Grunnleggende konsepter
The duration of starvation determines whether Drosophila forms appetitive short-term or longer-lasting intermediate memories. Insulin-like signaling in octopaminergic reward neurons integrates internal energy storage into memory formation, with octopamine acting as a negative regulator of memory.
Sammendrag
The study investigates how the internal energy status of Drosophila melanogaster influences the formation and stability of food-related memories.
Key highlights:
- Prolonged starvation leads to the formation of more stable, anesthesia-resistant intermediate and long-term memories, while mild starvation results in short-term memory.
- The neurotransmitter octopamine acts as a negative regulator of long-term memory formation. Blocking octopamine function in control flies or feeding octopamine to octopamine-deficient mutants enhances or suppresses long-term memory, respectively.
- Insulin receptor signaling in octopaminergic reward neurons integrates the internal energy status into memory formation. Reducing insulin receptor function in these neurons restores short-term memory in octopamine-deficient mutants.
- The internal glycogen levels in the muscles and fat bodies influence the strength of short-term memory. Decreasing glycogen levels enhances short-term memory, while increasing glycogen levels reduces it.
- Octopamine-deficient mutants show reduced sucrose preference and intake when mildly starved, but overconsume sucrose after prolonged starvation, correlating with their altered memory performance.
The results demonstrate that the internal energy status, as reflected by glycogen levels, is integrated into the reward system via insulin-octopamine signaling to regulate the formation and stability of food-related memories, which in turn influences feeding behavior.
Statistikk
Flies starved for 16 h showed short-term memory, while flies starved for 40 h formed more stable, anesthesia-resistant intermediate and long-term memories.
Octopamine-deficient TβhnM18 mutants starved for 16 h did not form short-term memory, but developed long-term memory, which became anesthesia-resistant after 40 h of starvation.
Reducing glycogen levels in the muscles or both muscles and fat bodies enhanced short-term memory, while increasing glycogen levels reduced it.
Octopamine-deficient mutants showed reduced sucrose intake when mildly starved, but overconsumption after prolonged starvation.
Sitater
"Prolonged starvation results in anesthesia-resistant ITM (Figure 2D). In contrast, mildly starved TβhnM18 mutants form a long-term memory that is sensitive to anesthesia-sensitive and detectable 24 h after the training. Prolonged starvation in TβhnM18 mutants leads to anesthesia-resistant long-term memory."
"Feeding 3 mM of the octopamine receptor antagonist epinastine for 1 h after training resulted in memory 6 h later in w1118 flies. Feeding 3 mM octopamine for 6 h after training suppresses LTM in TβhnM18."
"Blocking InR signaling in Tdc2-Gal4-targeted octopaminergic neurons in TβhnM18 mutants significantly increased 5% sucrose consumption."