involves a lasting increase after high-frequency stimulation. These two processes work together to shape neural circuits by weakening less important connections through LTD and strengthening relevant connections via LTP, contributing to learning and memory.
• What are the key molecular mechanisms involved in the induction of long-term depression, and how do they contribute to its effects on synaptic transmission?
  • The induction of long-term depression involves key molecular mechanisms such as the activation of NMDA receptors, leading to an influx of calcium ions (Ca²+) into the postsynaptic neuron. This calcium signaling triggers downstream pathways that ultimately result in the internalization of AMPA receptors from the synapse, decreasing synaptic strength. By modifying receptor availability at the synapse, LTD fine-tunes synaptic transmission and plays an essential role in processes like memory formation.
• Evaluate the implications of impaired long-term depression on cognitive function and its potential link to neurological disorders.
  • Impaired long-term depression can have significant consequences for cognitive function, as it disrupts the balance between synaptic strengthening and weakening. This disruption may lead to an inability to effectively prune unnecessary synapses or adjust neural circuits based on experience. Research has linked dysfunctional LTD to several neurological disorders, such as Alzheimer's disease and schizophrenia, suggesting that maintaining proper LTD is critical for cognitive health. Understanding these links can inform potential therapeutic strategies aimed at restoring normal synaptic function.

Related terms

Long-term potentiation: Long-term potentiation (LTP) is a lasting increase in synaptic strength that occurs after high-frequency stimulation of a synapse, complementing the effects of long-term depression.

Synaptic plasticity: Synaptic plasticity refers to the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity, and is fundamental for learning and memory.

Calcium ions: Calcium ions (Ca²+) play a significant role in signaling pathways involved in both long-term potentiation and long-term depression, acting as critical messengers that influence synaptic modifications.