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Updated: Sep 6, 2025
Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function
Published on: August 7, 2019
CKAMP44 controls synaptic function and strength of relay neurons during early development of the dorsal lateral
Florian Hetsch1, Danni Wang1, Xufeng Chen1
1Institute of Pathophysiology, Focus Program Translational Neurosciences (FTN), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Insights
The AMPA receptor auxiliary subunit CKAMP44 is crucial for retinogeniculate synapse maturation in the developing visual system. Its absence impairs synaptic strength and increases silent synapses but does not affect eye-specific input segregation.
Area of Science:
- Neuroscience
- Developmental Biology
- Synaptic Plasticity
Background:
- Relay neurons in the dorsal lateral geniculate nucleus (dLGN) receive visual input via retinogeniculate synapses.
- These synapses undergo significant pruning and strengthening after eye opening, involving AMPA receptor (AMPAR) insertion.
- CKAMP44 is an AMPAR auxiliary subunit implicated in synaptic function.
Purpose of the Study:
- To investigate the role of CKAMP44 in the development and function of retinogeniculate synapses.
- To determine the impact of CKAMP44 deletion on synaptic strength, AMPAR properties, and neuronal morphology in the dLGN.
Main Methods:
- Utilized CKAMP44 knockout (CKAMP44-/-) and wild-type mouse models.
- Assessed synaptic strength, AMPAR desensitization, and plateau potential induction in dLGN relay neurons.
- Analyzed dendritic arborization and eye-specific input segregation.
Main Results:
- CKAMP44 deletion decreased synaptic strength and increased silent synapses in young mice.
- Faster recovery from AMPAR desensitization and elevated plateau potential induction were observed in CKAMP44-/- mice.
- Transient changes in dendritic branching occurred, but eye-specific input segregation remained unaffected.
Conclusions:
- CKAMP44 is essential for retinogeniculate synapse maturation and function during visual system development.
- It modulates AMPAR properties and synaptic plasticity without altering eye-specific input segregation.
- CKAMP44 plays a key role in refining visual circuit development.
Abstract:
Relay neurons of the dorsal lateral geniculate nucleus (dLGN) receive inputs from retinal ganglion cells via retinogeniculate synapses. These connections undergo pruning in the first 2 weeks after eye opening. The remaining connections are strengthened several-fold by the insertion of AMPA receptors (AMPARs) into weak or silent synapses. In this study, we found that the AMPAR auxiliary subunit CKAMP44 is required for receptor insertion and function of retinogeniculate synapses during development. Genetic deletion of CKAMP44 resulted in decreased synaptic strength and a higher number of silent synapses in young (P9-11) mice. Recovery from desensitisation of AMPARs was faster in CKAMP44 knockout (CKAMP44-/- ) than in wild-type mice. Moreover, loss of CKAMP44 increased the probability of inducing plateau potentials, which are known to be important for eye-specific input segregation and retinogeniculate synapse maturation. The anatomy of relay neurons in the dLGN was changed in young CKAMP44-/- mice showing a transient increase in dendritic branching that normalised during later development (P26-33). Interestingly, input segregation in young CKAMP44-/- mice was not affected when compared to wild-type mice. These results demonstrate that CKAMP44 promotes maturation and modulates function of retinogeniculate synapses during early development of the visual system without affecting input segregation. KEY POINTS: Expression of CKAMP44 starts early during development of the dorsal lateral geniculate nucleus (dLGN) and remains stable in relay neurons and interneurons. Genetic deletion of CKAMP44 decreases synaptic strength and increases silent synapse number in dLGN relay neurons; increases the rate of recovery from desensitisation of AMPA receptors in dLGN relay neurons; and reduces synaptic short-term depression in retinogeniculate synapses. The probability of inducing plateau potentials is elevated in relay neurons of CKAMP44-/- mice. Eye-specific input segregation is unaffected in the dLGN of CKAMP44-/- mice. Deletion of CKAMP44 mildly affects dendritic arborisation of relay neurons in the dLGN.
