Spontaneous regeneration of the seriously injured sympathetic pathway projecting to the prostate over a long period in the dog

Abstract

the prostate to electrical stimulation of the lumbar splanchnic nerve (LSN) or the HGN proximal to the site removed, were assessed. RESULTSIn six dogs, 10 of the 17 LSNs (second to fourth) and four of the 10 HGNs stimulated elicited prostatic contraction. The pathways via the ipsilateral HGN and/or the contralateral HGN from the LSNs to the prostate were identified as having regenerated in four of six dogs. CONCLUSIONThese results indicate that the sympathetic pathways via the HGN to the canine prostate can regenerate spontaneously over a long period after serious injury, and that their cross-innervation system can also be repaired.

Progenitors from the central nervous system drive neurogenesis in cancer

“…In prostate cancer, the number of neurons per ganglia is increased, which suggests that a potential process of neurogenesis occurs in tumours and that this process supports tumour development and progression 13 . This process seems to be specific to cancer: in the healthy prostate, sympathetic innervation can regenerate after injury, which indicates a process of axonogenesis without any evidence for newly formed neurons 14 . In prostate cancer, the outgrowth of newly formed autonomic nerve fibres into the tumour contributes to the initiation and progression of cancer through the activation of β-adrenergic and muscarinic cholinergic signalling, respectively 5,8 .…”

Targeting tumor innervation: premises, promises, and challenges

“…However, it is worth noting that this process may be more cancer-specific. In healthy prostates, sympathetic nerves can regenerate after injury; studies have speculated that this may be a result of axonogenesis, with no evidence of neurogenesis [ 59 ]. In prostate cancer, compared to normal prostate tissues, the penetration of newly formed autonomic nerves into the tumors contributes to the initiation and progression of cancers through activation of beta-adrenergic and toxicological cholinergic signaling, respectively [ 60 , 61 ].…”