Hippocampus CA1 pyramidal GLU cell

- - HG - Hip - CA1 - PRINC - pyramidal - - glu
Properties are:  Present   Absent 
Input Receptors
Intrinsic Currents
Output Transmitters
Distal apical dendrite
Perforant pathway entorhinal pyramidal neuron terminals (T) Glutamate
Glutamate is commonly believed to be the primary excitatory neurotransmitter in the hippocampal formation generally (reviewed in Cotman et al., 1995), and in CA1 in particular (Storm-Mathisen J, 19771 ). (Randall AD and Collingridge GL, 19922 ). CA1 pyramidal neurons increase their firing (recorded extracellularly) in response to ionophoresed Glu within their apical dendritic fields or in the cell body layer (Dudar 1974 PMID#4437726).(Magee JC and Cook EP, 20003 ).
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
--- 		Gaba
Labeling for glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA, is heavy in the molecular layer of CA1 (Storm-Mathisen J, 19771 ). cited in Johnston and Amaral, 1998).
AMPA
EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse (He Y et al, 19985 ). Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA and NMDA receptors, respectively (Spruston N et al, 199512 ).
NMDA
The way that different parts of a neuron carry out multiple information processing roles is illustrated by the CA1 pyramidal cell in the hippocampus. The authors used 2-photon microscopy to obtain high resolution images of calcium signals in the apical dendrites while activating Schaffer collateral inputs to induce long-term potentiation (LTP) of different durations. Short-duration LTP (LTP 1) was associated with Ca increase in dendritic spines, due to activation of NMDA receptors and local ryanodine receptors (RyRs). Intermediate duration LTP (LTP 2) was associated with Ca increase in dendritic branches, due to activation of NMDA receptors and local IP3 receptors (IP3Rs). For Ca increase in long duration LTP (LTP3), see Ca channels in CA1 pyramidal cell apical dendrite. ...(Raymond CR and Redman SJ, 20064 ). EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse (He Y et al, 19985 ). Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA and NMDA receptors, respectively (Spruston N et al, 199512 ).
I A
A-current is reduced in the presence of amyloid-beta (Chen C, 200514 ). Patch-clamp recordings reveal a high density of A-type K channels in the dendritic tree, which increases with distance from the soma (Hoffman DA et al, 1997 [rat]13 ). A shift toward more depolarized potentials of the activation curve has also been observed in mid and distal dendrites (more than 100um) (Hoffman DA et al, 1997 [rat]13 ). These channels "prevent initiation of an action potential in the dendrites, limit the backpropagation of action potentials into the dendrites, and reduce excitatory synaptic events" (Hoffman DA et al, 1997 [rat]13 ). 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, 200115 ). CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 ?M) can convert neurons in both regions into firing bursting action potentials (Staff NP et al, 200016 ).
I p,q
action potential-mediated depolarization can...result in the elevation of dendritic intracellular Ca concentration (Regehr et al 1989, (Jaffe DB et al, 199229 ). which is important for the induction of long term changes in synaptic strength" (Spruston N et al, 1995 [mammal]30 ).
I T low threshold
Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density (Magee JC and Johnston D, 1995 [rat]22 ). However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the soma than in the dendrites (Christie BR et al, 199531 ).
I Na,t
Na impulses may underly "fast prepotentials" that boost distal EPSPs (Spencer WA and Kandel ER, 196132 ). Na action potentials support backpropagating impulses (Spruston N et al, 1995 [mammal]30 ). and can activate Ca action potentials (Spruston N et al, 1995 [mammal]30 ). 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]22 ). (Tsubokawa H et al, 200023 ). Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 199725 ). 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, 199926 ). 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, 200115 ).
I L high threshold
Ca fluorescence imaging shows that application of L-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a significantly greater effect in the proximal dendrites than in more distal dendrites (Christie BR et al, 199531 ).
I N
Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines (Mills LR et al, 199427 ).
I h
Membrane patches recorded in the cell-attached patch configuration from the soma and apical dendrites revealed an Ih that increased over sixfold from soma to distal dendrites. Ih demonstrated a mixed Na+-K+ conductance and was sensitive to low concentrations of external CsCl. As a result of Ih the propagation of subthreshold voltage transients is directionally specific.The elevated dendritic Ih density decreases EPSP amplitude and duration and reduces the time window over which temporal summation takes place (Magee JC, 1998 [Rat]40 ).
Middle apical dendrite
Hippocampus CA3 pyramidal GLU cell
 -Axon terminal.Glutamate
NMDA
The way that different parts of a neuron carry out multiple information processing roles is illustrated by the CA1 pyramidal cell in the hippocampus. The authors used 2-photon microscopy to obtain high resolution images of calcium signals in the apical dendrites while activating Schaffer collateral inputs to induce long-term potentiation (LTP) of different durations. Short-duration LTP (LTP 1) was associated with Ca increase in dendritic spines, due to activation of NMDA receptors and local ryanodine receptors (RyRs). Intermediate duration LTP (LTP 2) was associated with Ca increase in dendritic branches, due to activation of NMDA receptors and local IP3 receptors (IP3Rs). For Ca increase in long duration LTP (LTP3), see Ca channels in CA1 pyramidal cell apical dendrite. ...(Raymond CR and Redman SJ, 20064 ). The Schaeffer collateral/commissural pathway elicits EPSPs in CA1 that have an NMDA-receptor mediated component that can be blocked by APV under certain experimental circumstances (such as low bath Mg+ levels). Many authors have suggested that NMDA receptors may be involved in long-term potentiation in this region. (Reviewed in (Randall AD and Collingridge GL, 19922 ). EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse (He Y et al, 19985 ).
Hippocampus CA3 pyramidal GLU cell
 -Axon terminal.Glutamate
AMPA
The Schaeffer collateral/commissural pathway elicits EPSPs in CA1 that have a large AMPA receptor-mediated component that can be blocked by CNQX (Honoré T et al, 1988 [rat]6 ). Reviewed in (Randall AD and Collingridge GL, 19922 ). EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse (He Y et al, 19985 ). Using outside-out patches and a fast application system the properties and distribution of synaptic glutamate receptors an approximately twofold increase in AMPA-mediated current was observed in the dendritic region that receives a uniform density of Schaffer collateral input (100-250um from soma) (Andrasfalvy BK and Magee JC, 20017 ).
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
GabaA
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
GabaB
--- mGluR
Extracelluar ACPD (an mGluR agonist) application to apical or basal dendrites of CA1 pyramidal neurons causes local increases in calcium concentration that propagate throughout the cell, as measured by simultaneous whole cell recording and confocal microscopy with calcium imaging (Jaffe DB and Brown TH, 1994 [rat]8 ). suggesting the presence of mGluRs. (Bashir ZI et al, 19939 ). provide evidence that activation of these receptors is necessary for LTP induction .
Glutamate
(Magee JC and Cook EP, 20003 ).
I Potassium
A D-type potassium current is involved in dendritic calcium spikes initiation and repolarization (Golding NL et al, 199921 ).
I A
A-current is reduced in the presence of amyloid-beta (Chen C, 200514 ). Patch-clamp recordings reveal a high density of A-type K channels in the dendritic tree, which increases with distance from the soma (Hoffman DA et al, 1997 [rat]13 ). A shift toward more depolarized potentials of the activation curve has also been observed in mid and distal dendrites (more than 100um) (Hoffman DA et al, 1997 [rat]13 ). These channels "prevent initiation of an action potential in the dendrites, limit the backpropagation of action potentials into the dendrites, and reduce excitatory synaptic events" (Hoffman DA et al, 1997 [rat]13 ). 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, 200115 ). CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 µM) can convert neurons in both regions into firing bursting action potentials (Staff NP et al, 200016 ).
I p,q
action potential-mediated depolarization can...result in the elevation of dendritic intracellular Ca concentration (Regehr et al 1989, (Jaffe DB et al, 199229 ). which is important for the induction of long term changes in synaptic strength" (Spruston N et al, 1995 [mammal]30 ).
I Na,t
Na impulses may underly "fast prepotentials" that boost distal EPSPs (Spencer WA and Kandel ER, 196132 ). Na action potentials support backpropagating impulses (Spruston N et al, 1995 [mammal]30 ). and can activate Ca action potentials (Spruston N et al, 1995 [mammal]30 ). 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]22 ). (Tsubokawa H et al, 200023 ). Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 199725 ). 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, 199926 ). 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, 199833 ). 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, 200115 ).
I T low threshold
Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density (Magee JC and Johnston D, 1995 [rat]22 ). However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the dendrites than in the soma (Christie BR et al, 199531 ).
I L high threshold
Ca fluorescence imaging shows that application of L-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a significantly greater effect in the proximal dendrites than in more distal dendrites (Christie BR et al, 199531 ).
Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines (Mills LR et al, 199427 ).
I N
Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines (Mills LR et al, 199427 ).
I h
Membrane patches recorded in the cell-attached patch configuration from the soma and apical dendrites revealed an Ih that increased over sixfold from soma to distal dendrites. Ih demonstrated a mixed Na+-K+ conductance and was sensitive to low concentrations of external CsCl. As a result of Ih the propagation of subthreshold voltage transients is directionally specific.The elevated dendritic Ih density decreases EPSP amplitude and duration and reduces the time window over which temporal summation takes place (Magee JC, 1998 [Rat]40 ).
Proximal apical dendrite
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaB
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaA
GABA(A)-mediated (bicuculline-sensitive) inhibitory responses can be demonstrated in CA1 neurons by extracellular recording (Curtis et al, 1970) and by recording spontaneous synaptic currents (Collingridge, 1984).
CA1 Basket Cell terminals (T) Gaba
The baskets formed by inhibitory basket cells have high concentrations of glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA (Storm-Mathisen J, 19771 ).
--- mGluR
Extracelluar ACPD (an mGluR agonist) application to apical or basal dendrites of CA1 pyramidal neurons causes local increases in calcium concentration that propagate throughout the cell, as measured by simultaneous whole cell recording and confocal microscopy with calcium imaging (Jaffe DB and Brown TH, 1994 [rat]8 ). suggesting the presence of mGluRs. (Lipowsky R et al, 1996 [rat]10 ). provide evidence that activation of these receptors is necessary for LTP induction
Glutamate
(Magee JC and Cook EP, 20003 ).
AMPA
EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse (He Y et al, 19985 ).
NMDA
The way that different parts of a neuron carry out multiple information processing roles is illustrated by the CA1 pyramidal cell in the hippocampus. The authors used 2-photon microscopy to obtain high resolution images of calcium signals in the apical dendrites while activating Schaffer collateral inputs to induce long-term potentiation (LTP) of different durations. Short-duration LTP (LTP 1) was associated with Ca increase in dendritic spines, due to activation of NMDA receptors and local ryanodine receptors (RyRs). Intermediate duration LTP (LTP 2) was associated with Ca increase in dendritic branches, due to activation of NMDA receptors and local IP3 receptors (IP3Rs). For Ca increase in long duration LTP (LTP3), see Ca channels in CA1 pyramidal cell apical dendrite. ...(Raymond CR and Redman SJ, 20064 ). EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse (He Y et al, 19985 ).
I Potassium
A D-type potassium current is involved in dendritic calcium spikes initiation and repolarization (Golding NL et al, 199921 ). CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 µM) can convert neurons in both regions into firing bursting action potentials (Staff NP et al, 200016 ).
I Na,t
Na impulses may underly "fast prepotentials" that boost distal EPSPs (Spencer WA and Kandel ER, 196132 ). Na action potentials support backpropagating impulses (Spruston N et al, 1995 [mammal]30 ). and can activate Ca action potentials (Spruston N et al, 1995 [mammal]30 ). 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]22 ). However, channel density varied widely in the proximal compartment, possibly indicating the presence of hot spots. (Tsubokawa H et al, 200023 ). Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 199725 ). 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, 199926 ). 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, 200115 ).
I p,q
Ca fluorescence imaging shows that application of P-channel antagonists reduces the Ca influx associated with backpropagating action potentials (Storm-Mathisen J, 19771 ). action potential-mediated depolarization can...result in the elevation of dendritic intracellular Ca concentration (Regehr et al 1989, (Jaffe DB et al, 199229 ). which is important for the induction of long term changes in synaptic strength" (Spruston N et al, 1995 [mammal]30 ).
I T low threshold
Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density (Magee JC and Johnston D, 1995 [rat]22 ). However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the dendrites than in the soma (Storm-Mathisen J, 19771 ).
I L high threshold
Using a monoclonal antibody (Westenbroek RE et al, 199034 ). showed that the proximal dendrites and somata of hippocampal neurons label for L-type Ca2+ channels and that these channels tend to cluster near the bases of the neural processes. In patch recordings, "HVA-l channels reminiscent of L-type channels were occasionally encountered primarily in the more proximal dendrites" (and in the soma) (Magee JC and Johnston D, 1995 [rat]22 ). Ca fluorescence imaging shows that application of L-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a significantly greater effect in the proximal dendrites than in more distal dendrites (Christie BR et al, 199531 ).
I h
Membrane patches recorded in the cell-attached patch configuration from the soma and apical dendrites revealed an Ih that increased over sixfold from soma to distal dendrites. Ih demonstrated a mixed Na+-K+ conductance and was sensitive to low concentrations of external CsCl. As a result of Ih the propagation of subthreshold voltage transients is directionally specific.The elevated dendritic Ih density decreases EPSP amplitude and duration and reduces the time window over which temporal summation takes place (Magee JC, 1998 [Rat]40 ).
I A
A-current is reduced in the presence of amyloid-beta (Chen C, 200514 ). Patch-clamp recordings reveal a high density of A-type K channels in the dendritic tree, which increases with distance from the soma (Hoffman DA et al, 1997 [rat]13 ). These channels "prevent initiation of an action potential in the dendrites, limit the backpropagation of action potentials into the dendrites, and reduce excitatory synaptic events" (Hoffman DA et al, 1997 [rat]13 ). 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, 200115 ). CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 µM) can convert neurons in both regions into firing bursting action potentials (Staff NP et al, 200016 ).
I Na,p
Whole-cell somatic recording during TTX application to proximal dendrites suggests the presence of a persistent Na current (Lipowsky R et al, 1996 [rat]10 ).
I N
Ca fluorescence imaging shows that application of N-channel antagonists slightly reduces the Ca influx associated with backpropagating action potentials (Christie BR et al, 199531 ). Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines (Mills LR et al, 199427 ).
NO
Experimental findings support a cascade for induction of homosynaptic, NO-dependent LTD involving activation of guanylyl cyclase, production of guanosine 3',5' cyclic monophosphate and subsequent PKG activation. This process has an additional requirement for release of Ca2+ from ryanodine-sensitive stores (Reyes-Harde M et al, 199946 ).
Distal oblique dendrite
Hippocampus CA3 pyramidal GLU cell
 -Axon terminal.Glutamate
Shaffer collaterals (T) 		Glutamate
The CA1 oblique dendrites (also called radial oblique) are the main target of the Schaffer collaterals from CA3, and are therefore the primary sites of generation of LTP.
I A
The A current increases with distance from the soma normalizes Ca+ signals during AP propagation (Frick A et al, 2003 [rat]17 ). (Gasparini S et al, 2007 [rat]18 ). and (Migliore M et al, 200519 ). Individual branches can function as single integrative compartments where the fast oblique spike contains contributions from NMDA, VGCCs, and the A current (Losonczy A and Magee JC, 2006 [rat]20 ).
Middle oblique dendrite
Hippocampus CA3 pyramidal GLU cell
 -Axon terminal.Glutamate
Shaffer collaterals (T) 		Glutamate
The CA1 oblique dendrites (also called radial oblique) are the main target of the Schaffer collaterals from CA3, and are therefore the primary sites of generation of LTP.
I A
The A current increases with distance from the soma normalizes Ca+ signals during AP propagation (Frick A et al, 2003 [rat]17 ). (Gasparini S et al, 2007 [rat]18 ). and (Migliore M et al, 200519 ). Individual branches can function as single integrative compartments where the fast oblique spike contains contributions from NMDA, VGCCs, and the A current (Losonczy A and Magee JC, 2006 [rat]20 ).
Distal basal dendrite
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaA
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaB
Glutamate
P2
I K,Ca
Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the slow AHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids (Bekkers JM, 200042 ).
Middle basal dendrite
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaA
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaB
Glutamate
P2
I Na,t
Proximal basal dendrite
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaB
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaA
Glutamate
I Na,t
Soma
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaB
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaA
Hippocampus CA1 interneuron basket GABA cell
 -Axon terminal.Gaba
CA1 Basket Cell terminals (T) 		Gaba
The baskets formed by inhibitory basket cells have high concentrations of glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA (Storm-Mathisen J, 19771 ). 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 (Wierenga CJ and Wadman WJ, 1999 [rat]11 ).
AMPA
Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA and NMDA receptors, respectively (Spruston N et al, 199512 ).
NMDA
Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA and NMDA receptors, respectively (Spruston N et al, 199512 ).
I A
Patch-clamp recordings reveal A-type K channels in the soma(Hoffman DA et al, 1997 [rat]13 ).
I T low threshold
T-type channels are less dense in the soma than in the dendrites (Magee JC and Johnston D, 1995 [rat]22 ).
I 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]22 ). (Tsubokawa H et al, 200023 ). 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]24 ). Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs (Jung HY et al, 199725 ). 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, 199926 ).
I L high threshold
In patch recordings, "HVA-l channels reminiscent of L-type channels were occasionally encountered primarily in the more proximal dendrites" (and in the soma) (Magee JC and Johnston D, 1995 [rat]22 ).
I N
Patch recordings (Magee JC and Johnston D, 1995 [rat]22 ). Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines (Mills LR et al, 199427 ).
I p,q
Patch recordings indicate channels similar in basic characteristics to one or more of the HVAm channel types (most likely Q- or R-type channels)(Magee JC and Johnston D, 1995 [rat]22 ).
I K
The properties of voltage-gated potassium currents were studied in acutely isolated rat cells from area CA1 and CA3 at postnatal ages of day 6-8, 9-14, and 26-29 (P6-8, P9-14, and P26-29) with the use of the whole cell version of the patch-clamp technique. In CA1 cells IK was blocked by TEA at +30 mV with an IC50 of 0.98 mM. In CA3 cells the corresponding IC50 value was 1.05 mM. About 20% of IK were insensitive to TEA. IK was partially blocked by approximately 30% with 100 microM 4-AP. Mast cell degranulating peptide (100-200 nM) and dendrotoxin (50-300 nM) had no effect on IK. IK was upregulated with increasing postnatal age. This increase in the expression of IK was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat]28 ).
I M
Cells were voltage-clamped using a single microelectrode, at 23-30 degrees C. M-current resembled that of sympathetic ganglion cells. It was abolished by addition of carbachol, muscarine or bethanechol, as well as by 1 mM barium. It was suggested that activation of cholinergic septal inputs to the hippocampus facilitates repetitive firing of pyramidal cells by turning off the M-conductance, without much change in the resting potential of the cell (Halliwell JV and Adams PR, 1982 [guinea pig]35 ). It was was blocked by linopirdine in a reversible, concentration-dependent manner (Aiken SP et al, 1995 [rat]36 ). and by cholinergic agonists in slices (Sanchez-Andres JV and Alkon DL, 1991 [rabbit]37 ). Serotonin produced a slowly developing and long-lasting suppression of IM leading to depolarization end excitation (Colino A and Halliwell JV, 1987 [rat]38 ). It was decreased by cannabinoids (Schweitzer P, 200039 ).
I h
Depolarizing "sag" during larger hyperpolarizing voltage transients is indicative of Ih current in determinating the passive membrane properties of CA1 pyramidal neurons (Spruston N and Johnston D, 199241 ). Membrane patches recorded in the cell-attached patch configuration from the soma and apical dendrites revealed an Ih that increased over sixfold from soma to distal dendrites. Ih demonstrated a mixed Na+-K+ conductance and was sensitive to low concentrations of external CsCl. As a result of Ih the propagation of subthreshold voltage transients is directionally specific.The elevated dendritic Ih density decreases EPSP amplitude and duration and reduces the time window over which temporal summation takes place (Magee JC, 1998 [Rat]40 ).
I K,Ca
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 (Lancaster B and Adams PR, 198643 ). Cell-attached patches on the proximal 100um of the apical dendrite did not contain sAHP channels. Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the sAHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids (Bekkers JM, 200042 ). In situ hybridization of three cloned SK channel subunits (SK1-3), the prime candidates likely to underlie Ca(2+)-dependent AHPs showed high levels of expression in regions presenting prominent AHP currents including CA1-3 regions of the hippocampus (SK1 and SK2), reticularis thalami (SK1 and SK2), supraoptic nucleus (SK3), and inferior olivary nucleus (SK2 and SK3) (Stocker M and Pedarzani P, 200044 ). The role of large-conductance Ca2+-dependent K+ channels (BK) in spike broadening during repetitive firing was studied using sharp electrode and computer modelling. The amplitude of the fast after-hyperpolarization (fAHP) rapidly declined during each train. Suppression of BK-channel activity with the selective BK-channel blocker iberiotoxin, the non-peptidergic BK-channel blocker paxilline, or calcium-free medium, broadened the 1st spike to a similar degree ( approximately 60 %) (Shao LR et al, 1999 [rat]45 ).
Axon
Axon hillock
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaA
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Axon terminal.Gaba
Interneuron terminals (T) 		GabaB
I K
I Na,t
Axon fiber
I Na,t
Axon terminal
I N
Glutamate
Hippocampus CA1 interneuron oriens alveus GABA cell
 -Distal equivalent dendrite.AMPA
 -Middle equivalent dendrite.AMPA
 -Proximal equivalent dendrite.AMPA
Subiculum pyramidal neuron
Classical References: first publications on each compartmental property; search PubMed for complete list
1.  Storm-Mathisen J. (1977) Localization of transmitter candidates in the brain: the hippocampal formation as a model. Prog Neurobiol 8:119-81.
2.  Randall AD and Collingridge GL. (1992) Amino acid receptor-mediated synaptic currents in the CA1 region of the hippocampus. Ion Channels 3:63-81.
3.  Magee JC and Cook EP. (2000) Somatic EPSP amplitude is independent of synapse location in hippocampal pyramidal neurons. Nat Neurosci 3:895-903 [Journal] .
4.  Raymond CR and Redman SJ. (2006) Spatial segregation of neuronal calcium signals encodes different forms of LTP in rat hippocampus. J Physiol 570:97-111 [Journal] .
5.  He Y, Janssen WG and Morrison JH. (1998) Synaptic coexistence of AMPA and NMDA receptors in the rat hippocampus: a postembedding immunogold study. J Neurosci Res 54:444-9 [Journal] .
6.  Honoré T, Davies SN, Drejer J, Fletcher EJ, Jacobsen P, Lodge D and Nielsen FE. (1988) Quinoxalinediones: potent competitive non-NMDA glutamate receptor antagonists. Science 241:701-3.
7.  Andrasfalvy BK and Magee JC. (2001) Distance-dependent increase in AMPA receptor number in the dendrites of adult hippocampal CA1 pyramidal neurons. J Neurosci 21:9151-9.
8.  Jaffe DB and Brown TH. (1994) Metabotropic glutamate receptor activation induces calcium waves within hippocampal dendrites. J Neurophysiol 72:471-4 [Journal] .
9.  Bashir ZI, Bortolotto ZA, Davies CH, Berretta N, Irving AJ, Seal AJ, Henley JM, Jane DE, Watkins JC and Collingridge GL. (1993) Induction of LTP in the hippocampus needs synaptic activation of glutamate metabotropic receptors. Nature 363:347-50 [Journal] .
10.  Lipowsky R, Gillessen T and Alzheimer C. (1996) Dendritic Na+ channels amplify EPSPs in hippocampal CA1 pyramidal cells. J Neurophysiol 76:2181-91 [Journal] .
11.  Wierenga CJ and Wadman WJ. (1999) Miniature inhibitory postsynaptic currents in CA1 pyramidal neurons after kindling epileptogenesis. J Neurophysiol 82:1352-62 [Journal] .
12.  Spruston N, Jonas P and Sakmann B. (1995) Dendritic glutamate receptor channels in rat hippocampal CA3 and CA1 pyramidal neurons. J Physiol 482 ( Pt 2):325-52.
13.  Hoffman DA, Magee JC, Colbert CM and Johnston D. (1997) K+ channel regulation of signal propagation in dendrites of hippocampal pyramidal neurons. Nature 387:869-75 [Journal] .
14.  Chen C. (2005) beta-Amyloid increases dendritic Ca2+ influx by inhibiting the A-type K+ current in hippocampal CA1 pyramidal neurons. Biochem Biophys Res Commun 338:1913-9 [Journal] .
15.  Golding NL, Kath WL and Spruston N. (2001) Dichotomy of action-potential backpropagation in CA1 pyramidal neuron dendrites. J Neurophysiol 86:2998-3010 [Journal] .
16.  Staff NP, Jung HY, Thiagarajan T, Yao M and Spruston N. (2000) Resting and active properties of pyramidal neurons in subiculum and CA1 of rat hippocampus. J Neurophysiol 84:2398-408 [Journal] .
17.  Frick A, Magee J, Koester HJ, Migliore M and Johnston D. (2003) Normalization of Ca2+ signals by small oblique dendrites of CA1 pyramidal neurons. J Neurosci 23:3243-50.
18.  Gasparini S, Losonczy A, Chen X, Johnston D and Magee JC. (2007) Associative pairing enhances action potential back-propagation in radial oblique branches of CA1 pyramidal neurons. J Physiol 580:787-800 [Journal] .
19.  Migliore M, Ferrante M and Ascoli GA. (2005) Signal propagation in oblique dendrites of CA1 pyramidal cells. J Neurophysiol 94:4145-55 [Journal] .
20.  Losonczy A and Magee JC. (2006) Integrative properties of radial oblique dendrites in hippocampal CA1 pyramidal neurons. Neuron 50:291-307 [Journal] .
21.  Golding NL, Jung HY, Mickus T and Spruston N. (1999) Dendritic calcium spike initiation and repolarization are controlled by distinct potassium channel subtypes in CA1 pyramidal neurons. J Neurosci 19:8789-98.
22.  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 487:67-90.
23.  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.
24.  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.
25.  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.
26.  Mickus T, Jung Hy and Spruston N. (1999) Properties of slow, cumulative sodium channel inactivation in rat hippocampal CA1 pyramidal neurons. Biophys J 76:846-60 [Journal] .
27.  Mills LR, Niesen CE, So AP, Carlen PL, Spigelman I and Jones OT. (1994) N-type Ca2+ channels are located on somata, dendrites, and a subpopulation of dendritic spines on live hippocampal pyramidal neurons. J Neurosci 14:6815-24.
28.  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] .
29.  Jaffe DB, Johnston D, Lasser-Ross N, Lisman JE, Miyakawa H and Ross WN. (1992) The spread of Na+ spikes determines the pattern of dendritic Ca2+ entry into hippocampal neurons. Nature 357:244-6 [Journal] .
30.  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.
31.  Christie BR, Eliot LS, Ito K, Miyakawa H and Johnston D. (1995) Different Ca2+ channels in soma and dendrites of hippocampal pyramidal neurons mediate spike-induced Ca2+ influx. J Neurophysiol 73:2553-7 [Journal] .
32.  Spencer WA and Kandel ER. (1961) ELECTROPHYSIOLOGY OF HIPPOCAMPAL NEURONS: IV. FAST PREPOTENTIALS. J Neurophysiol 24:272-85 [Journal] .
33.  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.
34.  Westenbroek RE, Ahlijanian MK and Catterall WA. (1990) Clustering of L-type Ca2+ channels at the base of major dendrites in hippocampal pyramidal neurons. Nature 347:281-4 [Journal] .
35.  Halliwell JV and Adams PR. (1982) Voltage-clamp analysis of muscarinic excitation in hippocampal neurons. Brain Res 250:71-92.
36.  Aiken SP, Lampe BJ, Murphy PA and Brown BS. (1995) Reduction of spike frequency adaptation and blockade of M-current in rat CA1 pyramidal neurones by linopirdine (DuP 996), a neurotransmitter release enhancer. Br J Pharmacol 115:1163-8.
37.  Sanchez-Andres JV and Alkon DL. (1991) Voltage-clamp analysis of the effects of classical conditioning on the hippocampus. J Neurophysiol 65:796-807 [Journal] .
38.  Colino A and Halliwell JV. (1987) Differential modulation of three separate K-conductances in hippocampal CA1 neurons by serotonin. Nature 328:73-7 [Journal] .
39.  Schweitzer P. (2000) Cannabinoids decrease the K(+) M-current in hippocampal CA1 neurons. J Neurosci 20:51-8.
40.  Magee JC. (1998) Dendritic hyperpolarization-activated currents modify the integrative properties of hippocampal CA1 pyramidal neurons. J Neurosci 18:7613-24.
41.  Spruston N and Johnston D. (1992) Perforated patch-clamp analysis of the passive membrane properties of three classes of hippocampal neurons. J Neurophysiol 67:508-29 [Journal] .
42.  Bekkers JM. (2000) Distribution of slow AHP channels on hippocampal CA1 pyramidal neurons. J Neurophysiol 83:1756-9 [Journal] .
43.  Lancaster B and Adams PR. (1986) Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons. J Neurophysiol 55:1268-82 [Journal] .
44.  Stocker M and Pedarzani P. (2000) Differential distribution of three Ca(2+)-activated K(+) channel subunits, SK1, SK2, and SK3, in the adult rat central nervous system. Mol Cell Neurosci 15:476-93 [Journal] .
45.  Shao LR, Halvorsrud R, Borg-Graham L and Storm JF. (1999) The role of BK-type Ca2+-dependent K+ channels in spike broadening during repetitive firing in rat hippocampal pyramidal cells. J Physiol 521 Pt 1:135-46.
46.  Reyes-Harde M, Potter BV, Galione A and Stanton PK. (1999) Induction of hippocampal LTD requires nitric-oxide-stimulated PKG activity and Ca2+ release from cyclic ADP-ribose-sensitive stores. J Neurophysiol 82:1569-76 [Journal] .