Golgi polarity shift instructs dendritic refinement in the neonatal cortex by mediating NMDA receptor signaling
Naoki Nakagawa, Takuji Iwasato

Cell Reports 2023 Jul 28 DOI:10.1016/j.celrep.2023.112843

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• Uncovering how the Golgi apparatus impacts early postnatal neuron development

Neurons are the cells that constitute neural circuits and use chemicals and electricity to receive and send messages that allow the body to do everything, including thinking, sensing, moving, and more. Neurons have a long fiber called an axon that sends information to the subsequent neurons. Information from axons is received by branch-like structures that fan out from the cell body, called dendrites.

Dendritic refinement is an important part of early postnatal brain development during which dendrites are tailored to make specific connections with appropriate axons. In a recently published paper, researchers present evidence showing how a mechanism within the neurons of a rodent involving the Golgi apparatus initiates dendritic refinement with the help of the neuronal activity received by a receptor of a neurotransmitter called N-methyl-D-aspartate-type glutamate receptor (NMDAR).

The paper was published in Cell Reports on July 28. Read more>

Figure: The image shows a spiny stellate neuron (magenta) and its Golgi apparatus (white) in the mouse barrel cortex at postnatal day 5. The study found that the Golgi apparatus shows a biased distribution in one side of the neuron only during the postnatal critical period of circuit reorganization. This lateral Golgi polarity instructs the direction in which the neuron expands its dendrites for establishing precise neuronal circuit.

Dysregulated TDP-43 proteostasis perturbs excitability of spinal motor neurons during brainstem-mediated fictive locomotion in zebrafish
Kazuhide Asakawa, Hiroshi Handa, Koichi Kawakami

evelopment, Growth & Differentiation 2023 July 15 DOI:10.1111/dgd.12879

Amyotrophic lateral sclerosis (ALS) is a debilitating disease that causes muscle weakness and eventually fatal paralysis. A major hallmark of ALS is the deposition of the aggregate form of TDP-43 protein in motor neurons, a type of nerve cell that directs muscle contractions. This motor neuron pathology can occur without genetic mutations in the coding sequence of the TDP-43-encoding gene TARDBP. Whether and how wild-type TDP-43 drives pathological changes in motor neurons remain largely unexplored.

In the present study, Asakawa and colleagues used calcium imaging to directly compare the neural activity of motor neurons with and without excessive TDP-43 protein during fictive locomotion. They found that excessive amounts of TDP-43 protein reduced the excitability of motor neurons (Figure). This finding suggests that the reduced excitability caused by excessive TDP-43 potentially contributes to asymptomatic pathological lesions of motor neurons and movement disorders in patients with ALS.

This work was published in the journal Development Growth & Differentiation on the 15th of July, 2023. The study was conducted by a collaborative research group comprising the National Institute of Genetics (Kazuhide Asakawa and Koichi Kawakami) and Tokyo Medical University (Hiroshi Handa).

This work was supported by the Nakabayashi Trust For ALS Research (K.A.), The Kato Memorial Trust For Nambyo Research (K.A.), Daiichi-Sankyo Foundation of Life Science (K.A.), Takeda Science Foundation (K.A.), KAKENHI grant numbers JP16K07045 (K.A.), JP19K06933 (K.A.), JP22H02958 (K.A.), JP23H04266 (K.A.), JP21H02463 (K.K.) and AMED-PRIME grant number JP23gm6410011h0003 (K.A.), and the National BioResource Project (NBRP) (K.K.).

Figure: Excessive amounts of TDP-43 protein reduce motor neuron excitability

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