ABSTRACT
Monoamines are implicated in a cognitive processes in a variety of brain regions, including the hippocampal formation, where storage and retrieval of information are facilitated by synchronous network activities. We have investigated the effects of norepinephrine, serotonin, and dopamine on carbachol-, kainate-, and stimulus-induced hippocampal gamma-oscillations employing combined extra- and intracellular recordings. Monoamines dose-dependently and reversibly suppressed kainate- and carbachol-induced gamma-oscillations while increasing the frequency. The effect of serotonin was mimicked by fenfluramine, which releases serotonin from presynaptic terminals. Forskolin also suppressed kainate- and carbachol-induced gamma-oscillations. This effect was mimicked by 8-Br-cAMP and isoproterenol, an agonist of noradrenergic beta-receptor suggesting that the monoamines-mediated suppression of these oscillations could involve intracellular cyclic adenosine 3',5'-cyclic monophosphate (AMP). By contrast, stimulus-induced gamma-oscillations were dose-dependently augmented in power and duration after monoamines application. Intracellular recordings from pyramidal cells revealed that monoamines prolonged the stimulus-induced depolarization and membrane potential oscillations. Stimulus-induced gamma-oscillations were also suppressed by isoproterenol, the D1 agonist SKF-38393 forskolin, and 8-Br-cAMP. This suggests that the augmentation of stimulus-induced gamma-oscillations by monoamines involves--at least in part-different classes of cells than in case of carbachol- and kainate-induced gamma-oscillations.
Subject(s)
Biogenic Monoamines/pharmacology , Hippocampus/drug effects , Hippocampus/physiology , 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology , 8-Bromo Cyclic Adenosine Monophosphate/pharmacology , Animals , Carbachol/pharmacology , Central Nervous System Agents/pharmacology , Colforsin/pharmacology , Dopamine/pharmacology , Electric Stimulation , Fenfluramine/pharmacology , In Vitro Techniques , Isoproterenol/pharmacology , Kainic Acid/pharmacology , Membrane Potentials/drug effects , Norepinephrine/pharmacology , Pyramidal Cells/drug effects , Pyramidal Cells/physiology , Rats , Rats, Wistar , Serotonin/pharmacology , Serotonin Agents/pharmacologyABSTRACT
Sharp wave-ripple complexes (SPW-Rs) are characterized by approximately 60 ms field potential transients superimposed by ripple oscillations of approximately 200 Hz. In chronic epileptic rodents and humans, faster ripples have been recorded showing frequencies of up to 500 Hz. In this study, we tested whether the blockade of K currents by 4-aminopyridine (4-AP) contribute to the generation of high-frequency ripples, as changes in K channel expression have been observed in chronic epileptic tissue. We showed that 4-AP significantly increased the amplitudes and incidence of induced SPW-Rs without significantly changing their ripple frequency. alpha-Dendrotoxin or BDS-I did not mimick these changes suggesting that 4-AP acts via Kv1.4 channels. Thus, the incidence of SPW-Rs, but not the ripple frequency is regulated by 4-AP-sensitive potassium currents.
