@article {45923, title = {Action potential initiation and backpropagation in neurons of the mammalian CNS.}, journal = {Trends Neurosci}, volume = {20}, year = {1997}, month = {1997 Mar}, pages = {125-31}, abstract = {

Most neurons in the mammalian CNS encode and transmit information via action potentials. Knowledge of where these electrical events are initiated and how they propagate within neurons is therefore fundamental to an understanding of neuronal function. While work from the 1950s suggested that action potentials are initiated in the axon, many subsequent investigations have suggested that action potentials can also be initiated in the dendrites. Recently, experiments using simultaneous patch-pipette recordings from different locations on the same neuron have been used to address this issue directly. These studies show that the site of action potential initiation is in the axon, even when synaptic activation is powerful enough to elicit dendritic electrogenesis. Furthermore, these and other studies also show that following initiation, action potentials actively backpropagate into the dendrites of many neuronal types, providing a retrograde signal of neuronal output to the dendritic tree.

}, keywords = {Action Potentials, Animals, Central Nervous System, Neurons}, issn = {0166-2236}, author = {Stuart, G and Spruston, N and Sakmann, B and H{\"a}usser, M} } @article {45913, title = {Activity-dependent action potential invasion and calcium influx into hippocampal CA1 dendrites.}, journal = {Science}, volume = {268}, year = {1995}, month = {1995 Apr 14}, pages = {297-300}, abstract = {

The temporal and spatial profile of activity-evoked changes in membrane potential and intracellular calcium concentration in the dendrites of hippocampal CA1 pyramidal neurons was examined with simultaneous somatic and dendritic patch-pipette recording and calcium imaging experiments. Action potentials are initiated close to the soma of these neurons and backpropagate into the dendrites in an activity-dependent manner; those occurring early in a train propagate actively, whereas those occurring later fail to actively invade the distal dendrites. Consistent with this finding, dendritic calcium transients evoked by single action potentials do not significantly attenuate with distance from the soma, whereas those evoked by trains attenuate substantially. Failure of action potential propagation into the distal dendrites often occurs at branch points. Consequently, neighboring regions of the dendritic tree can experience different voltage and calcium signals during repetitive action potential firing. The influence of backpropagating action potentials on synaptic integration and plasticity will therefore depend on both the extent of dendritic branching and the pattern of neuronal activity.

}, keywords = {Action Potentials, Animals, Calcium, Calcium Channels, Dendrites, Ion Channel Gating, Neuronal Plasticity, Patch-Clamp Techniques, Pyramidal Cells, Rats, Rats, Wistar, Sodium Channels, Synapses, Tetrodotoxin}, issn = {0036-8075}, author = {Spruston, N and Schiller, Y and Stuart, G and Sakmann, B} } @article {45893, title = {Dendritic glutamate receptor channels in rat hippocampal CA3 and CA1 pyramidal neurons.}, journal = {J Physiol}, volume = {482 ( Pt 2)}, year = {1995}, month = {1995 Jan 15}, pages = {325-52}, abstract = {

1. Properties of dendritic glutamate receptor (GluR) channels were investigated using fast application of glutamate to outside-out membrane patches isolated from the apical dendrites of CA3 and CA1 pyramidal neurons in rat hippocampal slices. CA3 patches were formed (15-76 microns from the soma) in the region of mossy fibre (MF) synapses, and CA1 patches (25-174 microns from the soma) in the region of Schaffer collateral (SC) innervation. 2. Dual-component responses consisting of a rapidly rising and decaying component followed by a second, substantially slower, component were elicited by 1 ms pulses of 1 mM glutamate in the presence of 10 microM glycine and absence of external Mg2+. The fast component was selectively blocked by 2-5 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the slow component by 30 microM D-2-amino-5-phosphonopentanoic acid (D-AP5), suggesting that the fast and slow components were mediated by the GluR channels of the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and NMDA type, respectively. The peak amplitude ratio of the NMDA to AMPA receptor-mediated components varied between 0.03 and 0.62 in patches from both CA3 and CA1 dendrites. Patches lacking either component were rarely observed. 3. The peak current-voltage (I-V) relationship of the fast component was almost linear, whereas the I-V relationship of the slow component showed a region of negative slope in the presence of 1 mM external Mg2+. The reversal potential for both components was close to 0 mV. 4. Kainate-preferring GluR channels did not contribute appreciably to the response to glutamate. The responses to 100 ms pulses of 1 mM glutamate were mimicked by application of 1 mM AMPA, whereas 1 mM kainate produced much smaller, weakly desensitizing currents. This suggests that the fast component is primarily mediated by the action of glutamate on AMPA-preferring receptors. 5. The mean elementary conductance of AMPA receptor channels was about 10 pS, as estimated by non-stationary fluctuation analysis. The permeability of these channels to Ca2+ was low (approximately 5\% of the permeability to Cs+). 6. The elementary conductance of NMDA receptor channels was larger, with a main conductance state of about 45 pS. These channels were 3.6 times more permeable to Ca2+ than to Cs+.(ABSTRACT TRUNCATED AT 400 WORDS)

}, keywords = {2-Amino-5-phosphonovalerate, 6-Cyano-7-nitroquinoxaline-2,3-dione, alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid, Animals, Calcium, Cell Membrane Permeability, Dendrites, Electric Conductivity, Hippocampus, Kainic Acid, Magnesium, Patch-Clamp Techniques, Pyramidal Cells, Rats, Rats, Wistar, Receptors, AMPA, Receptors, N-Methyl-D-Aspartate, Time Factors, Zinc}, issn = {0022-3751}, author = {Spruston, N and Jonas, P and Sakmann, B} }