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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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Long-term Depression01:03

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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.
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Long-term Depression01:05

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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.
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Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

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Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
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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...
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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.
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Video Experimental Relacionado

Updated: Jan 13, 2026

Presynaptically Silent Synapses Studied with Light Microscopy
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Modulación viral de la poda sináptica: implicaciones para la neuropatología y la función cerebral

Shayan Aliakbari1,2, Sareh Asadi3, Mohammad Sayyah2

  • 1Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Journal of virology
|January 7, 2026
PubMed
Resumen

Las infecciones virales alteran la poda sináptica, un proceso clave del desarrollo cerebral, lo que puede causar deterioro cognitivo y trastornos del neurodesarrollo. Comprender esta conexión ayuda a desarrollar nuevas terapias para afecciones cerebrales asociadas a virus.

Palabras clave:
cascada del complementomicroglíadensidad sinápticapoda sinápticainfección viral

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Área de la Ciencia:

  • Neurociencia
  • Virología
  • Inmunología

Sus antecedentes:

  • La poda sináptica es vital para refinar los circuitos neuronales y las funciones cognitivas como el aprendizaje y la memoria.
  • Las infecciones virales son cada vez más reconocidas por su impacto significativo en los procesos del sistema nervioso.

Objetivo del estudio:

  • Revisar los mecanismos moleculares y celulares de la poda sináptica.
  • Examinar cómo los virus neurotrópicos afectan la poda sináptica.
  • Elucidar la interacción entre las infecciones virales y la poda sináptica para obtener información sobre la neuropatología.

Principales métodos:

  • Revisión de la literatura sobre mecanismos moleculares y celulares.
  • Análisis de estudios sobre los impactos virales en los procesos sinápticos.
  • Examen de la participación del sistema inmunitario (sistema del complemento, citoquinas).

Principales resultados:

  • Las infecciones virales alteran la plasticidad sináptica, la expresión de proteínas y los mecanismos de eliminación.
  • Las alteraciones son mediadas por respuestas inmunitarias y expresión de proteínas alterada.
  • La interferencia viral puede conducir a una pérdida o retención excesiva de sinapsis, lo que afecta la función cognitiva.

Conclusiones:

  • Las infecciones virales impactan significativamente la poda sináptica, contribuyendo a la neuropatología.
  • Comprender estas interacciones es crucial para abordar el deterioro cognitivo y los trastornos del neurodesarrollo.
  • Esta revisión informa la investigación futura y las estrategias terapéuticas en virología y neuroinmunología.