Cyclic AMP-dependent attenuation of oscillatory-activity-induced intercortical strengthening of horizontal pathways between insular and parietal cortices.
Cyclic AMP (cAMP) is a key intracellular second messenger, and the intracellular cAMP signaling pathway acts to modulate various brain functions. We have previously reported that low-frequency insular cortex stimulation in rat brain slices switches on a voltage oscillator in the parietal cortex that delivers signals horizontally back and forth under caffeine application. The oscillatory activities are N-methyl-D-aspartate (NMDA) receptor-dependent, and the role of oscillation is to strengthen functional intercortical connections. The present study investigated actions of the cAMP signaling pathway on caffeine-induced strengthening of intercortical connections and tried to confirm the role of oscillation on intercortical strengthening by focusing on the cAMP pathway. After induction of parietal oscillation by insular cortex stimulation in caffeine-containing medium, application of membrane-permeable cAMP analog, bromo-cAMP, diminished oscillatory signal delivery from the parietal cortex, but initial insulo-parietal signal propagation remained strong. When oscillatory activities were reduced with co-application of caffeine and bromo-cAMP from the beginning, initial insulo-parietal propagation was established, but amplitudes of propagating wavelets and propagating velocity were reduced. Thus, cAMP-dependent diminution of caffeine-induced NMDA-receptor-dependent oscillatory signal delivery causes attenuation of intercortical strengthening of horizontal pathways between insular and parietal cortices. This finding suggests that the intracellular cAMP signaling pathway has the ability to regulate extracellular communications at the network level, and also that full expression of strengthened intercortical signal communication requires sufficient NMDA-receptor-dependent oscillatory neural activities.
Yoshimura
Hiroshi
H
Department of Oral and Maxillofacial Surgery, Kanazawa Medical University, Ishikawa 920-0293, Japan. hyoshimu@kanazawa-med.ac.jp
Honjo
Makoto
M
Segami
Natsuki
N
Kaneyama
Keiseki
K
Sugai
Tokio
T
Mashiyama
Yuichi
Y
Onoda
Norihiko
N
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D000818:Animals; D000831:Animals, Newborn; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology*; D002110:Caffeine / Q000494:pharmacology; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D000242:Cyclic AMP / Q000502:physiology*; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D051381:Rats; D017208:Rats, Wistar; D012236:Rhodanine / Q000031:analogs & derivatives; D053778:Thiazolidines; D013997:Time Factors
D000697:Central Nervous System Stimulants; D018691:Excitatory Amino Acid Antagonists; D053778:Thiazolidines; D015124:8-Bromo Cyclic Adenosine Monophosphate; D002110:Caffeine; D015763:2-Amino-5-phosphonovalerate; C029653:NK 2761; D012236:Rhodanine; D000242:Cyclic AMP