Cholinergic modulation of slow cortical rhythm in urethane-anesthetized rats.
Slow cortical rhythm (SCR) is characterized by rhythmic cycling of active (UP) and silent (DOWN) states in cortical cells. In urethane anesthesia, SCR appears as alternation of almost isoelectrical EEG periods and low-frequency, high-amplitude large shifts with superimposed high-frequency activity in the local field potentials (LFPs). Dense cholinergic projection reaches the cortex from the basal forebrain (BF), and acetylcholine (ACh) has been demonstrated to play a crucial role in the regulation of cortical activity. In the present experiments, cholinergic drugs were administered topically to the cortical surface of urethane-anesthetized rats to examine the direct involvement of ACh and the BF cholinergic system in the SCR. SCR was recorded by a 16-pole vertical electrode array from the hindlimb area of the somatosensory cortex. Multiple unit activity (MUA) was recorded from layer V to VI in close proximity of the recording array. Neither a low dose (10 mM solution) of the muscarinic antagonist atropine or the nicotinic agonist nicotine (1 mM solution) had any effect on SCR. In contrast, the higher dose (100 mM solution) of atropine, the cholinergic agonist carbachol (32 mM solution), and the cholinesterase inhibitor physostigmine (13 mM solution) all decreased the number of UP states, delta power (0-3 Hz) and MUA. These results suggest that cholinergic system may influence SCR through muscarinic mechanisms during urethane anesthesia. Cholinergic activation obstructs the mechanisms responsible for local or global synchronization seen during SCR as this rhythm was disrupted or aborted. Muscarinic antagonism can evoke similar changes when high dose of atropine is applied.
Department of Physiology and Neurobiology, Eötvös Loránd University, Pázmány Péter sétány 1/C, Budapest 1117, Hungary. etn@freemail.hu
Attila
A
Toth
Tunde
T
Hajnik
Laszlo
L
Detari
D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology; D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D004569:Electroencephalography / Q000379:methods*; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D010830:Physostigmine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000187:drug effects / Q000502:physiology; D014520:Urethane / Q000494:pharmacology*
D018686:Anesthetics, Intravenous; D018679:Cholinergic Agonists; D002800:Cholinesterase Inhibitors; D018727:Muscarinic Antagonists; D018722:Nicotinic Agonists; D014520:Urethane; D009538:Nicotine; D001285:Atropine; D002217:Carbachol; D010830:Physostigmine; D000109:Acetylcholine