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Long-term Potentiation

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.

Long-term Potentiation

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 Depression

Long-term Depression

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...

Long-term Depression

Long-term Depression

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.

Calmodulin-dependent Signaling

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,...

Role of Neurotransmitters in Memory

Role of Neurotransmitters in Memory

Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is critical for...

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Updated: Jul 15, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

La fosforilación alfa de eIF2 regula bidireccionalmente el cambio de la plasticidad sináptica a corto y largo plazo y

Mauro Costa-Mattioli¹, Delphine Gobert, Elad Stern

¹Department of Biochemistry and McGill Cancer Center, McGill University, Montreal, Quebec, Canada. mauro.costa-mattioli@mail.mcgill.ca

|April 10, 2007

Resumen

La alteración de la fosforilación eIF2alfa afecta la memoria y la plasticidad sináptica. La fosforilación reducida mejora la memoria y la potenciación tardía a largo plazo (L-LTP), mientras que el aumento de la fosforilación los deteriora.

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Área de la Ciencia:

La neurociencia es la neurociencia.
Biología Molecular Biología Molecular
La plasticidad sináptica.

Sus antecedentes:

La potenciación a largo plazo de la fase tardía (LTP) y la memoria a largo plazo (LTM) dependen de la nueva expresión génica.
Los mecanismos moleculares precisos que rigen estos procesos siguen siendo incompletamente entendidos.
La fosforilación del factor de iniciación eucariota 2 alfa (eIF2alfa) inhibe globalmente la traducción pero selectivamente aumenta el ATF4, un represor de la LTP tardía (L-LTP) mediada por CREB y la LTM.

Objetivo del estudio:

Investigar el papel de la fosforilación eIF2alfa en la plasticidad sináptica y el aprendizaje conductual.
Para aclarar la función reguladora de la fosforilación eIF2alfa en la formación de L-LTP y LTM.

Principales métodos:

Utilizó un enfoque farmacogenético bidireccional en ratones.
Se examinaron los efectos de la fosforilación eIF2alpha reducida en ratones eIF2alpha ((+/S51A).
Investigó el impacto del aumento de la fosforilación eIF2alfa utilizando la pequeña molécula Sal003 en el hipocampo.

Principales resultados:

La reducción de la fosforilación eIF2alpha en ratones eIF2alpha ((+/S51A) redujo el umbral de L-LTP y mejoró la memoria.
El aumento de la fosforilación eIF2alfa a través de la inyección de Sal003 dio lugar sólo a LTP temprano y LTM deteriorado.
Estos hallazgos implican el sitio de fosforilación eIF2alfa como un regulador crítico.

Conclusiones:

La fosforilación eIF2alfa es un interruptor molecular clave que controla el L-LTP y el LTM.
La modulación de la fosforilación eIF2alfa ofrece un objetivo terapéutico potencial para los trastornos de la memoria.
El equilibrio de la fosforilación eIF2alfa es crucial para la consolidación de la memoria y la plasticidad sináptica.