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Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
Published on: April 23, 2019
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Upward synaptic scaling is dependent on neurotransmission rather than spiking
Ming-fai Fong1, Jonathan P Newman2, Steve M Potter3
11] Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA [2] Laboratory for Neuroengineering, Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332, USA [3] Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Nature Communications
|March 10, 2015
Summary
Reduced glutamatergic transmission directly triggers synaptic upscaling in neurons. This finding challenges the established view that neural firing rates are the primary driver of this homeostatic plasticity mechanism.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Neural Circuit Homeostasis
Background:
- Homeostatic plasticity stabilizes neural circuit firing rates through various mechanisms.
- Upward synaptic scaling (upscaling) is a key form of homeostatic plasticity, increasing excitatory synaptic strength.
- Traditionally, reduced neuronal firing rate is believed to trigger upscaling.
Purpose of the Study:
- To investigate whether reduced glutamatergic transmission directly triggers synaptic upscaling.
- To differentiate the roles of neuronal spiking versus synaptic transmission in initiating upscaling.
- To explore the signaling cascades involved in mediating synaptic upscaling.
Main Methods:
- Utilized chronic multielectrode recording to monitor neural activity.
- Employed closed-loop optogenetic stimulation to precisely control neuronal activity.
- Applied pharmacological interventions to manipulate glutamatergic transmission.
Main Results:
- Demonstrated that reduced glutamatergic transmission directly induces cell-wide synaptic upscaling.
- Showcased the critical role of synaptic activity in initiating the signaling pathways for upscaling.
- Provided evidence that synaptic activity, not just firing rate, is a direct trigger.
Conclusions:
- Reduced glutamatergic transmission is a direct trigger for synaptic upscaling.
- Synaptic activity plays a crucial role in initiating the cascades mediating homeostatic plasticity.
- The findings challenge the prevailing model of upscaling solely stabilizing neural firing rates.
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