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Neurotic Synapses Relations to Pain

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Steven Jacob

on 18 January 2016

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Transcript of Neurotic Synapses Relations to Pain

Neural Responses As Related To Pain
What is Pain?
Pain is defined as "a basic bodily sensation that is induced by a noxious stimulus, is received by naked nerve endings, is characterized by physical discomfort (as pricking, throbbing, or aching), and typically leads to evasive action" (Webster Medical Dictionary).
A Basic Context of the Nervous System
Specific Types of Neurons:

are the nerve cells that transmit information within the body.

are a collection of bundled neurons.

The Sensory neurons
transmit information from sensors that detect external stimuli or internal conditions. This information is integrated in the brain with immediate context and past experience.

The Interneurons
are known to form local circuits connecting various neurons in the brain.

motor neurons
are examples of neurons that extend out of processing centers and trigger muscle or gland activity.

Procedures and Data
Regarding Synaptic Control
Many processes have been used within Biological laboratories to track and study plethora of neurons and proteins related to Synapsis and pain. Such include Bioelectric Parameter measurments (through electrical conduction) and Synaptic Plasticity (for Pain Aversion).
By: Steven Jacob
Prashanth Ganesh
Jonathan Huang

What are synapses and how do they work?
Synaptic function can be characterized by the transmission of regulatory proteins (neurotransmitters) or electrical impulses between two adjacent neurons. The pathway gaps in which these communicating proteins cross are known as synapses.
Major Sources of Pain in the Human Body
recieve signals
transmits signals away from the neural cell body
The axon hillock is point where the summation of input signals from the dendrites are used to produce action potentials when a threshold barrier is crossed.
Synaptic terminals are part of the axon that forms the synapse. Neurotransmitters pass information from the transmitting neuron (presynaptic cell) to neuron/muscle/gland cell that recieves the signal (postsynaptic cell).
Inputs from other neurons or specific stimuli cause changes in the neuron's membrane potential that act as signals.

It is these rapid changes in membrane potential that enable us to see, read, study, make massive muscular gains, etc.
Gated ion channels open and close in response to stimuli, changing membrane potential
depolarization: ion channel opens so that the inside of the membrane becomes less negative than outside (Na+ flows in).
action potential: if the depolarization is large enough, it creates an electrical signal that travels along the membrane of a neuron as a nongraded (does not decay) depolarization.

It is generated at axon hillock, and is reinitiated in the neighboring region along the length of the axon. This is how the nerve impulse moves from the cell body to the synaptic terminal.
Arrival of the action potential depolarizes plasma membrane, opening ion channels to allow Ca+2 to enter the synaptic terminal. The increase in calcium ions cause some of the synaptic vesicles to fuse with the terminal membrane and release the neurotransmitter.
The Sensory Organ
Where the stimulus or pain is initially received and the beginning of the neurological response and synaptic responses.
This is the transition point between the Inter-neuron and the Motor-neuron in which neurotransmitters transfer from one neuron to another.
This is where the stimulus reaches the response and the neurons trigger the contraction of mucle cells
Proteins associated with Pain Signaling
According a study published in
, special presynaptic regulation proteins and kinases were discovered that lead to upregulation in pain induced signaling pathways. Such protein kinases include ERK 1/2 and CaMKII. The protein involved in such a process in called Synapsin I.
Works Cited
Bie B, Brown DL, Naguib M. 2011. Synaptic Plasticity and Pain Aversion. European Journal of Pharmacology (1st) [Internet]. [2011 Sept 30, cited 2013 Dec 2] Vol667(Issue 1-3) Location(e.g., 26-31). Available from: http://sciencedirect.com

White R, Zdeblik M. 2012. Method and Apparatus for Neural Signal Determination and Therapy Enhancement. (Patented) (1st) [Internet]. [2012 Mar 28, cited 2013 Dec 2] WO 2010135463 A2. Available from: http://www.google.com/

Kun-Long H, Su-Jane W, Ying-Chou W. 2013. Upregulation of presynaptic proteins and protein kinases associated with enhanced glutamate release from axonal terminals (synaptosomes) of the medial prefrontal cortex in rats with neuropathic pain. Pain Journal Online (1st) [Internet]. [2013 Nov 11, cited 2013 Dec 2] PII: S0304-3959(13)00570-8doi:10.1016/j.pain.2013.10.026. Available from: http://www.painjournalonline.com

How Does the Brain Respond to Pain?- Karen D. Davis. Dir. Karen D. Davis. YouTube. YouTube, 02 June 2014. Web. 17 Jan. 2016. <https://www.youtube.com/watch?v=I7wfDenj6CQ>.

Trumbull, FMG. "Central Nervous System Mechanisms of Pain Modulation." YouTube. YouTube, 19 Apr. 2011. Web. 17 Jan. 2016. <

The Three Levels of Pain: Pain, Excruciating Pain, and Stepping on a Lego. Digital image. Www.somecards.com. Www.somecards.com, n.d. Web. <http://www.someecards.com/usercards/viewcard/MjAxMi0yODE5ZmFkYjA1Mjc0NzEy>.
are specific types
sensory neurons that sends a collection of signals to the central nervous system as a response mechanism to potentially harmful/painful stimuli. The specific stimuli which could activate nociceptor activity include thermal variations, a break in the skin surface, and chemical stimulants.
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