PMID- 8841999
OWN - NLM
STAT- MEDLINE
DCOM- 19961220
LR  - 20190512
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 494 ( Pt 2)
IP  - Pt 2
DP  - 1996 Jul 15
TI  - Activity dependence and functional role of the apamin-sensitive K+ current in rat 
      supraoptic neurones in vitro.
PG  - 389-98
AB  - 1. Intracellular recordings were obtained from seventy-two magnocellular 
      neurosecretory cells (MNCs) in superfused explants of rat hypothalamus. The 
      current underlying the after-hyperpolarization (IAHP) following spike-evoked 
      trains of action potentials was characterized using the hybrid-clamp technique. 
      The activity-dependent requirements for the genesis of the AHP were determined. 
      The functional role of the conductance was investigated using saturating 
      concentrations (50-300 nM) of apamin, a selective blocker of the AHP in MNCs. 2. 
      IAHP was reversibly abolished by the removal of extracellular Ca2+. The amplitude 
      of IAHP varied linearly as a function of voltage and reversed at -100 +/- 3 mV in 
      3 mM external K+. Changes in the concentration of extracellular K+ resulted in 
      shifts of the reversal potential consistent with Nernst equation predictions for 
      a K+-selective conductance. 3. Action potentials triggered by brief depolarizing 
      pulses elicited an AHP during trains evoked at frequencies > 1 Hz. Onset of the 
      AHP progressed exponentially, reaching a maximum after the first fifteen to 
      twenty impulses. The steady-state amplitude of the AHP increased logarithmically 
      between 1 and 20 Hz. 4. Switching to voltage clamp during periods of continuous 
      cell activity (firing rate > 4 Hz) confirmed the presence of an apamin-sensitive 
      Ca2(+)-dependent K+ current. 5. Application of apamin produced a threefold 
      increase in the mean firing rate of spontaneously active cells, but was without 
      effect when applied to silent cells (firing rate < 0.5 Hz). 6. Apamin did not 
      affect the ability of MNCs to fire in a phasic manner but caused a dramatic 
      increase in the mean intraburst firing rate. Moreover, inhibition of IAHP by 
      apamin strongly attenuated spike accommodation normally seen at the onset of 
      phasic bursts. 7. While apamin did not enhance the amplitude of depolarizing 
      after-potentials following single spikes, post-train plateau potentials and 
      associated after-discharges were enhanced. 8. The possible consequences of IAHP 
      modulation are discussed in the context of the regulation of firing rate and 
      pattern in MNCs.
FAU - Kirkpatrick, K
AU  - Kirkpatrick K
AD  - Centre for Research in Neuroscience, Montreal General Hospital, Quebec, Canada.
FAU - Bourque, C W
AU  - Bourque CW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Potassium Channels)
RN  - 24345-16-2 (Apamin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Action Potentials/drug effects
MH  - Animals
MH  - Apamin/*pharmacology
MH  - Calcium/pharmacology
MH  - Electric Stimulation
MH  - Kinetics
MH  - Male
MH  - Neurons/drug effects/*physiology
MH  - Neurosecretory Systems
MH  - Organ Culture Techniques
MH  - Patch-Clamp Techniques
MH  - Potassium Channels/drug effects/*physiology
MH  - Rats
MH  - Supraoptic Nucleus/*physiology
MH  - Time Factors
PMC - PMC1160642
EDAT- 1996/07/15 00:00
MHDA- 1996/07/15 00:01
PMCR- 1996/07/15
CRDT- 1996/07/15 00:00
PHST- 1996/07/15 00:00 [pubmed]
PHST- 1996/07/15 00:01 [medline]
PHST- 1996/07/15 00:00 [entrez]
PHST- 1996/07/15 00:00 [pmc-release]
AID - 10.1113/jphysiol.1996.sp021500 [doi]
PST - ppublish
SO  - J Physiol. 1996 Jul 15;494 ( Pt 2)(Pt 2):389-98. doi: 
      10.1113/jphysiol.1996.sp021500.