Propagation of synchronous burst discharges from entorhinal cortex to morphologically and electrophysiologically identified neurons of rat lateral amygdala.
Intracellular and field potential recordings were taken from the lateral nucleus of the amygdala in a rat horizontal brain slice preparation that included hippocampal formation. Pyramidal cells comprised the majority of labeled cells (77%). Electrophysiological classification based on hyperpolarizing or depolarizing afterpotentials subdivided both the pyramidal and non-pyramidal cell classes, although pyramidal cells tended to have hyperpolarizing afterpotentials (70%) and non-pyramidal cells tended to have depolarizing afterpotentials (63%). Synchronous population bursts were triggered with single extracellular stimuli in the deep layers of entorhinal cortex. These events propagated from deep layers of entorhinal cortex into the lateral nucleus of the amygdala. Latencies were consistent with a direct entorhinal to amygdala projection. Individual lateral nucleus neurons exhibited responses ranging from a long burst response that included an initial period of 200 Hz firing and a tail of gamma frequency firing lasting over 100 ms (grade 1) to an epsp with no firing (grade 4). Half of pyramidal cells responding to events initiated in entorhinal cortex were found to receive epsps strong enough to trigger firing. Only one stellate neuron fired in response to entorhinal stimulation. Excitatory postsynaptic responses included NMDA and non-NMDA receptor mediated components. We demonstrate that synchronous population events can propagate from entorhinal cortex to the lateral nucleus of the amygdala and that pyramidal neurons of the lateral nucleus are more common targets than stellate neurons. We conclude that other synchronous events such as sharp waves and interictal spikes can spread from entorhinal cortex to amygdala in the same manner.
Funahashi
M
M
Department of Physiology, Okayama University Dental School, 2-5-1 Shikata-cho, 700-8525, Okayama, Japan. mfuna@dent.okayama-u.ac.jp
Matsuo
R
R
Stewart
M
M
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000679:Amygdala / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D048429:Cell Size / Q000502:physiology; D003344:Cortical Synchronization / Q000379:methods*; D003712:Dendrites / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D004558:Electric Stimulation; D018728:Entorhinal Cortex / Q000166:cytology / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000166:cytology / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D010852:Picrotoxin / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D051381:Rats; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000378:metabolism
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D018691:Excitatory Amino Acid Antagonists; D010852:Picrotoxin; D010879:Piperazines; D011963:Receptors, GABA-A; D016194:Receptors, N-Methyl-D-Aspartate; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid