Microglia And Neurodegeneration A Synaptic Stripping

Transection of the facial nerve is a useful model for studying microglial responses in the absence of infiltrating macrophages, as shown by the seminal work of Kreutzberg and colleagues. The facial nerve is cut outside the brain and the reactions of facial motoneur-ons and their glial environment to retrograde axonal degeneration can be studied in the brain stem, which shows no disturbance of the BBB in this lesion paradigm. After transection of the facial nerve micro-glia proliferated within 3 or 4 days mainly around the corresponding motoneurons and expressed longstanding activation markers (CD4, MHC class I and II, and cell adhesion molecules), amyloid precursor protein, and the cytokines TNF-a and TGF-b. TGF-b is a cytokine with a potential role in tissue repair. From Day 4 after axotomy onward, proliferating perineuronal microglia ensheathed the soma of the injured motoneurons and detached afferent synaptic terminals from the motoneuron surface, a process designated synaptic stripping. Synaptic stripping is an important process in synaptic reorganization after injury. Interestingly, microglia were activated but did not phagocytose unless the motoneurons underwent lethal injury. After selective death of motoneurons induced by retrogradly transported toxic ricin, a paradigm that also leaves the BBB intact, surrounding microglia transformed into phagocytes and removed dying neurons without the aid of hematogenous macrophages. Similarly, kainic acid-induced neuronal degeneration led to phagocytic transformation of microglia in the hippocampus.

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Aspergers Answers Revealed

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