Change in the central control of the bladder function of rats with focal cerebral infarction induced by photochemically-induced thrombosis

PLoS One. 2021 Nov 9;16(11):e0255200. doi: 10.1371/journal.pone.0255200. eCollection 2021.

Abstract

The photochemically-induced thrombosis (photothrombosis) method can create focal cerebral infarcts anywhere in the relatively superficial layers of the cerebrum; it is easy to implement and minimally invasive. Taking advantage of this versatility, we aimed to establish a new rat model of urinary frequency with focal cerebral infarction, which was characterized by its simplicity, nonlethal nature, and high reproducibility. The prefrontal cortex and the anterior cingulate cortex, which are involved in lower urinary tract control, were targeted for focal cerebral infarction, and urinary parameters were measured by cystometrogram. Cystometric analysis indicated that micturition intervals significantly shortened in photothrombosis-treated rats compared with those in the sham operative group on Days 1 and 7 (P < 0.01), but prolonged after 14 days, with no difference between the two groups. Immunopathological evaluation showed an accumulation of activated microglia, followed by an increase in reactive astrocytes at the peri-infarct zone after photothrombotic stroke. Throughout this study, all postphotothrombosis rats showed cerebral infarction in the prefrontal cortex and anterior cingulate cortex; there were no cases of rats with fatal cerebral infarction. This model corresponded to the clinical presentation, in that the micturition status changed after stroke. In conclusion, this novel model combining nonlethality and high reproducibility may be a suitable model of urinary frequency after focal cerebral infarction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cerebral Infarction / complications
  • Cerebral Infarction / physiopathology*
  • Disease Models, Animal
  • Female
  • Rats
  • Rats, Wistar
  • Thrombosis
  • Urinary Bladder / physiopathology*
  • Urinary Bladder, Overactive / etiology
  • Urinary Bladder, Overactive / physiopathology*

Grants and funding

This work was supported by GSK Japan Research Grant 2019 (https://jp.gsk.com/jp/research/glaxosmithkline-research-grant-2019/) and a grant awarded by the Japan Society for the Promotion of Science (https://www.jsps.go.jp/j-grantsinaid/), Grant Number 19k18568, all to Y.O..