| 81 |
|
| 82 |
|
| 83 |
|
| 84 |
|
| 85 |
|
| 86 |
|
| 87 |
|
| 88 |
|
| 89 |
|
| 90 |
|
| 91 |
|
| 92 |
|
| 93 |
|
| 94 |
|
| 95 |
|
| 96 |
|
| 97 |
|
| 98 |
|
| 99 |
|
| 100 |
|
| 101 |
[ed. note: These data disagree on the presence of NMDA receptors in the soma. For a full description of the properties of NMDA receptors in CA3 pyramidal neurons, please see the apical dendritic compartments.] Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively |
| 102 |
[ed. note: we are not aware of glutamatergic synapses onto the soma] Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively |
| 103 |
1990) causing hyperpolarization, and presynaptic GABAb receptors causing enhancement of synaptic inhibition (Cameron and Williams, 1993). (Reviewed in |
| 104 |
2 types: one is a slow I AHP type current; weak in LGN, strong in peritenial; the other is fast. |
| 105 |
5-HT excites 5-HT2 receptors in interneurons and 5-HT1C receptors in pyramidal neurons |
| 106 |
5HT increases excitability and input resistance |
| 107 |
90% of cat brainstem input to LGN is cholinergic |
| 108 |
A 40-50% reduction in a small fraction of (peri-) somatic synapses with large or complex postsynaptic structure after kindling has been found. This functionally relevant reduction may be related to the loss of a specific class of interneurons, and could underlie the enhanced seizure susceptibility after kindling epileptogenesis |
| 109 |
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 |
| 110 |
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 |
| 111 |
A D-type potassium current is involved in dendritic calcium spikes initiation and repolarization |
| 112 |
A distinction was made between axon-bearing and axon-lacking dendrites. |
| 113 |
a fast voltage activated potassium current that generates the afterhyperpolarization following a fast spike." (data from |
| 114 |
A linear increase has been found (9 pA/100um) in the density of these channels with distance from soma. It was suggested that this generates site independence of EPSP time course |
| 115 |
A long duration component of the spike afterhyperpolarization determined the period of the oscillation and was generated by an apamin-sensitive calcium-activated potassium current..” |
| 116 |
A non-inactivating, Ca-independent, K+ current may limit the amplitude of membrane depolarizations associated with prolonged excursions into the depolarized state |
| 117 |
A persistent sodium current was the source of current during the depolarizing phase of the oscillation.” |
| 118 |
A shift toward more depolarized potentials of the activation curve has also been observed in mid and distal dendrites (more than 100um) |
| 119 |
A single-electrode voltage-clamp technique was employed on slices to examine slow AHP. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+ close to that predicted by the Nernst equation. It could be blocked by Cd2+ or norepinephrine, showed a requirement for voltage-dependent Ca2+ entry, but did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential |
| 120 |
A slow, noninactivating current may have a role to define the limits on the depolarized state, and to govern the spike discharge characteristics once the depolarized state has been reached |
