Cortical Eeg Following Bilateral Lateral Hypothalamic Damage: Effects of Drugs Acting on Some Components of the Reticular Formation (Hippocampus, Animal-Model, Pharmacology)
Shoham, Shai
This item is only available for download by members of the University of Illinois community. Students, faculty, and staff at the U of I may log in with your NetID and password to view the item. If you are trying to access an Illinois-restricted dissertation or thesis, you can request a copy through your library's Inter-Library Loan office or purchase a copy directly from ProQuest.
Permalink
https://hdl.handle.net/2142/69653
Description
Title
Cortical Eeg Following Bilateral Lateral Hypothalamic Damage: Effects of Drugs Acting on Some Components of the Reticular Formation (Hippocampus, Animal-Model, Pharmacology)
Author(s)
Shoham, Shai
Issue Date
1984
Department of Study
Psychology
Discipline
Psychology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Psychology, Physiological
Abstract
Following large bilateral lateral hypothalamic damage (BLH) rats are somnolent (appear behaviorally asleep) and show cortical EEG of high voltage and slow waves (HVS) all the time. The failure to maintain cortical low voltage and fast EEG (LVF) as the normal rat does, may reflect disruption of some neurotransmitter components of the reticular formation known to contribute to cortical LVF-activation. The purpose of this investigation was to find whether drugs which enhance or mimic the action of these reticular neurotransmitter systems (agonists) can establish normal-like cortical LVF. Drugs acting on acetylcholine, dopamine, norepinephrine, and serotonin were found able to advance BLH damaged rats from a condition of early recovery to a condition of later recovery and even to a normal-like cortical EEG. This is the first pharmacological evidence that the damage-induced cortical HVS is due to removal of cortical LVF-activation.
Only serotonin agonists could advance a rat from the most severe consequence of BLH damage ('BLH 1'--total loss of cortical LVF). The advance, with increasing dose, was through a series of stages (of EEG-behavior correlation) seen in natural (non-drug aided) recovery from BLH damage. Acetylcholine and direct catecholamines agonists could advance a BLH damaged rat only when some cortical LVF was already present. Until direct stimulation of cholinergic receptors is tested it is impossible to generalize that cholinergic mechanisms of LVF-activation are abolished under a BLH 1 condition. However, given neuroanatomical studies the hypothesis is offered that under condition BLH 1, cholinergic neurons are sufficiently disrupted to fail to establish cortical LVF.
It was discovered in the present investigation that drugs acting on serotonin can establish cortical LVF in the presence of atropine sulfate in both recovering BLH damaged rats and normal rats. This discovery combined with the discovery that only serotonin agonists advance a rat from condition BLH 1, suggest serotonin can contribute to cortical LVF-activation and that this contribution is not dependent on ACh release.
Use this login method if you
don't
have an
@illinois.edu
email address.
(Oops, I do have one)
IDEALS migrated to a new platform on June 23, 2022. If you created
your account prior to this date, you will have to reset your password
using the forgot-password link below.
