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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