Differential expression of connexin26 and connexin32 in the pre-Botzinger complex of neonatal and adult rat

Citation
Ic. Solomon et al., Differential expression of connexin26 and connexin32 in the pre-Botzinger complex of neonatal and adult rat, J COMP NEUR, 440(1), 2001, pp. 12-19
Citations number
51
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF COMPARATIVE NEUROLOGY
ISSN journal
00219967 → ACNP
Volume
440
Issue
1
Year of publication
2001
Pages
12 - 19
Database
ISI
SICI code
0021-9967(20011105)440:1<12:DEOCAC>2.0.ZU;2-8
Abstract
The pre-Botzinger complex (pre-BotC) is hypothesized to be the site for res piratory rhythm generation in mammals. Studies examining the cellular mecha nisms mediating rhythm generation have focused on the role of chemically me diated synaptic interactions; however, electrotonic synaptic interactions ( i.e., electrotonic coupling), which occur by means of gap junctions, may al so play a role. Here, we used immunoblot and immunohistochemical analyses t o determine whether the pre-BotC contains the gap junction proteins necessa ry for electrotonic communication and whether the presence and distribution of these gap junction proteins show a developmental change in expression. We found that both connexin26 (Cx26) and connexin32 (Cx32) were expressed i n pre-BotC neurons of neonatal and adult rats; however, the relative amount s and their distribution varied by age. Cx26 labeling was seen in a high pr oportion of pre-BotC neurons in neonatal rats less than or equal to 7 days postnatal (P7) but declined with increasing age. In contrast, Cx32 labeling was sparse in pre-BotC neurons of neonatal rats less than or equal to P7, but increased with increasing age; the highest proportion was seen in adult rats. These data suggest the potential for gap junctional communication in the pre-BotC of both neonatal and adult rats, and we propose that the gap junction proteins Cx26 and Cx32 form the neuroanatomic substrate for this g ap junctional communication, which may be important in the synchronization of neural activity generating respiratory rhythm. (C) 2001 Wiley-Liss, Inc.