Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats.
Pontine noradrenergic neurons of the locus coeruleus (LC) and sub-coeruleus (SubC) region cease firing during rapid eye movement sleep (REMS). This plays a permissive role in the generation of REMS and may contribute to state-dependent modulation of transmission in the CNS. Whether all pontomedullary catecholaminergic neurons, including those in the A1/C1, A2/C2 and A7 groups, have REMS-related suppression of activity has not been tested. We used Fos protein expression as an indirect marker of the level of neuronal activity and linear regression analysis to determine whether pontomedullary cells identified by tyrosine hydroxylase (TH) immunohistochemistry have reduced Fos expression following REMS-like state induced by pontine microinjections of a cholinergic agonist, carbachol in urethane-anesthetized rats. The percentage of Fos-positive TH cells was negatively correlated with the cumulative duration of REMS-like episodes induced during 140 min prior to brain harvesting in the A7 and rostral A5 groups bilaterally (P < 0.01 for both), and in SubC neurons on the side opposite to carbachol injection (P < 0.05). Dorsal medullary A2/C2 neurons did not exhibit such correlation, but their Fos expression (and that in A7, rostral A5 and SubC neurons) was positively correlated with the duration of the interval between the last REMS-like episode and the time of perfusion (P < 0.05). In contrast, neither of these correlations was significant for A1 /C1 or caudal A5 neurons. These findings suggest that, similar to the prototypic LC neurons, neurons of the A7, rostral A5 and A2/C2 groups have reduced or abolished activity during REMS, whereas A1 /IC1 and caudal A5 neurons do not have this feature. The reduced activity of A2/C2, A5 and A7 neurons during REMS, and the associated decrements in norepinephrine release, may cause state-dependent modulation of.transmission in brain somato- and viscerosensory, somatomotor, and cardiorespiratory pathways.
D018686:Anesthetics, Intravenous / Q000494:pharmacology; D000818:Animals; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology*; D002217:Carbachol / Q000008:administration & dosage*; D002395:Catecholamines / Q000378:metabolism; D018679:Cholinergic Agonists / Q000008:administration & dosage*; D004569:Electroencephalography; D007150:Immunohistochemistry; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology; D008845:Microinjections; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D011149:Pons / Q000187:drug effects / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012895:Sleep, REM / Q000502:physiology*; D014446:Tyrosine 3-Monooxygenase / Q000096:biosynthesis; D014520:Urethane / Q000494:pharmacology
D018686:Anesthetics, Intravenous; D002395:Catecholamines; D018679:Cholinergic Agonists; D016760:Proto-Oncogene Proteins c-fos; D014520:Urethane; D002217:Carbachol; D014446:Tyrosine 3-Monooxygenase
autonomic regulation; brainstem; locus coeruleus; motor control; norepinephrine