| Neuron | Compartment | Property | Connectivity | Notes |
|---|
| Hippocampus CA3 pyramidal GLU cell | Distal apical dendrite | NMDA | Perforant pathway entorhinal pyramidal neuron terminals (T) | 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, 19852 ). 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]1 ). 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]3 ). see also (Jahr CE and Stevens CF, 1987 [rat]4 ). 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]5 ). 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, 19966 ). While NMDA receptor activation may be necessary for LTP at the commissural/associational synapses (Gorter JA and Brady RJ, 1995 [rat]7 ). 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]7 ). (Harris EW and Cotman CW, 19868 ). 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, 19959 ). |
| Hippocampus CA3 pyramidal GLU cell | Middle apical dendrite | NMDA | CA3 Pyramidal neuron terminals (T) | 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, 19852 ). 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]1 ). 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]3 ). see also (Jahr CE and Stevens CF, 1987 [rat]4 ). 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]5 ). 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, 19966 ). While NMDA receptor activation may be necessary for LTP at the commissural/associational synapses (Gorter JA and Brady RJ, 1995 [rat]7 ). 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]7 ). (Harris EW and Cotman CW, 19868 ). Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by (Chattarji S et al, 198910 ). |
| Hippocampus CA3 pyramidal GLU cell | Soma | 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, 19852 ). 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]1 ). [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, 19959 ). |
