Intracellular calcium ion dynamics involved in long-term potentiation in hippocampal CA1 neurons in mice lacking the IP3 type 1 receptor

• Published in: Neuroscience research Vol. 67; no. 2; pp. 149 - 155
• Main Authors: Yoshioka, Masatomo, Yamazaki, Yoshihiko, Fujii, Satoshi, Kaneko, Kenya, Kato, Hiroshi, Mikoshiba, Katsuhiko
• Format: Journal Article
• Language: English
• Published: Ireland 01-06-2010
• Subjects: Animals; Animals, Newborn; Biophysics; CA1 Region, Hippocampal - cytology; Calcium - metabolism; Electric Stimulation - methods; Excitatory Amino Acid Antagonists - pharmacology; In Vitro Techniques; Inositol 1,4,5-Trisphosphate Receptors - deficiency; Intracellular Fluid - metabolism; Long-Term Potentiation - genetics; Long-Term Potentiation - physiology; Mice; Mice, Knockout; Neurons - metabolism; Valine - analogs & derivatives; Valine - pharmacology
• ISSN: 0168-0102; 1872-8111
• DOI: 10.1016/j.neures.2010.03.002

In the present study, mice lacking the type 1 inositol-1,4,5-trisphosphate receptor (IP(3)R) were used to study the role of type 1 IP(3)Rs in the induction of long-term potentiation (LTP) in hippocampal CA1 neurons. The magnitude of the LTP induced by high frequency stimulation (HFS) consisting of 20 pulses at 30Hz in mice lacking type 1 IP(3)Rs was significantly larger than that in wild-type mice in terms of the field excitatory postsynaptic potential and population spike. By measuring changes in the intracellular Ca(2+) concentration ([Ca(2+)](i)) in CA1 pyramidal neurons using fluorometry, we found that the decay time of the transient increase in the [Ca(2+)](i) evoked by the HFS in mutant mice was significantly longer than that in wild-type mice, whereas the [Ca(2+)](i) at rest and the magnitude of the [Ca(2+)](i) increases caused by the HFS were no different from those in wild-type mice. In slices from the mutant mice, paired-pulse stimulation (PPS) delivered at an interval of 10ms resulted in significantly weaker paired-pulse inhibition (PPI) than in wild-type mice, suggesting that lack of type 1 IP(3)Rs reduces the PPI induced by PPS in the CA1 region. These results indicate that a lack of type 1 IP(3)Rs causes a slower decay of the transient [Ca(2+)](i) in CA1 pyramidal neurons and attenuates the activity of inhibitory interneurons, resulting in enhancement of LTP induction.