1. (LMNs). In contrast, LMNs are located in the

1. Upper motor neurons (UMNs), whose nuclei
are located in the motor region of the cerebral cortex (these nerves
play a role in the pyramidal tract) or in the brainstem (these nerves are part
of the extrapyramidal tract), do not innervate tissues but do synapse
(and thus communicate) with lower motor neurons in the anterior or ventral horn
of the spinal cord. UMNs generally function to carry and transmit signals from the
cerebral cortex or brainstem to the lower motor neurons (LMNs). In
contrast, LMNs are located in the brainstem or spinal cord and innervate
skeletal muscle, glands, and smooth muscle. LMNs generally function to
connect the UMNs, interneurons, and/or sensory neurons to muscles or glands to
promote action. LMNs connect the central nervous system to the peripheral body.



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Astrocytes are multifaceted in function with an overlying duty of
neuronal support. Some of its physiologic duties include regulation of neuronal
metabolism by the export and transfer of glucose or lactate, the regulation of
ions and water, the clearance of neurotransmitters including the excitatory
glutamate, the regulation of endothelial cells and their supporting pericytes
during development, the interaction with microglia, and the production and/or alteration
of the extracellular matrix. During an induced pathological state, astrocytes
have been shown to proliferate to provide more support to neuronal cells. For
example, during a state of ischemia, this proliferation may function to provide
more metabolic substrate, like glucose (which can be metabolized via glycolysis
without oxygen), for neuronal cells to prevent neuronal death. During states of inflammation and hypoxia, it is known
that astrocytes aid in neuronal survival, possibly through their
release of neurotropic factors.

Microglia, commonly known as the
macrophages of the brain, broadly function to aid in neuronal pruning during
development and also play a role in inflammation/immune function in
the central nervous system. These cells are known to migrate to
sites of injury and release neurotropic factors. During an induced
pathological state, like inflammation, microglia respond and migrate. They express receptors that, when triggered by signals of inflammation, are
involved in promoting cytokine release and initiating phagocytosis. These
processes may harm surrounding neuronal cells. Microglia have been shown to be
both neurodegenerative, as in Alzheimer’s Disease and their role in synapse
loss, and neuroprotective, as in states of ischemia.

Oligodendroglia function to produce
myelin, necessary for saltatory conduction, in the central nervous system. Defects in oligodendroglia would lead to a lack of myelination on neurons of
the central nervous system, and thus errors in signal transmission would arise.

This would cause movement and sensory defects and may induce a pathological
state. For example, in multiple sclerosis, a disease characterized by imbalance,
weakness, and possibly vision distortion, oligodendroglia are the
target of immune cells in conditions of chronic inflammation.



Associated with fear, emotion, and physiological signs of panic including
increased respiration, blood pressure, startle response, and heart rate, the amygdala is an appealing pharmaceutical target to alleviate symptoms of
generalized anxiety disorder (GAD). Specifically, within the amygdala lies the
basolateral complex (BAL), which relays signals to the central nucleus of the
amygdala (CeA), which transmits signals to the rest of the brain. The BAL-CeA axis is a potential therapeutic target of GAD because it is the
pathway necessary to transmit feelings of anxiety from the amygdala to the rest
of the brain. Intercalated neurons, neurons that act to inhibit BAL activation
of CeA, naturally release the neurotransmitter gamma-aminobutyric acid (GABA)
into neuronal synapses. GABA is a neurotransmitter that is
inhibitory to neurons in the central nervous system, and it is associated with reduced
anxiety. Thus, GABA is a possible neurotransmitter that therapeutics
may mimic to reduce symptoms of GAD via inhibition of the neurons between BAL
and CeA.