1. 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 [Journal] .

NeuronCompartmentPropertyConnectivityNotes
Hippocampus CA3 pyramidal GLU 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, 19971 ). 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]2 ). 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]3 ).
Hippocampus CA3 pyramidal GLU 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, 19971 ). 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]2 ). 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]3 ).
Hippocampus CA3 pyramidal GLU 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, 19971 ). 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]2 ). 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]3 ).
Hippocampus CA3 pyramidal GLU 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, 19971 ). 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]2 ). 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]3 ).

Classical References: first publications on each compartmental property; search PubMed for complete list
1.  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 [Journal] .
2.  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] .
3.  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.