Highlights d Local basolateral amygdala (BLA) circuits generate sharpwave ripples (SWs) ex vivo d SWs occur with simultaneous synaptic burst inputs in BLA neurons d A chandelier interneuron discharge can initiate SW bursts through local circuits. d In silico chandelier-interneuron-driven modular microcircuits reproduce SW bursts
We have previously shown that in the basolateral amygdala (BLA), action potentials in one type of parvalbumin (PV)‐expressing GABAergic interneuron can evoke a disynaptic feedback excitatory postsynaptic potential (fbEPSP) onto the same presynaptic interneuron. Here, using whole‐cell recordings from PV‐expressing interneurons in acute brain slices we expand on this finding to show that this response is first detectable at 2‐week postnatal, and is most prevalent in animals beyond 3 weeks of age (>P21). This circuit has a very high fidelity, and single action potential evoked fbEPSPs display few failures. Reconstruction of filled neurons, and electron microscopy show that interneurons that receive feedback excitation make symmetrical synapses on both the axon initial segments (AIS), as well as the soma and proximal dendrites of local pyramidal neurons, suggesting fbEPSP interneurons are morphologically distinct from the highly specialized chandelier neurons that selectively target the axon initial segment of pyramidal neurons. Single PV interneurons could trigger very large (~ 1 nA) feedback excitatory postsynaptic currents (fbEPSCs) suggesting that these neurons are heavily reciprocally connected to local glutamatergic principal cells. We conclude that in the BLA, a subpopulation of PV interneurons forms a distinct neural circuit in which a single action potential can recruit multiple pyramidal neurons to discharge near simultaneously and feed back onto the presynaptic interneuron.
Neural circuits in the basolateral amygdala (BLA) play a pivotal role in the learning and memory formation, and processing of emotionally salient experiences, particularly aversive ones. A diverse population of GABAergic neurons present in the BLA orchestrate local circuits to mediate emotional memory functions. Targeted manipulation of GABAergic neuronal subtypes has shed light on cell-type specific functional roles in the fear learning and memory, revealing organizing principles for the operation of inhibitory circuit motifs in the BLA.
Visual hallucinations are common symptoms of seizures affecting primary and association cortices, and can provide vital information about the ictal onset zone. Epileptic kinetopsia, defined as illusionary movement of stationary objects in the visual field, was reported in a patient with a tumor in the temporal-parietal-occipital (TPO) junction. Intracranial stimulation of TPO junction did not evoke kinetopsia and the site of onset of this phenomenon is unknown. 1 We describe a patient with ictal kinetopsia whose seizure onset zone was localized with intracranial EEG.Case report. A 33-year-old right-handed woman had had pharmacoresistant focal epilepsy since age 15 months. Her habitual seizures started at age 16 years, characterized by visual perception of stationary objects located on her right side shift to the center or to the left. During these episodes, she described difficulties differentiating near and far objects, without blurring, double vision, scotomas, headache, or light hypersensitivity. This progressed to forceful blinking, tingling sensation of the left cheek and arm, followed by left arm posturing and left foot-jerking movements with preserved awareness. Postictally, visual field and color vision were normal. Scalp EEG revealed interictal epileptiform spikes or polyspikes over right centroparietal region (CP2, CP4, C4.P4, CZ, F4). Brain MRI showed area of cortical dysplasia in the right superior parietal lobule (SPL) and intraparietal sulcus (IPS) with cortical thickening on T1 and fluidattenuated inversion recovery signal change in the underlying white matter ( figure 1, A and B).Intracranial EEG recording and stimulation. Intracranial EEG was performed to determine the ictal onset zone and map sensory and motor functions. The patient underwent implantation of 8 3 7 contact subdural grid (10-mm spacing, AD-Tech, Watertown, WI) covering the area of cortical dysplasia and precentral and postcentral gyrus. Three depth electrodes were placed targeting the lesion (anteriorly D1, 1 3 6 contacts 5-mm spaced), posteriorly (D2, 1 3 4 contacts 5-mm spaced), and inferiorly (D3, 1 3 4 contacts 10-mm spaced) ( figure 1C). Interictally, frequent spikes were seen in the SPL and IPS. We recorded 51 seizures with kinetopsia at the onset, progressing to bilateral eye blinking and sometimes left hand-tingling sensation. In the postictal period, visual fields, language, and motor skills were normal. Ictal EEG showed stereotypical fast activity in right SPL and IPS (electrode contacts GA12 . GA13 . D2, ;70 Hz) ( figure 1D). Bipolar electrocortical stimulation of contact GA 13 (against distant electrode GA 53) evoked kinetopsia time locked to the electrical stimulus (figure e-1 on the Neurology ® Web site at Neurology.org); following stimulation, habitual interictal spikes returned on GA 12, 13, and D2. Resection was carried out at the posterior parietal cortex and pathology revealed Taylor type IIb focal cortical dysplasia. Postoperatively, there were no visual deficits. Transient difficulties to reach for objects wi...
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