Neuroglia in the Aging Brain (Contemporary Neuroscience)

Neuroglia in the Aging Brain (Contemporary Neuroscience)

Language: English

Pages: 513

ISBN: 1617370886

Format: PDF / Kindle (mobi) / ePub


A distinguished panel of internationally recognized neuroscientists comprehensively review the involvement of and changes in glial cells both during the normal aging process and in the major disorders of old age. Topics range from the cellular and molecular changes that occur with aging-especially aging-associated activation of astrocytes and microglia and its relation to neuronal injury and repair-to neuron-glia intercommunication. The contributors show how glial signals may be modulated by hormones, growth factors, neurotransmitters, intracellular metabolism, and intercellular exchanges, as well as by aging of the blood-brain barrier.

The Human Brain Book (2nd Edition)

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The Ravenous Brain: How the New Science of Consciousness Explains Our Insatiable Search for Meaning

A Hole in the Head: More Tales in the History of Neuroscience

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

inhibits astrocyte activation and induces NGF secretion. J. Neuroimmunol 81, 20–30. Gliosis Growth Factors 175 45. Streit, W.J., Hurley, S.D., McGraw, T.S., and Semple-Rowland, S.L. (2000) Comparative evaluation of cytokine profiles and reactive gliosis supports a critical role for interleukin-6 in neuronglia signaling during regeneration. J. Neurosci. Res. 61, 10–20. 46. Loddick, S.A., Turnbull, A.V., and Rothwell, N.J. (1998) Cerebral interleukin-6 is neuroprotective during permanent focal

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(16, Fig. 3). AMPA/KA-R stimulation affected astrocytes both when they were isolated from slices and when neuronal action potentials were blocked, indicating that AMPA/KA-R agonists were directly affecting astrocytes (10,12,28) (Shelton and McCarthy, Neurochemistry). When AMPA/KA-R responses have been closely examined, they appear to occur via AMPA-Rs in hippocampal cells presumed to be astrocyte progenitors (10,28). In addition to the physiological evidence for AMPA/KA-Rs, there is also evidence

that these potentials were due to acetylcholine release by Schwann cells. Later, Dennis and Miledi (77) showed that electrically stimulated denervated Schwann cells released acetylcholine in a nonquantal form. In giant axons of the squid, Lieberman et al. (78) have reported that nerve stimulation caused Schwann cell hyperpolarization. They suggested that glutamate released by axons caused Schwann cell depolarization which in turn triggered the release of acetylcholine and caused by an autocrine

peripheral nerve development has not yet been reported but appears plausible. The growth cones of developing neurons are known to release neurotransmitters. This has been shown in vitro for mammalian CNS (99) and PNS (100) neurons. It is therefore conceivable that like other transmitters, ATP could be released from growth cones and/or along axons of peripheral neurons during development and modulates apoptosis of surrounding Schwann cells. 5.2.2. Schwann Cell Apoptosis During Pathological

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