title: NMDA-Receptor-dependent synaptic activation of voltage-dependent calcium channels in basolateral amygdala.
abstract: Afferent stimulation of pyramidal cells in the basolateral amygdala produced mixed excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors during whole cell current-clamp recordings. In the presence of GABA(A) receptor blockade, the mixed EPSPs recruited a large "all-or-none" depolarizing event. This recruited event was voltage dependent and had a distinct activation threshold. An analogous phenomenon elicited by exogenous glutamate in the presence of tetrodotoxin (TTX) was blocked by Cd(2+), suggesting that the event was a Ca(2+) spike. Selective glutamatergic blockade revealed that these Ca(2+) spikes were recruited readily by single afferent stimulus pulses that elicited NMDA EPSPs. In contrast, non-NMDA EPSPs induced by single stimuli failed to elicit the Ca(2+) spike even at maximal stimulus intensities although these non-NMDA EPSPs depolarized the soma more effectively than mixed EPSPs. Elongation of non-NMDA EPSPs by cyclothiazide or brief trains of stimulation were also unable to elicit the Ca(2+) spike. Blockade of K(+) channels with intracellular Cs(+) enabled single non-NMDA EPSPs to activate the Ca(2+) spike. The finding that voltage-dependent calcium channels are activated preferentially by NMDA-receptor-mediated EPSPs provides a mechanism for NMDA-receptor-dependent plasticity independent of Ca(2+) influx through the NMDA receptor.
authors.affiliation: Department of Psychiatry, Durham, North Carolina 27705, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Calton
authors.forename: M H
authors.initials: MH
authors.lastname: Kang
authors.forename: W A
authors.initials: WA
authors.lastname: Wilson
authors.forename: S D
authors.initials: SD
authors.lastname: Moore
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000679:Amygdala / Q000737:chemistry* / Q000502:physiology; D000818:Animals; D001640:Bicuculline / Q000031:analogs & derivatives / Q000494:pharmacology; D002118:Calcium / Q000493:pharmacokinetics; D015220:Calcium Channels / Q000502:physiology*; D002586:Cesium / Q000494:pharmacology; D016291:Dizocilpine Maleate / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D018698:Glutamic Acid / Q000494:pharmacology; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D026902:Potassium Channel Blockers; D011810:Quinoxalines; D016194:Receptors, N-Methyl-D-Aspartate; D002586:Cesium; D018698:Glutamic Acid; C017069:bicuculline methiodide; D013779:Tetrodotoxin; C056723:FG 9041; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate; D015763:2-Amino-5-phosphonovalerate; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; D002118:Calcium; D001640:Bicuculline