1. Upper motor neurons (UMNs), whose nucleiare located in the motor region of the cerebral cortex (these nervesplay a role in the pyramidal tract) or in the brainstem (these nerves are partof the extrapyramidal tract), do not innervate tissues but do synapse(and thus communicate) with lower motor neurons in the anterior or ventral hornof the spinal cord.
UMNs generally function to carry and transmit signals from thecerebral cortex or brainstem to the lower motor neurons (LMNs). Incontrast, LMNs are located in the brainstem or spinal cord and innervateskeletal muscle, glands, and smooth muscle. LMNs generally function toconnect the UMNs, interneurons, and/or sensory neurons to muscles or glands topromote action. LMNs connect the central nervous system to the peripheral body. 2.Astrocytes are multifaceted in function with an overlying duty ofneuronal support. Some of its physiologic duties include regulation of neuronalmetabolism by the export and transfer of glucose or lactate, the regulation ofions and water, the clearance of neurotransmitters including the excitatoryglutamate, the regulation of endothelial cells and their supporting pericytesduring development, the interaction with microglia, and the production and/or alterationof the extracellular matrix. During an induced pathological state, astrocyteshave been shown to proliferate to provide more support to neuronal cells.
Forexample, during a state of ischemia, this proliferation may function to providemore metabolic substrate, like glucose (which can be metabolized via glycolysiswithout oxygen), for neuronal cells to prevent neuronal death. During states of inflammation and hypoxia, it is knownthat astrocytes aid in neuronal survival, possibly through theirrelease of neurotropic factors. Microglia, commonly known as themacrophages of the brain, broadly function to aid in neuronal pruning duringdevelopment and also play a role in inflammation/immune function inthe central nervous system. These cells are known to migrate tosites of injury and release neurotropic factors.
During an inducedpathological state, like inflammation, microglia respond and migrate. They express receptors that, when triggered by signals of inflammation, areinvolved in promoting cytokine release and initiating phagocytosis. Theseprocesses may harm surrounding neuronal cells. Microglia have been shown to beboth neurodegenerative, as in Alzheimer’s Disease and their role in synapseloss, and neuroprotective, as in states of ischemia.Oligodendroglia function to producemyelin, necessary for saltatory conduction, in the central nervous system. Defects in oligodendroglia would lead to a lack of myelination on neurons ofthe central nervous system, and thus errors in signal transmission would arise.This would cause movement and sensory defects and may induce a pathologicalstate. For example, in multiple sclerosis, a disease characterized by imbalance,weakness, and possibly vision distortion, oligodendroglia are thetarget of immune cells in conditions of chronic inflammation.
3.Associated with fear, emotion, and physiological signs of panic includingincreased respiration, blood pressure, startle response, and heart rate, the amygdala is an appealing pharmaceutical target to alleviate symptoms ofgeneralized anxiety disorder (GAD). Specifically, within the amygdala lies thebasolateral complex (BAL), which relays signals to the central nucleus of theamygdala (CeA), which transmits signals to the rest of the brain. The BAL-CeA axis is a potential therapeutic target of GAD because it is thepathway necessary to transmit feelings of anxiety from the amygdala to the restof the brain. Intercalated neurons, neurons that act to inhibit BAL activationof CeA, naturally release the neurotransmitter gamma-aminobutyric acid (GABA)into neuronal synapses. GABA is a neurotransmitter that isinhibitory to neurons in the central nervous system, and it is associated with reducedanxiety. Thus, GABA is a possible neurotransmitter that therapeuticsmay mimic to reduce symptoms of GAD via inhibition of the neurons between BALand CeA.