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Neurons
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Some interneurons are named according to anatomical features. Stellate cells are interneurons having several dendrites radiating from the cell body in a star-like manner. They are found in the cerebral and cerebellar cortices and could be excitatory or inhibitory. Basket cells are inhibitory interneurons having highly branched axonal arborizations that are like baskets surrounding part of the soma of the target cell. Basket cells are found throughout the brain. Chandelier cells are inhibitory interneurons so called because their axons make highly specialized candle-shaped synaptic “cartridges” on initial segments of axons of pyramidal neurons. Double-bouquet cells are numerous cortical inhibitory interneurons characterized by tightly interwoven bundles of vertically oriented axonal arborizations resembling a horsetail. Martinotti cells are small inhibitory interneurons found in various layers of the cerebral cortex. Their axons project vertically to layer I and terminate on the dendritic tufts of pyramidal neurons.
Experimental Models of Status Epilepticus
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
The perforant path stimulation model results in cell death, primarily in the ipsilateral dentate hilus.19 While vulnerable cell populations include hilar mossy cells, and somatostatin- and neuropeptide Y (NPY)-containing neurons, GABA-containing neurons in the hilus and granule cell layer and granule cells survive.19 The lesion induced by perforant path stimulation is similar to the lesion found in sclerotic hippocampi removed from cryptogenic epileptic patients.90,113 The survival of GABAergic neurons led to the formation of the dormant basket cell hypothesis to explain the seizure-induced loss of inhibition.91 The dormant basket cell hypothesis states that inhibition in the dentate gyrus depends on the tonic activation of inhibitory interneurons by hilar mossy cells. A loss of mossy cells results in a functional loss of inhibition not because the inhibitory neurons are dead but because the inhibitory neurons are not receiving sufficient activation to respond to remaining inputs.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
These are NON-PYRAMIDAL NEURONS, found in the CEREBRAL CORTEX, HIPPOCAMPUS (see HILAR CELLS) and the cerebellum (see CEREBELLUM- ANATOMICAL ORGANIZATION) which function as INTERNEURONS. They are called basket cells (or basket neurons) because they make so many synaptic connections that they appear to surround-to make a basket for-the neurons they make contact with.
Ataxia and ophthalmoplegia: an atypical case of Miller Fisher syndrome (MFS) with anti-GAD antibody
Published in International Journal of Neuroscience, 2022
Ali R. Shoraka, Xiang Fang, Diaa Hamouda, Bhanu Gogia, Xiangping Li
The GAD-Ab works against the glutamic acid decarboxylase (GAD) enzyme. GAD converts glutamate to gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the vertebrate central nervous system [12]. Previous reports have shown that several neurological syndromes were associated with GAD-Ab, such as stiff-person syndrome, limbic encephalitis, cerebellar ataxia, and autoimmune epilepsy. Collectively, these syndromes could be known as ‘anti-GAD positive neurological syndromes’ [13]. Moreover, two cases of autonomic neuropathy have been demonstrated in association of significantly elevated anti GAD-Ab [14]. A possible pathogenic role of GAD-Ab has been suggested by several observations but has not been definitely proven. Also, the reason for different clinical phenotypes associated with GAD-Ab is still unclear [15]. Intrathecal production of GAD-Ab has been detected in patients with ataxia but their role in pathogenesis remains unknown. CSF from GAD-Ab positive patients reduces GABA synthesis and inhibits postsynaptic currents in Purkinje cells of rat cerebellar slices, possibly representing a reduction in the GABA-mediated inhibitory activity of basket cells on Purkinje neurons. Also, the presence of GAD in nerve terminal of neuromuscular junctions was reported [16].
Synaptic remodeling, lessons from C. elegans
Published in Journal of Neurogenetics, 2020
Andrea Cuentas-Condori, David M. Miller, 3rd
In C. elegans, as in mammals, GABA-dependent inhibition determines circuit function (Lehmann, Steinecke, & Bolz, 2012; Pelkey et al., 2017; Schuske, Beg, & Jorgensen, 2004). Strong conservation of key molecular determinants of GABAergic function, including the GABA biosynthetic enzyme, GAD (UNC-25), vesicular GABA transporter, VGAT (UNC-47) and GABA ionotropic (UNC-49) and metabotropic (GBB-1/2) receptors highlight striking molecular similarities and suggest that developmental mechanisms that control GABA-dependent circuit refinement might also be conserved (Jin et al., 1999; Mclntire et al., 1993a; 1993b). GABAergic neurons constitute about 20–30% of the mammalian cortex, typically provide inhibitory input to glutamatergic neurons and are structurally and functionally diverse (Hendry, Schwark, & Jones, 1987; Pelkey et al., 2017; Sherwood et al., 2010). Similar to DD neurons, some mammalian GABAergic neurons receive excitatory input through dendritic spines and others innervate target cells through en-passant boutons (Kawaguchi, Karube, & Kubota, 2006; Pelkey et al., 2017). GABAergic interneurons can also be extensively refined during postnatal development. Of particular interest, the elimination of perisomatic inputs from GABAergic basket cells to glutamatergic pyramidal neurons depends on a mechanism that requires GABA signaling (Sullivan et al., 2018; Wu et al., 2012). The parallel role of GABA in promoting the removal of presynaptic termini in developing DD neurons in C. elegans could be indicative of shared cell biological pathways for synaptic remodeling (Miller-Fleming, 2016).
Brain circuits and neurochemical systems in essential tremor: insights into current and future pharmacotherapeutic approaches
Published in Expert Review of Neurotherapeutics, 2018
Sara M Schaefer, Ana Vives Rodriguez, Elan D Louis
Whole-scalp neuromagnetometry recordings of brain activity with simultaneous arm muscle electromyography in ET patients during postural tremor, and subsequent analysis of cerebro-muscular coherence and cerebro-cerebral coherence, suggest that tremor production involves a circuit that includes some or perhaps all of the following brain structures – the contralateral cerebral cortex and thalamus, the brainstem, and the ipsilateral cerebellum [5]. A basic schematic of this circuit is shown in Figure 1. In the normal brain, neurons in the deep cerebellar nuclei (DCNs) output to the thalamus, which outputs to the cerebral cortex, modulating movement. The DCNs are simultaneously inhibited by PCs from the cerebellar cortex and excited by neuronal input from the ION [10]. In addition to projecting excitatory impulses to DCNs, the ION also excites PCs through climbing fiber collaterals, thus modulating the activity of the cerebellum by directly exciting and indirectly inhibiting (through PCs) DCNs [10]. Cerebellar output is further modulated within the cerebellum itself by a number of other neurons, including basket cells (which inhibit PCs), cerebellar granule cells (which excite PCs), and PCs (which can directly inhibit other PCs through recurrent collaterals) [8,9,11,12]. In addition to the inhibitory neurons (i.e. GABAergic neurons) noted earlier (i.e. basket cells, PCs), other neurons in the cerebellum are also GABAergic (e.g. Golgi cells, stellate cells, projection neurons from the DCN to the ION), adding further complexity to the network. Within this complex system across several brain regions, the location and physiological driving force of the dysfunction that leads to tremor in ET is under debate. The ION and the cerebellum, most notably the PC layer, have both been implicated; these two models are discussed in detail in other reviews [2,3].