Amphetamine-produced convulsive (bursting) firings in the neuron of the giant African snail Achatina fulica: Effects of inhibitors of phosphodiesterases

• Published in: Journal of evolutionary biochemistry and physiology 2006-03, Vol.42 (2), p.166-173
• Main Authors: Lin, CH, Lin, P J, Chen, I M, Chen, Y H, Lin, P L, Zhuravlev, V L, Tsai, M C
• Format: Article
• Language: English
• Subjects: Achatina fulica; Amphetamines; Kinases; Proteins
• ISSN: 0022-0930; 1608-3202
• DOI: 10.1134/S0022093006020086

Effects of inhibitors of phosphodiesterases (PDE) on bursting activity, produced by d-amphetamine (d-AM) was studied in PPa4 neurons of the giant African snail Achatina fulica F. Action of the following PDE inhibitors was analyzed: vinpocetine (selective to PDE I), erythro-9-(2-hydroxi-3-nonyl) adenine (EHNA; selective to PDE 2), milrinone (selective to PDE 3), rolipram (selective to PDE 4), sildenafil citrate (Viagra^sup @^; selective to PDE 5), and caffeine, a non-selective phosphodiesterase inhibitor. Amphetamine at a low concentration (67.5 × 10^sup -5^ M) did not produce the bursting firing in the neurons; however, the convulsive activity appeared on addition to this solution of any if the PDE inhibitors except for sildenafil. Forskolin (an adenylyl cyclase activator, 10^sup -4^ M) also decreased the neuronal threshold to the d-AM action. The bursting activity produced by d-AM did not develop after a previous administration of the protein kinase A inhibitor KT-5720. The phospholipase C blocker U73122 had no effect on the bursting activity produced by d-AM. It is concluded that the neuronal convulsive activity induced by d-AM is associated with the phosphodiesterase activity.[PUBLICATION ABSTRACT]