436. Mickus T, Jung H and Spruston N. (1999) Properties of slow, cumulative sodium channel inactivation in rat hippocampal CA1 pyramidal neurons. Biophys J 76:846-60.

NeuronCompartmentPropertyConnectivityNotes
Hippocampus CA1 pyramidal cellSomaI Na,t.Patch recordings yield an approximate channel density of 45 pS/micron^2 (compared with 28 pS/micron^2 in dendrites) in juvenile rats < 4 wks of age, rising modestly to 56 pS/micron^2 (compared with 61 pS/micron^2 in dendrites) in older rats (Magee JC and Johnston D, 1995 [rat ]140 ). Tsubokawa H et al, 2000180 . Recordings using the intracellular perfusion method showed no differences between the I-V characteristics of CA1 and CA3 neurones for this current. In contrast to this, the steady-state inactivation of both types of neurones was significantly different (Steinhäuser C et al, 1990 [rats ]292 ). Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 1997435 ). Slow inactivation of sodium channels in dendrites and soma will modulate neuronal excitability in a way that depends in a complicated manner on the resting potential and previous history of action potential firing (Mickus T et al, 1999436 ).
Hippocampus CA1 pyramidal cellDistal apical dendriteI Na,t.Na impulses may underly "fast prepotentials" that boost distal EPSPs (Spencer WA and Kandel ER, 196175 ). Na action potentials support backpropagating impulses (Spruston N et al, 1995 [mammal ]57 ), and can activate Ca action potentials (Spruston N et al, 1995 [mammal ]57 ). Patch recordings yield an approximate channel density of 28 pS/micron^2 in juvenile rats < 4 wks of age, rising to 61 pS/micron^2 in older rats. Channel density was similar in other dendritic compartments (Magee JC and Johnston D, 1995 [rat ]140 ). Tsubokawa H et al, 2000180 . Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 1997435 ). Slow inactivation of sodium channels in dendrites and soma will modulate neuronal excitability in a way that depends in a complicated manner on the resting potential and previous history of action potential firing (Mickus T et al, 1999436 ). Single action potential backpropagations show dichotomy of either strong attenuation (26-42%) or weak attenuation (71-87%). The dichotomy seems to be conferred primarily by differences in distribution, density, etc. of voltage dependent sodium and potassium channel (A-type, especially ) along the somatodendritic axis (Golding NL et al, 2001439 )
Hippocampus CA1 pyramidal cellMiddle apical dendriteI Na,t.Na impulses may underly "fast prepotentials" that boost distal EPSPs (Spencer WA and Kandel ER, 196175 ). Na action potentials support backpropagating impulses (Spruston N et al, 1995 [mammal ]57 ), and can activate Ca action potentials (Spruston N et al, 1995 [mammal ]57 ). Patch recordings yield an approximate channel density of 28 pS/micron^2 in juvenile rats < 4 wks of age, rising to 61 pS/micron^2 in older rats. Channel density was similar in other dendritic compartments (Magee JC and Johnston D, 1995 [rat ]140 ). Tsubokawa H et al, 2000180 . Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 1997435 ). Slow inactivation of sodium channels in dendrites and soma will modulate neuronal excitability in a way that depends in a complicated manner on the resting potential and previous history of action potential firing (Mickus T et al, 1999436 ). Dendritic can fire sodium spikes that can precede somatic action potentials (APs), the probability and amplitude of which depend on previous synaptic and firing history. Some dendritic spikes could occur in the absense of somatic APs, indicating that their propagation to soma is unreliable (Golding NL and Spruston N, 1998437 ). Single action potential backpropagations show dichotomy of either strong attenuation (26-42%) or weak attenuation (71-87%). The dichotomy seems to be conferred primarily by differences in distribution, density, etc. of voltage dependent sodium and potassium channel (A-type, especially ) along the somatodendritic axis (Golding NL et al, 2001439 )
Hippocampus CA1 pyramidal cellProximal apical dendriteI Na,t.Na impulses may underly "fast prepotentials" that boost distal EPSPs (Spencer WA and Kandel ER, 196175 ). Na action potentials support backpropagating impulses (Spruston N et al, 1995 [mammal ]57 ), and can activate Ca action potentials (Spruston N et al, 1995 [mammal ]57 ). Patch recordings yield an approximate channel density of 28 pS/micron^2 in juvenile rats < 4 wks of age, rising to 61 pS/micron^2 in older rats. Channel density was similar in other dendritic compartments (Magee JC and Johnston D, 1995 [rat ]140 ). However, channel density varied widely in the proximal compartment, possibly indicating the presence of hot spots. Tsubokawa H et al, 2000180 . Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 1997435 ). Slow inactivation of sodium channels in dendrites and soma will modulate neuronal excitability in a way that depends in a complicated manner on the resting potential and previous history of action potential firing (Mickus T et al, 1999436 ). Single action potential backpropagations show dichotomy of either strong attenuation (26-42%) or weak attenuation (71-87%). The dichotomy seems to be conferred primarily by differences in distribution, density, etc. of voltage dependent sodium and potassium channel (A-type, especially ) along the somatodendritic axis (Golding NL et al, 2001439 )

References
140. Magee JC and Johnston D. (1995) Characterization of single voltage-gated Na+ and Ca2+ channels in apical dendrites of rat CA1 pyramidal neurons. J Physiol 487 ( Pt 1):67-90.
180. Tsubokawa H, Offermanns S, Simon M and Kano M. (2000) Calcium-dependent persistent facilitation of spike backpropagation in the CA1 pyramidal neurons. J Neurosci 20:4878-84.
292. Steinhäuser C, Tennigkeit M, Matthies H and Gündel J. (1990) Properties of the fast sodium channels in pyramidal neurones isolated from the CA1 and CA3 areas of the hippocampus of postnatal rats. Pflugers Arch 415:756-61.
435. Jung HY, Mickus T and Spruston N. (1997) Prolonged sodium channel inactivation contributes to dendritic action potential attenuation in hippocampal pyramidal neurons. J Neurosci 17:6639-46.
436. Mickus T, Jung H and Spruston N. (1999) Properties of slow, cumulative sodium channel inactivation in rat hippocampal CA1 pyramidal neurons. Biophys J 76:846-60.
75. Spencer WA and Kandel ER. (1961) ELECTROPHYSIOLOGY OF HIPPOCAMPAL NEURONS: IV. FAST PREPOTENTIALS. J Neurophysiol 24:272-85.
57. Spruston N, Schiller Y, Stuart G and Sakmann B. (1995) Activity-dependent action potential invasion and calcium influx into hippocampal CA1 dendrites. Science 268:297-300.
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437. Golding NL and Spruston N. (1998) Dendritic sodium spikes are variable triggers of axonal action potentials in hippocampal CA1 pyramidal neurons. Neuron 21:1189-200.
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