Research reportAxon terminals of GABAergic chandelier cells are lost at epileptic foci
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Cited by (88)
Reclusive chandeliers: Functional isolation of dentate axo-axonic cells after experimental status epilepticus
2023, Progress in NeurobiologyChandelier cells shine a light on the formation of GABAergic synapses
2023, Current Opinion in NeurobiologyMolecular mechanisms of axo-axonic innervation
2021, Current Opinion in NeurobiologyCitation Excerpt :For instance, altered regulation of PC firing activity has been found in movement disorders as well as cognitive dysfunction, including autism spectrum disorder (ASD) [45]. ChC connectivity defects have also been tied to ASD, in addition to schizophrenia and epilepsy, likely due to imbalances in E/I homeostasis [46–49]. Lastly, in the spinal cord, deficits in presynaptic inhibition of sensory neurons by GABApre terminals have been observed in individuals with Huntington and Parkinson diseases [50].
Etiology-related Degree of Sprouting of Parvalbumin-immunoreactive Axons in the Human Dentate Gyrus in Temporal Lobe Epilepsy
2020, NeuroscienceCitation Excerpt :Data are abundant about the sprouting of granule cell axons (mossy fibers) into the molecular layer of the DG. While mossy fibers normally terminate on both excitatory and inhibitory neurons of the CA3 region and those of the dentate hilus (Frotscher, 1985, 1989; Ribak, 1985; Claiborne et al., 1986; Soriano and Frotscher, 1993; Acsády et al., 1998), in the epileptic human hippocampal formation as well as in animal models of TLE, mossy terminals form synapses on granule cell dendrites in the molecular layer of the DG (Houser et al., 1990; Cavazos et al., 1991; Represa et al., 1993; Mathern et al., 1994; Franck et al., 1995). Sprouting of pyramidal cells’ axons in the CA1 region may result in a stronger excitatory input to neighboring pyramidal neurons (Lehmann et al., 2000, 2001).
Shedding Light on Chandelier Cell Development, Connectivity, and Contribution to Neural Disorders
2020, Trends in NeurosciencesAxo-axonic Innervation of Neocortical Pyramidal Neurons by GABAergic Chandelier Cells Requires AnkyrinG-Associated L1CAM
2019, NeuronCitation Excerpt :The striking selectivity of ChC innervation at the AIS of PyNs has intrigued neuroscientists ever since the initial discovery of ChCs in the 1970s (Jones, 1975; Somogyi, 1977; Szentágothai and Arbib, 1974). This interest has heightened with accruing evidence showing that this unique form of subcellular innervation allows ChCs to exert powerful yet precise control over cortical PyN spiking and population output (Howard et al., 2005; Inan and Anderson, 2014; Lu et al., 2017) and, in particular, given increasing reports linking ChC connectivity defects to neurological conditions, such as schizophrenia and epilepsy (Ariza et al., 2018; Del Pino et al., 2013; Lewis, 2011; Ribak, 1985; Rocco et al., 2017). Despite these findings, little to nothing is known about the mechanisms underlying the subcellular innervation of neocortical PyN AISs by ChCs.