scholarly journals Serotonin Signals Modulate Mushroom Body Output Neurons for Sustaining Water-Reward Long-Term Memory in Drosophila

Author(s):  
Wang-Pao Lee ◽  
Meng-Hsuan Chiang ◽  
Li-Yun Chang ◽  
Wei-Huan Shyu ◽  
Tai-Hsiang Chiu ◽  
...  

Memory consolidation is a time-dependent process through which an unstable learned experience is transformed into a stable long-term memory; however, the circuit and molecular mechanisms underlying this process are poorly understood. The Drosophila mushroom body (MB) is a huge brain neuropil that plays a crucial role in olfactory memory. The MB neurons can be generally classified into three subsets: γ, αβ, and α′β′. Here, we report that water-reward long-term memory (wLTM) consolidation requires activity from α′β′-related mushroom body output neurons (MBONs) in a specific time window. wLTM consolidation requires neurotransmission in MBON-γ3β′1 during the 0–2 h period after training, and neurotransmission in MBON-α′2 is required during the 2–4 h period after training. Moreover, neurotransmission in MBON-α′1α′3 is required during the 0–4 h period after training. Intriguingly, blocking neurotransmission during consolidation or inhibiting serotonin biosynthesis in serotoninergic dorsal paired medial (DPM) neurons also disrupted the wLTM, suggesting that wLTM consolidation requires serotonin signals from DPM neurons. The GFP Reconstitution Across Synaptic Partners (GRASP) data showed the connectivity between DPM neurons and MBON-γ3β′1, MBON-α′2, and MBON-α′1α′3, and RNAi-mediated silencing of serotonin receptors in MBON-γ3β′1, MBON-α′2, or MBON-α′1α′3 disrupted wLTM. Taken together, our results suggest that serotonin released from DPM neurons modulates neuronal activity in MBON-γ3β′1, MBON-α′2, and MBON-α′1α′3 at specific time windows, which is critical for the consolidation of wLTM in Drosophila.

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jie-Kai Wu ◽  
Chu-Yi Tai ◽  
Kuan-Lin Feng ◽  
Shiu-Ling Chen ◽  
Chun-Chao Chen ◽  
...  

2013 ◽  
Vol 110 (19) ◽  
pp. 7898-7903 ◽  
Author(s):  
T.-P. Pai ◽  
C.-C. Chen ◽  
H.-H. Lin ◽  
A.-L. Chin ◽  
J. S.-Y. Lai ◽  
...  

PLoS Genetics ◽  
2020 ◽  
Vol 16 (8) ◽  
pp. e1008963
Author(s):  
Wang-Pao Lee ◽  
Meng-Hsuan Chiang ◽  
Li-Yun Chang ◽  
Jhen-Yi Lee ◽  
Ya-Lun Tsai ◽  
...  

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Pierre-Yves Plaçais ◽  
Éloïse de Tredern ◽  
Lisa Scheunemann ◽  
Séverine Trannoy ◽  
Valérie Goguel ◽  
...  

2002 ◽  
Vol 22 (4) ◽  
pp. 1414-1425 ◽  
Author(s):  
Ildikó Kemenes ◽  
György Kemenes ◽  
Richard J. Andrew ◽  
Paul R. Benjamin ◽  
Michael O'Shea

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e59075 ◽  
Author(s):  
Chang Yang ◽  
Jian-Feng Liu ◽  
Bai-Sheng Chai ◽  
Qin Fang ◽  
Ning Chai ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Xiao-Wen Yu ◽  
Daniel M Curlik ◽  
M Matthew Oh ◽  
Jerry CP Yin ◽  
John F Disterhoft

The molecular mechanisms underlying age-related cognitive deficits are not yet fully elucidated. In aged animals, a decrease in the intrinsic excitability of CA1 pyramidal neurons is believed to contribute to age-related cognitive impairments. Increasing activity of the transcription factor cAMP response element-binding protein (CREB) in young adult rodents facilitates cognition, and increases intrinsic excitability. However, it has yet to be tested if increasing CREB expression also ameliorates age-related behavioral and biophysical deficits. To test this hypothesis, we virally overexpressed CREB in CA1 of dorsal hippocampus. Rats received CREB or control virus, before undergoing water maze training. CREB overexpression in aged animals ameliorated the long-term memory deficits observed in control animals. Concurrently, cells overexpressing CREB in aged animals had reduced post-burst afterhyperpolarizations, indicative of increased intrinsic excitability. These results identify CREB modulation as a potential therapy to treat age-related cognitive decline.


2018 ◽  
Author(s):  
Melissa C. Chubak ◽  
Max H. Stone ◽  
Nicholas Raun ◽  
Shelby L. Rice ◽  
Mohammed Sarikahya ◽  
...  

AbstractTechnology has led to rapid progress in the identification of genes involved in neurodevelopmental disorders like intellectual disability (ID), but our functional understanding of the causative genes is lagging. Here, we show that the SWI/SNF chromatin remodeling complex is one of the most overrepresented cellular components disrupted in ID. We systematically investigated the role of individual subunits of this large protein complex in post-mitotic memory forming neurons of the Drosophila mushroom body (MB). Using this approach, we have identified novel differential roles for the two prominent conformations of the Drosophila SWI/SNF complex, known as BAP and PBAP. The PBAP conformation is required post-mitotically for remodeling of the MB γ neurons during morphogenesis and is essential for both short and long-term memory. In contrast, the BAP conformation appears to preferentially effect long-term memory and is associated with γ neuron survival. Our results suggest that different subunits of the SWI/SNF complex may influence learning and memory through diverse and distinct roles in regulating structural plasticity, survival, and functionality of post-mitotic neurons. This study provides novel insight into the neuronal function of individual SWI/SNF subunits and will serve as a basis for understanding SWI/SNF-mediated gene regulatory mechanisms in post-mitotic neurons.


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