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Brain Motor Centers and Pathways
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Two main feedback inhibitory connections can be identified: (i) one in the cerebellar cortex, involving granule cells and Golgi cells (Figure 12.15a), and (ii) the other outside the cerebellar cortex, involving the inferior olive and the cerebellar nuclei, through the CF afferents (Figure 12.15b). Two additional feedback paths have been identified involving cerebellar nuclei: (i) inhibitory cerebellar nuclear cells project back to the cerebellar cortex where they terminate on Golgi cells and disinhibit granule cells, and (ii) axon collaterals of some cerebellar nuclear output cells project back as MFs to the cerebellar cortex, terminating on granule cells that excite Golgi cells that, in turn, inhibit Purkinje cells that project to the same nuclear cells, thereby providing a positive feedback loop.
Motor Function and ControlDescending Tracts
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The cerebellum lies above the fourth ventricle in the posterior fossa of the cranium. It consists of the anterior, posterior and flocculonodular lobes. The cerebellar cortex consists of an outer layer containing basket and stellate cells, a middle layer containing Purkinje cells and an inner layer containing granular cells with interneurons called Golgi cells.
Glutamine, Glutamate, and GABA in Human Diseases
Published in Elling Kvamme, Glutamine and Glutamate in Mammals, 1988
GABA content is moderately reduced in the cerebellar cortex and is often markedly reduced in the dentate nucleus, the dominantly inherited OPCAs,31 and ataxia telangiectasia33 (Table 4). In these disorders, the GABA deficiency probably is due to specific loss of Purkinje neurons and cerebellar cortical intemeurons. GABA is almost certainly the inhibitory neurotransmitter of most of the Purkinje cells,47-49 and it is probably the neurotransmitter of one or more of the three types of inhibitory intemeurons in the cerebellar cortex; the basket, stellate, and Golgi cells.48,49 GABA content is also markedly reduced in the globus pallidus and substantia nigra in Hallervorden-Spatz disease (Table 4), in this case because of the extensive loss of neurons in the globus pallidus where neuropathological changes are maximal and because of the loss of GABAergic neurons running from or through the globus pallidus to the substantia nigra.50
Revisiting the pathoanatomy of pseudobulbar affect: mechanisms beyond corticobulbar dysfunction
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2018
The modulatory role of the cerebellum in emotional expression is increasingly recognized as an important physiological function, integrating inputs from motor, association and limbic cortices, and acting as a gating mechanism to allow socially appropriate emotional responses. Dysfunction of corticopontocerebellar networks is regarded as a key factor in exhibiting context-inappropriate emotional responses (38). MS studies have also confirmed impaired cerebellar gate-control mechanisms and sensory network disruptions in PCL (39). At a cellular level, the microscopic gate-control function of the cerebellum has been primarily linked to Golgi cells which under physiological conditions inhibit weakly activated granule cells and reduce Purkinje cell firing (40). While cerebellar degeneration in ALS is relatively well established (41,42), it is seldom linked directly to PCL (15). With the ever expanding non-motor functions of the cerebellum, PCL is sometimes referred to as ‘affective dysmetria’ (43). Consistent with this model, the study of Christidi et al. confirms inferior and middle cerebellar peduncle degeneration in patients with PCL.
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].
The Effect of Induced Diabetes Mellitus on the Cerebellar Cortex of Adult Male Rat and the Possible Protective Role of Oxymatrine: A Histological, Immunohistochemical and Biochemical Study
Published in Ultrastructural Pathology, 2021
Amany Mohamed Shalaby, Adel Mohamed Aboregela, Mohamed Ali Alabiad, Mona Tayssir Sadek
Examination of the cerebellar cortex from the control group revealed regular arrangement of myelin sheaths in the molecular layer (Figure 3A). The perikaryons of Purkinje cells in the Purkinje cell layer contained large euchromatic nuclei with prominent nucleoli, mitochondria and rER (Figure 3B). The granular layer displayed two cell types: granule cells with heterochromatic nuclei surrounded by thin rim of cytoplasm and Golgi cells (Figure 3C). The cerebellar cortex had many synapses in which multiple synaptic vesicles were present and each synaptic site showed dense presynaptic and postsynaptic membranes (Figure 3D). The blood capillaries were enveloped by processes of astrocytes (Figure 3E). On the other hand, sections from the induced diabetic group (subgroup IIIa) showed irregularity and splitting of the myelin sheaths in the molecular layer (Figure 4A). Moreover, many Purkinje cells were shrunken and dark with ill-defined nuclei and dilated Golgi saccules. Vacuolation of the surrounding neuropil was also detected (Figure 4B). Other Purkinje cells had irregular nuclei with dilated perinuclear cisternae, dilated rER and vacuolated cytoplasm (Figure 4C). Cells in the granular layer appeared dark with irregular nuclear outlines and vacuolated cytoplasm. Some cells revealed shrunken nuclei (Figure 4D). Multiple synapses containing numerous synaptic vesicles were demonstrated (Figure 4E). In addition many processes of astrocytes related to blood capillaries were swollen and markedly enlarged (Figure 4F). As regards the induced diabetic-oxymatrine group (subgroup IIIb), it displayed partial preservation of the cerebellar cortex structure. Most of the nerve fibers in the molecular layer showed regular arrangement of the myelin sheaths. However, few nerve fibers revealed irregularity of their myelin sheaths (Figure 5A). Most of the Purkinje cells appeared normal (Figure 5B). Others had dark cytoplasm (Figure 5C). Also, most of the granule cells were normal, whereas some cells revealed rarefaction of their cytoplasm (Figure 5D). Many synapses containing synaptic vesicles were present (Figure 5E). The blood capillaries were surrounded by moderately enlarged processes of astrocytes (Figure 5F).