NeuronDB: Neuron Details

Hippocampus CA3 pyramidal GLU cell

- - HG - Hip - CA3 - PRINC - pyramidal - - glu

Properties are:

Present

Absent

Input Receptors

Intrinsic Currents

Output Transmitters

Distal apical dendrite

Perforant pathway entorhinal pyramidal neuron terminals (T)	AMPA
Quantitative autoradiography has been used to localize [3H]AMPA binding sites. It was found that AMPARs are found in a high concentration in the hippocampus relative to other areas in the brain. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare (Monaghan DT et al, 1984 [rat]¹ ). The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that a CNQX-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of AMPA channel opening). It was calculated that AMPA channels had a mean elementary conductance of 10 pS (estimated by non-stationary fluctuation analysis) and was found that the channels had a low permeability to Ca2+. The reversal potential for AMPA receptors was found to be about 0 mV with an almost linear peak current-voltage relationship (Spruston N et al, 1995 [mammal]² ). see also (Jahr CE and Stevens CF, 1987 [rat]³ ). It has also been found that CNQX does not block the intracellular calcium concentration increase normally associated with stratum lucidum stimulation (Pozzo Miller LD et al, 1996⁴ ). 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 (Spruston N et al, 1995⁵ ).
Perforant pathway entorhinal pyramidal neuron terminals (T)	NMDA
Quantitative autoradiography has been used to localize sites at which L-[3H]-glutamate is displaced by NMDA. The labelling of these receptors was somewhat lower than in CA1 overall, being highest in s. oriens and s. radiatum and very low in s.pyramidale and s. lucidum (Monaghan DT and Cotman CW, 1985⁶ ). In contrast, a study using radioactive in situ hybridization histochemistry looked at mRNA coding an NMDA glutamate binding protein and at NMDAR1 (an NMDAR subunit) expression and found heavy labeling for both in the pyramidal and polymorphic layers but little in the molecular layer (Sato K et al, 1995 [rat]⁷ ). The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that an APV-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of NMDA channel opening). It was calculated that NMDA channels had a main conductance state conductance of 45 pS and it was confirmed that the channel was permeable to Ca2+. The NMDAR-mediated conductance was blocked by Mg2+ in a voltage-dependent way and by Zn2+ in a non-voltage-dependent fashion (Spruston N et al, 1995 [mammal]² ). see also (Jahr CE and Stevens CF, 1987 [rat]³ ). NMDA iontophoretically applied to basal dendrites evoked inward currents near resting potential. Changing levels of bath calcium concentration downwards by 50% caused an increase in the inward current (Gerber U et al, 1993 [rat]⁸ ). MK801 (an NMDAR antagonist) blocks the transient intracellular Ca2+ release normally associated with stratum lucidum stimulation (found by simultaneous Ca imaging and intracellular recording in rat brain slices by (Pozzo Miller LD et al, 1996⁴ ). While NMDA receptor activation may be necessary for LTP at the commissural/associational synapses (Gorter JA and Brady RJ, 1995 [rat]⁹ ). it has been shown to occur at mossy fiber synapses even in the presence of NMDA receptor antagonists under certain conditions (Gorter JA and Brady RJ, 1995 [rat]⁹ ). (Harris EW and Cotman CW, 1986¹⁰ ). Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by #R#158#E#. 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 (Spruston N et al, 1995⁵ ).

I p,q

I K
Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997²⁷ ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a I(K) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat]²⁸ ). 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 (Sheng M et al, 1994 [rat]¹¹ ).

Middle apical dendrite

-Axon terminal.Glutamate CA3 Pyramidal Neuron terminals (T)	Glutamate

-Axon terminal.Glutamate CA3 Pyramidal neuron terminals (T)	AMPA
Quantitative autoradiography has been used to localize [3H]AMPA binding sites. It was found that AMPARs are found in a high concentration in the hippocampus relative to other areas in the brain. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare (Monaghan DT et al, 1984 [rat]¹ ). The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that a CNQX-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of AMPA channel opening). It was calculated that AMPA channels had a mean elementary conductance of 10 pS (estimated by non-stationary fluctuation analysis) and was found that the channels had a low permeability to Ca2+. The reversal potential for AMPA receptors was found to be about 0 mV with an almost linear peak current-voltage relationship (Spruston N et al, 1995 [mammal]² ). see also (Jahr CE and Stevens CF, 1987 [rat]³ ). It has also been found that CNQX does not block the intracellular calcium concentration increase normally associated with stratum lucidum stimulation (Sheng M et al, 1994 [rat]¹¹ ).
-Axon terminal.Glutamate CA3 Pyramidal neuron terminals (T)	NMDA
Quantitative autoradiography has been used to localize sites at which L-[3H]-glutamate is displaced by NMDA. The labelling of these receptors was somewhat lower than in CA1 overall, being highest in s. oriens and s. radiatum and very low in s.pyramidale and s. lucidum (Monaghan DT and Cotman CW, 1985⁶ ). In contrast, a study using radioactive in situ hybridization histochemistry looked at mRNA coding an NMDA glutamate binding protein and at NMDAR1 (an NMDAR subunit) expression and found heavy labeling for both in the pyramidal and polymorphic layers but little in the molecular layer (Sato K et al, 1995 [rat]⁷ ). The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that an APV-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of NMDA channel opening). It was calculated that NMDA channels had a main conductance state conductance of 45 pS and it was confirmed that the channel was permeable to Ca2+. The NMDAR-mediated conductance was blocked by Mg2+ in a voltage-dependent way and by Zn2+ in a non-voltage-dependent fashion (Spruston N et al, 1995 [mammal]² ). see also (Jahr CE and Stevens CF, 1987 [rat]³ ). NMDA iontophoretically applied to basal dendrites evoked inward currents near resting potential. Changing levels of bath calcium concentration downwards by 50% caused an increase in the inward current (Gerber U et al, 1993 [rat]⁸ ). MK801 (an NMDAR antagonist) blocks the transient intracellular Ca2+ release normally associated with stratum lucidum stimulation (found by simultaneous Ca imaging and intracellular recording in rat brain slices by (Pozzo Miller LD et al, 1996⁴ ). While NMDA receptor activation may be necessary for LTP at the commissural/associational synapses (Gorter JA and Brady RJ, 1995 [rat]⁹ ). it has been shown to occur at mossy fiber synapses even in the presence of NMDA receptor antagonists under certain conditions (Gorter JA and Brady RJ, 1995 [rat]⁹ ). (Harris EW and Cotman CW, 1986¹⁰ ). Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by (Chattarji S et al, 1989¹² ).
Receptor Notes Dentate Granule Cell mossy terminals (T)	mGluR
Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K, Ca) and voltage-gated I(K) (Charpak S et al, 1990¹³ ). A subsequent study in rat slice cultures has shown that bath application of MCPG (a mGluR antagonist) blocks the inward Ca-dependent K-current associated with ACPD application or mossy fiber stimulation in the presence on ionotropic GluR antagonists (Gerber U et al, 1993 [rat]⁸ ). Another study using bath application of 1S,3R-ACPD in rat slice cultures during single electrode voltage clamp recording showed that depolarizing current steps revealed a suppression of K currents leading to a negative slope conductance at potential between -55mV and -40 mV (Lüthi A et al, 1997¹⁴ ). mGluR2 knockout mice show normal LTP and synaptic transmission but not LTD (Yokoi M et al, 1996 [mice]¹⁵ ). It has also been shown (using whole and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al, 1996).
Hippocampus CA3 interneuron basket GABA cell -Axon terminal.Gaba CA3 Basket Cell terminals (T)	Gaba
A study using simultaneous intracellular recording from interneurons and pyramidal neurons combined with biocytin cell fills and morphological reconstructions revealed that the interneurons made connections onto the soma and proximal dendrites of the pyramidal neuron and that stimulation of the interneurons evoked IPSPs in the pyramidal neurons. EM microscopy revealed differential numbers of terminals depending on the subcellular locus of the connections. (Miles R et al, 1996¹⁶ ).
Hippocampus CA3 interneuron basket GABA cell -Axon terminal.Gaba CA3 Basket Cell terminals (T)	GabaA
Intracellular recording from organotypic rat hippocampal cultures have shown that approximately 25% of single spikes in CA3 pyramidal neurons are followed by IPSPs at a fixed latency, presumeably a result of feedback inhibition from inhibitory interneurons. The addition of bicuculline (a competitive GABA(A) antagonist) completely abolished these responses, but they were insensitive to CGP35348, a GABA(B) antagonist (Fortunato C et al, 1996¹⁷ ). There is also evidence that Zn+ can modulate bicuculline-sensitive responses to GABA early in development in rat (studied less than 8 days old)(Martina M et al, 1996 [rat]¹⁸ ).
Hippocampus CA3 interneuron basket GABA cell -Axon terminal.Gaba CA3 Basket Cell terminals (T)	GabaB
Hilar stimulation has been used to elicit (pharmacologically isolated) IPSPs in CA3 pyramidal neurons (recorded by means of intracellular or whole cell methods depending on the age of the animal). Paired pulse stimulation in this preparation resulted in paired pulse depression, which could be reduced by bath application of CGP35348 (a GABA(B)R antagonist) in adult rats. Neonatal rats (5-7 days old) showed paired pulse depression only within a much shorter range of interstimulus intervals and it was not affected by CGP35348 unless transmitter release was facilitated by raising the bath [Ca2+] and lowering the bath [Mg+] (Caillard O et al, 1998¹⁹ ).

I p,q

I K
Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997²⁷ ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat]²⁸ ). 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 (Sheng M et al, 1994 [rat]¹¹ ).
I L high threshold
In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, L-currents were found in 34% of the patches and found to have single channel conductances of 23-27 pS (Johnston D et al, 1992³⁰ ). (Fisher RE et al, 1990³¹ ). Whole cell recording experiments have revealed a sustained, partially nimodipine-sensitve current in steps to -50mV, suggesting that they play a role in CA2+ signalling at low voltages as well as a their classical high voltages (Johnston D et al, 1992³⁰ ). It has been suggested that voltage-gated calcium channels play a role in LTP (Johnston D et al, 1992³⁰ ). and it has been shown that nimodipine (an L-channel antagonist) prevents certain mossy fiber LTP-types from taking place (Kapur A et al, 1998³² ).
I T low threshold
In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, T-currents were found in 72% of the patches and found to have single channel conductances of 8 pS (Johnston D et al, 1992³⁰ ). (Fisher RE et al, 1990³¹ ). Whole cell recording from acutely isolated rat CA3 pyramidal neurons revealed a transient (59 msec decay time constant) that was inhibited by Ni2+ and amiloride (Avery RB and Johnston D, 1996 [rat]³³ ).

Proximal apical dendrite

Dentate gyrus granule GLU cell -Axon terminal.Glutamate Dentate Granule Cell mossy terminals (T)	Glutamate

I p,q

I Na,t
Extracellular recordings in vivo suggested that the dendritic density of these channels rapidly decreases with distance from soma (Buzsáki G et al, 1996²⁵ ).
I K
Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997²⁷ ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat]²⁸ ). 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 (Sheng M et al, 1994 [rat]¹¹ ).

Distal basal dendrite

-Axon terminal.Glutamate CA3 Pyramidal Neuron terminals (T)	Glutamate

Middle basal dendrite

-Axon terminal.Glutamate CA3 Pyramidal Neuron terminals (T)	Glutamate

Proximal basal dendrite

-Axon terminal.Glutamate CA3 Pyramidal Neuron terminals (T)	Glutamate

Soma

-----	AMPA
Quantitative autoradiography has been used to localize [3H]AMPA binding sites. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare (Monaghan DT et al, 1984 [rat]¹ ). [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 (Spruston N et al, 1995⁵ ).
-----	NMDA
Quantitative autoradiography has been used to localize sites at which L-[3H]-glutamate is displaced by NMDA. The labelling of these receptors was somewhat lower than in CA1 overall, being highest in s. oriens and s. radiatum and very low in s.pyramidale and s. lucidum (Monaghan DT and Cotman CW, 1985⁶ ). In contrast, a study using radioactive in situ hybridization histochemistry looked at mRNA coding an NMDA glutamate binding protein and at NMDAR1 (an NMDAR subunit) expression and found heavy labeling for both in the pyramidal and polymorphic layers but little in the molecular layer (Sato K et al, 1995 [rat]⁷ ). [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 (Spruston N et al, 1995⁵ ).
-----	mGluR
Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K,Ca) and voltage-gated I(K) (Charpak S et al, 1990¹³ ). A subsequent study in rat slice cultures has shown that bath application of MCPG (a mGluR antagonist) blocks the inward Ca-dependent K-current associated with ACPD application or mossy fiber stimulation in the presence on ionotropic GluR antagonists (Gerber U et al, 1993 [rat]⁸ ). Another study using bath application of 1S,3R-ACPD in rat slice cultures during single electrode voltage clamp recording showed that depolarizing current steps revealed a suppression of K currents leading to a negative slope conductance at potential between -55mV and -40 mV (Lüthi A et al, 1997¹⁴ ). mGluR2 knockout mice show normal LTP and synaptic transmission but not LTD (Yokoi M et al, 1996 [mice]¹⁵ ). It has also been shown (using whole cell and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al. 1996 #8680866).
Hippocampus CA3 interneuron basket GABA cell -Axon terminal.Gaba CA3 Basket Cell terminals (T)	Gaba
A study using simultaneous intracellular recording from interneurons and pyramidal neurons combined with biocytin cell fills and morphological reconstructions revealed that the interneurons made connections onto the soma and proximal dendrites of the pyramidal neuron and that stimulation of the interneurons evoked IPSPs in the pyramidal neurons. EM microscopy revealed differential numbers of terminals depending on the subcellular locus of the connections. (Miles R et al, 1996¹⁶ ).
Hippocampus CA3 interneuron basket GABA cell -Axon terminal.Gaba CA3 Basket Cell terminals (T)	GabaA
Intracellular recording from organotypic rat hippocampal cultures have shown that approximately 25% of single spikes in CA3 pyramidal neurons are followed by IPSPs at a fixed latency, presumeably a result of feedback inhibition from inhibitory interneurons. The addition of bicuculline (a competitive GABA(A) antagonist) completely abolished these responses, but they were insensitive to CGP35348, a GABA(B) antagonist (Fortunato C et al, 1996¹⁷ ). There is also evidence that Zn+ can modulate bicuculline-sensitive responses to GABA early in development in rat (studied less than 8 days old)(Martina M et al, 1996 [rat]¹⁸ ).
Hippocampus CA3 interneuron basket GABA cell -Axon terminal.Gaba CA3 Basket Cell terminals (T)	GabaB
Hilar stimulation has been used to elicit (pharmacologically isolated) IPSPs in CA3 pyramidal neurons (recorded by means of intracellular or whole cell methods depending on the age of the animal). Paired pulse stimulation in this preparation resulted in paired pulse depression, which could be reduced by bath application of CGP35348 (a GABA(B)R antagonist) in adult rats. Neonatal rats (5-7 days old) showed paired pulse depression only within a much shorter range of interstimulus intervals and it was not affected by CGP35348 unless transmitter release was facilitated by raising the bath [Ca2+] and lowering the bath [Mg+] (Caillard O et al, 1998¹⁹ ).
Septum principal ACh cell -Axon terminal.Acetylcholine	Nicotinic

I K,Ca
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) (Shao LR et al, 1999 [rat]²⁶ ).
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, 1992²⁹ ).
I Na,t
Subthreshold membrane potential oscillations are blocked by bath application of tetrodotoxin (TTX), a potent Na(t)-current antagonist, in rats 3-17 days old (Psarropoulou C and Avoli M, 1995³⁴ ). 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]³⁵ ).
I L high threshold
In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, L-currents were found in 34% of the patches and found to have single channel conductances of 23-27 pS (Johnston et al. 1992; (Fisher RE et al, 1990³¹ ). Whole cell recording experiments have revealed a sustained, partially nimodipine-sensitve current in steps to -50mV, suggesting that they play a role in CA2+ signalling at low voltages as well as a their classical high voltages (Avery RB and Johnston D, 1996 [rat]³³ ). It has been suggested that voltage-gated calcium channels play a role in LTP (Johnston et al. 1992), and it has been shown that nimodipine (an L-channel antagonist) prevents certain mossy fiber LTP-types from taking place (Kapur A et al, 1998³² ).
I N
In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, N-currents were found in 63% of the patches and found to have single channel conductances of 14 pS (Johnston et al. 1992; (Fisher RE et al, 1990³¹ ). Bath application of omega-conotoxin MVIIC blocked (with rapid kinetics) approximately 20% of the high-voltage activated Ca2+ current, suggesting the presence of N-channels measured in whole-cell recordings (McDonough SI et al, 1996 [rat]³⁶ ).
I T low threshold
In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, T-currents were found in 72% of the patches and found to have single channel conductances of 8 pS (Johnston et al. 1992, (Fisher RE et al, 1990³¹ ). Whole cell recording from acutely isolated rat CA3 pyramidal neurons revealed a transient (59 msec decay time constant) that was inhibited by Ni2+ and amiloride (Avery RB and Johnston D, 1996 [rat]³³ ).
I p,q
Bath application of omega-conotoxin MVIIC (an antagonist of N and P channels) blocked (with slow kinetics) approximately 30% of the high-voltage activated Ca2+ current measured in whole-cell recordings (McDonough SI et al, 1996 [rat]³⁶ ).
I A
In a study of acutely isolated rat cells under whole cell recording across developmental states (Day 6 - Day 29), I(A) was separated from I(K) by subtraction methods. It was found that I(A) was rapidly activated and inactivated and was 80% blocked by 4-AP (4-aminopyridine), but was insensitive to TEA (tetraethylammonium) and dendrotoxin (Klee et al, 1995). The current has also been shown to be modulated by K concentration (Eder et al, 1996), though this effect appears to be restricted to very early in development (Klee et al, 1997).
I K
Bath application of Pb2+ shifted the neurons'' current-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons" (Madeja M et al, 1997²⁷ ). In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a I(K) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50% (Klee R et al, 1995 [rat]²⁸ ). 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 (Sheng M et al, 1994 [rat]¹¹ ).

Axon hillock

I Na,t

I K

Axon fiber

I Na,t

Axon terminal

	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, 1999²⁰ ).
	NMDA
Presynaptic terminal and axon NMDAR's have been found withimmunocytochemical techniques (Siegel SJ et al, 1994 [monkey]²¹ ). (DeBiasi S et al, 1996 [rat]²² ). (Paquet M et al, 1997 [squirrel monkey]²³ ). Unlike postsynaptic NMDAR's, they are potentiatedby physiologically relevant concentrations of taurine (Suárez LM and Solís JM, 2006 [rat]²⁴ ).

I N

Glutamate	Hippocampus CA1 pyramidal GLU cell -Middle apical dendrite.NMDA -Middle apical dendrite.AMPA -Distal oblique dendrite.Glutamate -Middle oblique dendrite.Glutamate -Middle apical dendrite.Glutamate -Middle apical dendrite.AMPA -Middle apical dendrite.NMDA -Distal basal dendrite.Glutamate -Middle basal dendrite.Glutamate -Proximal basal dendrite.Glutamate CA1 Pyramidal Neuron: Dam

Classical References: first publications on each compartmental property; search PubMed for complete list
1.	Monaghan DT, Yao D and Cotman CW. (1984) Distribution of [3H]AMPA binding sites in rat brain as determined by quantitative autoradiography. Brain Res 324:160-4.
2.	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.
3.	Jahr CE and Stevens CF. (1987) Glutamate activates multiple single channel conductances in hippocampal neurons. Nature 325:522-5 [Journal] .
4.	Pozzo Miller LD, Petrozzino JJ, Golarai G and Connor JA. (1996) Ca2+ release from intracellular stores induced by afferent stimulation of CA3 pyramidal neurons in hippocampal slices. J Neurophysiol 76:554-62 [Journal] .
5.	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.
6.	Monaghan DT and Cotman CW. (1985) Distribution of N-methyl-D-aspartate-sensitive L-[3H]glutamate-binding sites in rat brain. J Neurosci 5:2909-19.
7.	Sato K, Mick G, Kiyama H and Tohyama M. (1995) Expression patterns of a glutamate-binding protein in the rat central nervous system: comparison with N-methyl-D-aspartate receptor subunit 1 in rat. Neuroscience 64:459-75.
8.	Gerber U, Lüthi A and Gähwiler BH. (1993) Inhibition of a slow synaptic response by a metabotropic glutamate receptor antagonist in hippocampal CA3 pyramidal cells. Proc Biol Sci 254:169-72 [Journal] .
9.	Gorter JA and Brady RJ. (1995) Modulation of N-methyl-D-aspartic acid receptors by extracellular calcium in immature and adult hippocampal slices: whole cell recordings in CA3 pyramidal cells. Neurosci Lett 194:209-13.
10.	Harris EW and Cotman CW. (1986) Long-term potentiation of guinea pig mossy fiber responses is not blocked by N-methyl D-aspartate antagonists. Neurosci Lett 70:132-7.
11.	Sheng M, Tsaur ML, Jan YN and Jan LY. (1994) Contrasting subcellular localization of the Kv1.2 K+ channel subunit in different neurons of rat brain. J Neurosci 14:2408-17.
12.	Chattarji S, Stanton PK and Sejnowski TJ. (1989) Commissural synapses, but not mossy fiber synapses, in hippocampal field CA3 exhibit associative long-term potentiation and depression. Brain Res 495:145-50.
13.	Charpak S, Gähwiler BH, Do KQ and Knöpfel T. (1990) Potassium conductances in hippocampal neurons blocked by excitatory amino-acid transmitters. Nature 347:765-7 [Journal] .
14.	Lüthi A, Gähwiler BH and Gerber U. (1997) 1S, 3R-ACPD induces a region of negative slope conductance in the steady-state current-voltage relationship of hippocampal pyramidal cells. J Neurophysiol 77:221-8 [Journal] .
15.	Yokoi M, Kobayashi K, Manabe T, Takahashi T, Sakaguchi I, Katsuura G, Shigemoto R, Ohishi H, Nomura S, Nakamura K, Nakao K, Katsuki M and Nakanishi S. (1996) Impairment of hippocampal mossy fiber LTD in mice lacking mGluR2. Science 273:645-7.
16.	Miles R, Tóth K, Gulyás AI, Hájos N and Freund TF. (1996) Differences between somatic and dendritic inhibition in the hippocampus. Neuron 16:815-23.
17.	Fortunato C, Debanne D, Scanziani M, Gähwiler BH and Thompson SM. (1996) Functional characterization and modulation of feedback inhibitory circuits in area CA3 of rat hippocampal slice cultures. Eur J Neurosci 8:1758-68.
18.	Martina M, Mozrzymas JW, Strata F and Cherubini E. (1996) Zinc modulation of bicuculline-sensitive and -insensitive GABA receptors in the developing rat hippocampus. Eur J Neurosci 8:2168-76.
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