Synapse-Glia Interactions at the Vertebrate Neuromuscular Junction

Abstract

Glial cells are widely distributed throughout the nervous system, including at the chemical synapse. However, our knowledge of the role of glial cells at the synapse is rudimentary. Recent studies using a model synapse, the vertebrate neuromuscular junction (NMJ), have demonstrated that perisynaptic Schwann cells (PSCs), which are the glia juxtaposed to the nerve terminal at the NMJ, play active and essential roles in synaptic function, maintenance, and development. PSCs can respond to nerve activity by increasing intracellular calcium and are capable of modulating synaptic function in response to pharmacological manipulations. Studies using PSC ablation in vivo have shown that PSCs are essential for the long-term maintenance of synaptic structure and function at the adult NMJ. In vivo observations have also shown that PSCs guide presynaptic nerve terminal extension and dictate the pattern of innervation during synaptic regeneration and remodeling at adult NMJs. PSCs may also induce postsynaptic acetylcholine receptor aggregation. Furthermore, PSCs play an essential role in synaptic growth and maintenance during development of NMJs in vivo, and Schwann cell-derived factors can promote synaptogenesis and enhance synaptic transmission in tissue culture. These recent findings advance the emerging concept that glial cells help make bigger, stronger, and more stable synapses.

Association of IL-1B genetic polymorphisms with an increased risk of opioid and alcohol dependence

“…Novel candidate genes need to be identified to account for more of the heritability of opioid dependence. With mounting evidence showing the involvement of IL-1b in opioid dependence [31][32][33][34], genetic variability in the IL-1 gene family could be a possible candidate that alters opioid abuse liability. The proposed mechanism of how IL-1b is involved in modifying abuse potential is most likely related to altered opioid-induced reward and neuroplasticity ( Fig.…”

“…This mechanism is supported by both animal and human studies, which have highlighted the role of IL-1b after glial activation by opioids and alcohol. Chronic administration of morphine has been shown to induce CNS proinflammation and upregulation of IL-1b in animal [31][32][33][34] and human [35] studies. Blocking IL-1b, by intrathecal administration of an IL-1 receptor antagonist, reversed established morphine tolerance [32].…”

Opposite effects of CBP and p300 in glucocorticoid signaling in astrocytes

“…In peripheral nerves, Schwann cells elaborate myelin sheaths and play an important role in regeneration processes. Moreover, perisynaptic astrocytes, as well as terminal Schwann cells, can be viewed as integral modulatory elements of synapses [13].…”

The Synaptic Remodeling Between Regenerated Perforant Pathway and Granule Cells in Slice Culture

“…Peripheral nerves have the capacity to self-regenerate after traumatic injury (Kang et al 2003;Pfister et al 2007). There is evidence that regenerated axons can even form functional neuromuscular junctions with muscles (Koirala et al 2003;Feng et al 2005). However, the CNS in adult mammals is notorious for its poor capacity to regenerate axons after injury (Fawcett 2006).…”