192. Bekkers JM. (2000) Distribution of slow AHP channels on hippocampal CA1 pyramidal neurons. J Neurophysiol 83:1756-9 [Journal] .

NeuronCompartmentPropertyConnectivityNotes
Hippocampus CA1 pyramidal cellSomaI K,Ca.A single-electrode voltage-clamp technique was employed on slices to examine slow AHP. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+ close to that predicted by the Nernst equation. It could be blocked by Cd2+ or norepinephrine, showed a requirement for voltage-dependent Ca2+ entry, but did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential (Lancaster B and Adams PR, 1986191 ). Cell-attached patches on the proximal 100um of the apical dendrite did not contain sAHP channels. Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the sAHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids (Bekkers JM, 2000192 ). In situ hybridization of three cloned SK channel subunits (SK1-3), the prime candidates likely to underlie Ca(2+)-dependent AHPs showed high levels of expression in regions presenting prominent AHP currents including CA1-3 regions of the hippocampus (SK1 and SK2), reticularis thalami (SK1 and SK2), supraoptic nucleus (SK3), and inferior olivary nucleus (SK2 and SK3) (Stocker M and Pedarzani P, 2000193 ). The role of large-conductance Ca2+-dependent K+ channels (BK) in spike broadening during repetitive firing was studied using sharp electrode and computer modelling. The amplitude of the fast after-hyperpolarization (fAHP) rapidly declined during each train. Suppression of BK-channel activity with the selective BK-channel blocker iberiotoxin, the non-peptidergic BK-channel blocker paxilline, or calcium-free medium, broadened the 1st spike to a similar degree ( approximately 60 %) (Shao LR et al, 1999 [rat ]194 ).
Hippocampus CA1 pyramidal cellDistal basal dendriteI K,Ca.Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the slow AHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids (Bekkers JM, 2000192 ).

References
191. Lancaster B and Adams PR. (1986) Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons. J Neurophysiol 55:1268-82 [Journal] .
192. Bekkers JM. (2000) Distribution of slow AHP channels on hippocampal CA1 pyramidal neurons. J Neurophysiol 83:1756-9 [Journal] .
193. Stocker M and Pedarzani P. (2000) Differential distribution of three Ca(2+)-activated K(+) channel subunits, SK1, SK2, and SK3, in the adult rat central nervous system. Mol Cell Neurosci 15:476-93.
194. Shao LR, Halvorsrud R, Borg-Graham L and Storm JF. (1999) The role of BK-type Ca2+-dependent K+ channels in spike broadening during repetitive firing in rat hippocampal pyramidal cells. J Physiol 521 Pt 1:135-46.
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