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Journal of Neuroscience, Vol 16, 1523-1537, Copyright © 1996 by Society for Neuroscience
Histaminergic descending inputs to the mesopontine tegmentum and their role in the control of cortical activation and wakefulness in the cat
JS Lin, Y Hou, K Sakai and M Jouvet
Departement de Medecine Experimentale, Institut National de la Sante et de la Recherche Medicale U52, Faculte de Medecine, Universite Claude Bernard, Lyon, France.
We have demonstrated previously the importance of histaminergic neurons in
arousal mechanisms. In addition to their ascending axons, these neurons
also send heavy descending inputs to the mesopontine tegmentum (MPT), which
plays a key role in cortical activation during wakefulness (W). This
anatomical link suggests histaminergic control of the mechanisms of the MPT
relevant to behavioral states. In this study, we sought to demonstrate, at
the light microscopy level, hypothalamotegmental histaminergic pathways and
their topographical interaction with MPT neurons in the cat and to explore
further their involvement in sleep-wake control. Using immunohistochemistry
of histamine (HA), either alone or together with that of choline-
acetyltransferase or tyrosine hydroxylase, a large number of very fine,
short and varicose HA-positive fibers and terminal-like dots were detected
in the MPT, including the laterodorsal tegmental nucleus, locus coeruleus
(LC), LC alpha, and peri-LC alpha. Furthermore, these fibers and
terminal-like structures were found in close proximity to a great number of
cholinergic or noradrenergic neurons. We also investigated the effects of
microadministration of HA agonists and antagonist into the mediodorsal
pontine tegmentum on the cortical electroencephalogram (EEG) power spectra
and the sleep-wake cycle in freely moving cats. Microinjection of HA or
2-thiazolylethylamine (an H1-receptor agonist) caused a long-lasting
suppression of cortical slow activity and an increase in quiet wakefulness
(W). Paradoxical sleep, however, was less affected. The effects of HA were
attenuated by systemic or in situ pretreatment with mepyramine (an
H1-receptor antagonist), which when injected alone produced an increase in
slow wave sleep. Microinjection of impromidine (an H2-receptor agonist)
into the same area had no effect on either the cortical EEG or W. Because
MPT ascending and presumed cholinergic neurons discharge tonically during
cortical activation of W and because HA causes excitation of MPT
cholinergic neurons via H1 receptors, we hypothesize that the histaminergic
descending afferents in the MPT would promote cortical desynchronization
and W, at least partially, via activation of H1 receptors situated on
cholinergic neurons and that the interactions between histaminergic and
cholinergic neurons constitute an important circuit in cortical activation
during W.
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