title: Developmental changes in pedunculopontine nucleus (PPN) neurons.
abstract: The developmental decrease in rapid-eye-movement (REM) sleep in man occurs between birth and after puberty. We hypothesize that if this decrease in REM sleep does not occur, lifelong increases in REM sleep drive may ensue. Such disorders are characterized by hypervigilance and sensory-gating deficits, such as are present in postpubertal onset disorders like schizophrenia, panic attacks (a form of anxiety disorder), and depression. The decrease in REM sleep in the rat occurs between 10 and 30 days of age. We studied changes in size and physiological properties of pedunculopontine nucleus (PPN) cells involved in the control of arousal, i.e., waking and REM sleep. During the largest decrease in REM sleep (12-21 days), cholinergic PPN neurons doubled in cell area, the hypertrophy peaking at 15-16 days, then decreasing in area by 20-21 days. Noncholinergic PPN cells did not change in area during this period. We confirmed the presence of two populations of PPN neurons based on action potential (AP) duration, with the proportion of short-AP-duration cells increasing and long AP duration decreasing between 12 and 21 days. Most cholinergic and noncholinergic cells had short AP durations. Afterhyperpolarization (AHP) duration became segregated into long and short AHP duration after 15 days. Cells with short AP duration also had short AHP duration. The proportion of PPN cells with Ih current increased gradually, peaking at 15 days, then decreased by 21 days. These changes in morphological and physiological properties are discussed in relation to the developmental decrease in REM sleep.
authors.affiliation: Center for Translational Neuroscience, Department of Anatomy and Neurobiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: C
authors.initials: C
authors.lastname: Good
authors.forename: J
authors.initials: J
authors.lastname: Biedermann
authors.forename: C
authors.initials: C
authors.lastname: Barnes
authors.forename: R D
authors.initials: RD
authors.lastname: Skinner
authors.forename: E
authors.initials: E
authors.lastname: Garcia-Rill
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001360:Avidin / Q000031:analogs & derivatives* / Q000378:metabolism; D002317:Cardiovascular Agents / Q000494:pharmacology; D002452:Cell Count; D048429:Cell Size; D005260:Female; D005452:Fluoresceins / Q000378:metabolism; D007150:Immunohistochemistry / Q000379:methods; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009249:NADP / Q000378:metabolism; D009474:Neurons / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D011247:Pregnancy; D011743:Pyrimidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013681:Tegmentum Mesencephali / Q000166:cytology* / Q000196:embryology / Q000254:growth & development; D013779:Tetrodotoxin / Q000494:pharmacology; D014966:Xanthenes / Q000378:metabolism
chemical_list: D002317:Cardiovascular Agents; D005452:Fluoresceins; D011743:Pyrimidines; D026941:Sodium Channel Blockers; D014966:Xanthenes; C049445:fluorescein-avidin; C082246:ICI D2788; D001360:Avidin; D013779:Tetrodotoxin; D009249:NADP; C034657:Texas red