Neurobiology of Pain: Case Study, Neural Pathways, and Transmitters

This case study examines the neurobiology of pain, focusing on a patient, Katie, who dislocated her shoulder. The analysis explores how factors such as previous injuries and anxiety can exacerbate pain. The study details the activation of brain regions like the ACC and insular cortex during pain perception. It discusses the role of neurotransmitters, including glutamate, serotonin, and GABA, in pain modulation. The document outlines the pain pathway, from transduction by nociceptors to perception, including the roles of Aδ and C fibers, and the release of neurotransmitters like substance P. The modulation of nociceptive transmission, involving both inhibitory and excitatory mechanisms, is also discussed. The study references several scientific articles to support its findings.

Running head: NEUROBIOLOGY OF PAIN
NEUROBIOLOGY OF PAIN
Name of the Student
Name of the university
Author’s note

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The case study states, that Katie has dislocated her right shoulder during the last game of the
session. In this case the fact one of the factor that can influence pain is that, this was Katie’s
second injury, which might have exacerbated the pain. Furthermore, Katie is anxious that she
would miss the finals, which might have increased the pain further.
People suffering from pain presents an activation of the limbic areas, as well as cerebral
alterations. There is an activation of the medial prefrontal cortex, the hippocampus and the
anterior cingulate cortex and the insular cortex1. The ACC joins the neurons joins the neurons of
the frontal cortex, the amygdala and the thalamus. Studies have proved the ACC injuries reduces
the sensitivity of pain. The Insular cortex is another area of the cortex that is recruited in the
pain. The posterior portion insular cortex takes part in the somatosensory characteristics of the
pain and the interior portion is related to the affective respect1. Again pain is controlled by some
neurotransmitters like Glutamate, serotonin and γ-amino butyric acid (GABA). Loss of the
GABA neurotransmission present in the dorsal horn of the spinal cord is an important
mechanism leading to the development of the neuropathic pain. Monoamine neurotransmitters,
such as the serotonin (5-HT), dopamine (DA), and norepinephrine (NE), have been studied for
understanding the molecular mechanisms that are responsible for chronic pain and depression2.
According to the classical monoamine hypothesis, depression might occur due to decreased
accessibility of monoamine neurotransmitters like 5-HT and NE in the central nervous system2.
The pain pathway consists of three order of neurons that carry action potentials signaling
the pain. The pain occurs in five phases like 1) Transduction 2) Conduction 3) Transmission 4)
Modulation 5) Perception. The first order neurons contains specialist receptors known as

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nociceptor that are stimulated by various toxic stimuli. These nociceptors are present at the free
nerve endings present in the primary afferent neuron4. Mechanical, thermal and the mechano-
thermal nociceptor signals are conducted to the dorsal horn of the spinal cord by the help of the
Aδ fibres. These fibers have less threshold for the firing and the fast transmission speed the
means that they are the reason for the transmission of the first felt pain. The polymodel
nociceptors transfers their signals to the dorsal horn with the help of the C fibers. These fibers
are responsible for the secondary pain that is being felt as a dull, deep and throbbing pain4.
C fibers are terminated in Rexed laminae I and II and helps in the secretion of the
neurotransmitter substance P. Some of the other neurotransmitters are generated by the primary
afferent neurons that are ending within the spinal cord like aspartate and vasoactive peptide.
The nociceptor pain consists of high activation threshold. Hence intense stimulation is
required for the generation of the threshold5. Injury to the neurons and the surrounding tissue
exposes the neighboring nociceptors to irritating substances like the neurotransmitters,
bradykinin, serotonin, creating a condition that can be termed as hyperesthesia5. Modulation of
the nociceptive transmission is an adaptive process that involves both inhibitory and the
excitatory mechanism of pain. Perception of the nociceptive pain depends upon the neural
processing occurring in the spinal cord.

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References
1. Denk F, McMahon SB, Tracey I. Pain vulnerability: a neurobiological perspective.
Nature neuroscience. 2014 Feb;17(2):192.
2. Sheng J, Liu S, Wang Y, Cui R, Zhang X. The Link between Depression and Chronic
Pain: Neural Mechanisms in the Brain. Neural Plast. 2017;2017:9724371.
doi:10.1155/2017/9724371
3. Cohen SP, Mao J. Neuropathic pain: mechanisms and their clinical implications. Bmj.
2014 Feb 5;348:f7656.
4. Han C, Pae CU. Pain and depression: a neurobiological perspective of their relationship.
Psychiatry investigation. 2015 Jan;12(1):1.
5. Schwaller F, Fitzgerald M. The consequences of pain in early life: Injury‐induced
plasticity in developing pain pathways. European journal of neuroscience. 2014 Feb
1;39(3):344-52.