162. Klee R, Ficker E and Heinemann U. (1995) Comparison of voltage-dependent potassium currents in rat pyramidal neurons acutely isolated from hippocampal regions CA1 and CA3. J Neurophysiol 74:1982-95 [Journal] .

NeuronCompartmentPropertyConnectivityNotes
Hippocampus CA1 pyramidal cellSomaI K.The properties of voltage-gated potassium currents were studied in acutely isolated rat cells from area CA1 and CA3 at postnatal ages of day 6-8, 9-14, and 26-29 (P6-8, P9-14, and P26-29) with the use of the whole cell version of the patch-clamp technique. In CA1 cells IK was blocked by TEA at +30 mV with an IC50 of 0.98 mM. In CA3 cells the corresponding IC50 value was 1.05 mM. About 20% of IK were insensitive to TEA. IK was partially blocked by approximately 30% with 100 microM 4-AP. Mast cell degranulating peptide (100-200 nM) and dendrotoxin (50-300 nM) had no effect on IK. IK was upregulated with increasing postnatal age. This increase in the expression of IK was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat ]162 ).
Hippocampus CA3 pyramidal cellDistal apical dendriteI K.Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997164 ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a I(K) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat ]162 ). A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which may correspond to I(K) channels) is concentrated in the dendrites of CA3 neurons (Sheng M et al, 1994 [rat ]173 ).
Hippocampus CA3 pyramidal cellMiddle apical dendriteI K.Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997164 ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat ]162 ). A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which probably corresponds to I(K) channels) is concentrated in the dendrites of CA3 neurons (Sheng M et al, 1994 [rat ]173 ).
Hippocampus CA3 pyramidal cellSomaI K.Bath application of Pb2+ shifted the neurons'' current-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997164 ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a I(K) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat ]162 ). A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which may correspond to I(K) channels) is concentrated in the dendrites of CA3 neurons (Sheng M et al, 1994 [rat ]173 ).
Hippocampus CA3 pyramidal cellProximal apical dendriteI K.Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997164 ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat ]162 ). A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which probably corresponds to I(K) channels) is concentrated in the dendrites of CA3 neurons (Sheng M et al, 1994 [rat ]173 ).

References
162. Klee R, Ficker E and Heinemann U. (1995) Comparison of voltage-dependent potassium currents in rat pyramidal neurons acutely isolated from hippocampal regions CA1 and CA3. J Neurophysiol 74:1982-95 [Journal] .
164. Madeja M, Musshoff U, Binding N, Witting U and Speckmann EJ. (1997) Effects of Pb2+ on delayed-rectifier potassium channels in acutely isolated hippocampal neurons. J Neurophysiol 78:2649-54.
173. Sheng M, Tsaur ML, Jan YN and Jan LY. (1994) Contrasting subcellular localization of the Kv1.2 K+ channel subunit in different neurons of rat brain. J Neurosci 14:2408-17.
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