scholarly journals Reduced Mg2+ block of N-methyl-D-aspartate receptor-mediated synaptic potentials in developing visual cortex.

1993 ◽  
Vol 90 (15) ◽  
pp. 7114-7118 ◽  
Author(s):  
N. Kato ◽  
H. Yoshimura
Keyword(s):  
Visual Cortex ◽  
Synaptic Potentials ◽  
Aspartate Receptor

scholarly journals Input-specific maturation of NMDAR-mediated transmission onto parvalbumin-expressing interneurons in layers 2/3 of the visual cortex

2018 ◽  
Vol 120 (6) ◽  
pp. 3063-3076 ◽  
Author(s):  
Camilo Ferrer ◽  
Helen Hsieh ◽  
Lonnie P. Wollmuth
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Pyramidal Neurons ◽  
Temporal Integration ◽  
Developmental Changes ◽  
Evoked Responses ◽  
Developmentally Regulated ◽  
Low Frequencies ◽  
Aspartate Receptor ◽  
Synaptic Responses

Parvalbumin-expressing (PV) GABAergic interneurons regulate local circuit dynamics. In terms of the excitation driving PV interneuron activity, the N-methyl-d-aspartate receptor (NMDAR)-mediated component onto PV interneurons tends to be smaller than that onto pyramidal neurons but makes a significant contribution to their physiology and development. In the visual cortex, PV interneurons mature during the critical period. We hypothesize that during the critical period, the NMDAR-mediated signaling and functional properties of glutamatergic synapses onto PV interneurons are developmentally regulated. We therefore compared the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and NMDAR-mediated synaptic responses before (postnatal days 15–20, P15–P20), during (P25–P40), and after (P50–P60) the visual critical period. AMPAR miniature excitatory postsynaptic currents (mEPSCs) showed a developmental decrease in frequency, whereas NMDAR mEPSCs were absent or showed extremely low frequencies throughout development. For evoked responses, we consistently saw a NMDAR-mediated component, suggesting pre- or postsynaptic differences between evoked and spontaneous neurotransmission. Evoked responses showed input-specific developmental changes. For intralaminar inputs, the NMDAR-mediated component significantly decreased with development. This resulted in adult intralaminar inputs almost exclusively mediated by AMPARs, suited for the computation of synaptic inputs with precise timing, and likely having NMDAR-independent forms of plasticity. In contrast, interlaminar inputs maintained a stable NMDAR-mediated component throughout development but had a shift in the AMPAR paired-pulse ratio from depression to facilitation. Adult interlaminar inputs with facilitating AMPAR responses and a substantial NMDAR component would favor temporal integration of synaptic responses and could be modulated by NMDAR-dependent forms of plasticity. NEW & NOTEWORTHY We show for the first time input-specific developmental changes in the N-methyl-d-aspartate receptor component and short-term plasticity of the excitatory drive onto layers 2/3 parvalbumin-expressing (PV) interneurons in the visual cortex during the critical period. These developmental changes would lead to functionally distinct adult intralaminar and interlaminar glutamatergic inputs that would engage PV interneuron-mediated inhibition differently.

Neurophysiology of glutamatergic signalling and anthelmintic action in Ascaris suum: pharmacological evidence for a kainate receptor

Parasitology ◽  
1998 ◽  
Vol 116 (5) ◽  
pp. 471-486 ◽  
Author(s):  
R. E. DAVIS
Keyword(s):  
Parasitic Nematode ◽  
Excitatory Amino Acid ◽  
Ascaris Suum ◽  
Induced Response ◽  
Primary Target ◽  
Synaptic Potentials ◽  
Aspartate Receptor ◽  
Amino Acid Analogues ◽  
Locomotory Behaviour ◽  
Reversal Potentials

Electrophysiological and pharmacological techniques were used to study glutamatergic signalling in the parasitic nematode, Ascaris suum. Glutamate or kainate injections into whole worms produced a paralysed quasi-static posture similar to the waveform in behaving worms. The DE2 motorneuron class is a primary target. Several glutamatergic substances produced pronounced conductance increases and depolarization in DE2; domoate and kainate were the most potent agonists tested. Glutamate responses and spontaneous excitatory post-synaptic potentials in DE2 were reversibly blocked in sodium-free saline. DE2 sensitivity to exogenous glutamate was sustained during block of synaptic transmission suggesting that glutamatergic receptors are located on DE2 neurons. The glutamate-induced response was localized to the DE2 dendrite, coincident with the synapses responsible for spontaneous potentials in DE2. Steady-state potentials reached during glutamate superfusion were similar to the reversal potentials for both the spontaneous post-synaptic potentials and glutamate, also suggesting that these potentials may be glutamatergic. Non-N-methyl-D-aspartate receptor antagonists partially blocked spontaneous DE2 excitatory potentials and responses elicited by exogenous glutamate and kainate. This glutamatergic pathway may play a role in nematode locomotory behaviour and account for the paralysing anthelmintic action of excitatory amino acid analogues like kainate and domoate.

Actions of glutamate antagonists on synaptic potentials in cat visual cortex

1989 ◽  
Vol 9 ◽  
pp. 135
Author(s):  
Ayahiko Nishigori ◽  
Tetsuya Shirokawa ◽  
Tadaharu Tsumoto ◽  
Fumitaka Kimura
Keyword(s):  
Visual Cortex ◽  
Glutamate Antagonists ◽  
Synaptic Potentials ◽  
Cat Visual Cortex

Glycine Binding Sites of Presynaptic NMDA Receptors May Tonically Regulate Glutamate Release in the Rat Visual Cortex

2007 ◽  
Vol 97 (1) ◽  
pp. 817-823 ◽  
Author(s):  
Yan-Hai Li ◽  
Tai-Zhen Han
Keyword(s):  
Visual Cortex ◽  
Binding Site ◽  
Binding Sites ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Excitatory Neurotransmitter ◽  
Aspartate Receptor ◽  
Neurotransmitter Glutamate ◽  
Presynaptic Nmda Receptors ◽  
Nmda Receptor Blocker

In the CNS, activation of N-methyl-d-aspartate receptor (NMDA-R) glycine binding sites is a prerequisite for activation of postsynaptic NMDA-Rs by the excitatory neurotransmitter glutamate. Here we provide electrophysiological evidence that the glycine binding sites of presynaptic NMDA-Rs regulate glutamate release in layer II/III pyramidal neurons of the rat visual cortex. Specifically, our results reveal that the frequency of miniature excitatory postsynaptic currents is significantly reduced by 7-chloro-kynurenic acid (7-Cl KYNA), a NMDA-R glycine binding site antagonist, and glycine or d-serine reverses this effect. Similar results are obtained when the open-channel NMDA receptor blocker, MK-801, is included in the recording pipette. Our data indicate that the glycine binding site of postsynaptic NMDA-Rs is not saturated. Moreover, they suggest that presynaptic NMDA-Rs are located in layer II/III pyramidal neurons of the rat visual cortex and that the glycine binding site of presynaptic NMDA-Rs tonically regulates glutamate release.

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