Tyrosine kinase inhibitors enhance a Ca(2+)‐activated K+ current (IAHP) and reduce IAHP suppression by a metabotropic glutamate receptor agonist in rat dentate granule neurones.

Tyrosine kinases and synaptic transmission

“…Published data on ion channel modification needs to be extended to cell/synaptic function in situ. For example, a Ca 2ϩactivated K ϩ current of hippocampal pyramidal cells is under tonic regulation by PTK and block of this current by mGluRs requires PTK (Abdul-Ghani et al, 1996) which is consistent with biochemical observations (Siciliano et al, 1996). Postsynaptic NMDA receptors can be modified by PTK activity (Lancaster et al, 1995;Yu et al, 1997); although mGluRs might also be the natural stimulus for such an effect, Ca 2ϩ entry through the NMDA receptor channel itself could potentially stimulate PTK activity in dendritic spines.…”

Role of tyrosine phosphorylation in leptin activation of ATP‐sensitive K+ channels in the rat insulinoma cell line CRI‐G1

“…Thus genistein activates the CFTR chloride channel in a number of expression systems (Illek, Fischer, Santos, Widdicombe, Machen & Reenstra, 1995; Yang, Cheng, Wang, Price & Hwang, 1997), whereas orthovanadate inhibits genistein‐induced channel activation (Illek et al 1995). Tyrosine kinase inhibitors are also reported to increase the activity of other channel types including Ca 2+ ‐activated K + channels in smooth muscle cells (Xiong, Burnette & Cheung, 1995) and hippocampal neurones (Abdul‐Ghani, Valiante, Carlen & Pennefather, 1996) and cation channels in leech pressure‐sensitive neurones (Aniksztejn, Catarsi & Drapeau, 1997). In contrast, the activity of voltage‐dependent Ca 2+ channels is reduced by tyrosine kinase inhibitors in GH 3 pituitary cells (Cataldi et al .…”

SK channels and the varieties of slow after‐hyperpolarizations in neurons

“…The hippocampal sAHP is suppressed by monoamines and peptides that act via cyclic adenosine monophosphate (cAMP) and protein kinase A (Madison & Nicoll, 1986; Nicoll, 1988; Storm, 1990; Pedarzani & Storm, 1993; Haug & Storm, 2000; Storm et al ., 2000), and by muscarinic receptors at least partly via calcium–calmodulin‐dependent protein kinase II (CaMKII) (Müller et al ., 1992; Pedarzani & Storm, 1996). The modulation by metabotropic glutamate receptors has been reported to require tyrosine kinase (Abdul‐Ghani et al ., 1996), whereas an unconventional metabotropic inhibition of the sAHP by kainate receptors seems to be mediated by PKC (Melyan et al ., 2002). Similar modulation of the sAHP has also been found in other central neurons, including human neocortical cells (McCormick & Williamson, 1989; see Table 1).…”