Amino acid-mediated regulation of spontaneous synaptic activity patterns in the rat basolateral amygdala.
1. Spontaneous postsynaptic currents (PSCs) were examined in the basolateral amygdala using whole cell patch-clamp recordings in coronal slices (400 microns) from young rats (postnatal day 6-25). In most cells, Cs+ was used in the electrode to block putative voltage-activated K(+)-currents. Both inward and outward spontaneous PSCs were examined. 2. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist, 6,7-nitroquinoxaline-2,3-dione (DNQX) blocked all inward PSCs, which reversed near 0 mV. They therefore were considered to be glutamate-mediated excitatory postsynaptic currents (EPSCs). Averaged EPSCs had a rapid 10-90% rise time (1.0 +/- 0.04 ms; mean +/- SD) and monoexponential decay (tau = 3.6 +/- 0.18 ms) at potentials negative to about -50 mV. Above this potential, a second, slower time constant (tau 1 = 41 +/- 4.5 ms at -30 mV), accounting for 10-30% of the total EPSC amplitude was resolved in 8 of 10 cells examined. The slower decay time constant was sensitive to the N-methyl-D-aspartate (NMDA)-receptor antagonist, DL-2-amino-5-phosphonovaleric acid (AP5) and therefore probably was due to activation of NMDA receptors. 3. The gamma-aminobutyric acid-A (GABAA) antagonist, bicuculline, blocked all outward PSCs, which reversed near -70 mV. They therefore were considered to be GABA-mediated inhibitory postsynaptic currents (IPSCs). Averaged IPSCs displayed rapid 10-90% rise times (1.0 +/- 0.03 ms) and monoexponential decay time constants (tau = 5.16 +/- 0.14 ms). 4. Tetrodotoxin (TTX) reduced the frequency of synaptic activity and eliminated the largest PSCs, thus reducing slightly the mean EPSC and IPSC amplitude. Most cells received bursts of spontaneous IPSCs and/or EPSCs (30-68 Hz lasting 0.5-6 s), which were also TTX sensitive. The TTX data suggest that the somata of the cells responsible for the largest PSCs and the PSC bursts were contained within the slice. 5. In addition to blocking EPSCs, DNQX blocked the bursts of IPSCs, but not all individual IPSCs. DNQX had similar effects as TTX on the bursts and frequency of the IPSCs. 6. Bicuculline enhanced spontaneous EPSC frequency (231 +/- 90%). Much of this increase was due to an increase in the bursts of EPSCs. 7. Neurons in the basolateral amygdala therefore appear to receive both excitatory (glutamatergic) and inhibitory (GABAergic) synaptic input from local neurons. The activity of the neurons responsible for these inputs are themselves largely regulated by glutamatergic and GABAergic inputs. The relevance of this local circuitry to seizures and epilepsy is discussed briefly.
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins 80523, USA.
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Smith
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Dudek
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology*; D018408:Patch-Clamp Techniques; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018377:Neurotransmitter Agents; D011810:Quinoxalines; D018698:Glutamic Acid; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid; C056723:FG 9041; D001640:Bicuculline