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|Title:||Cortical Eeg Following Bilateral Lateral Hypothalamic Damage: Effects of Drugs Acting on Some Components of the Reticular Formation (Hippocampus, Animal-Model, Pharmacology)|
|Department / Program:||Psychology|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|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.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1984.
|Date Available in IDEALS:||2014-12-15|