Information

Why do neurons die so quickly (relative to other cells) when deprived of oxygen?


This question could be considered a follow-up question to Why is a lack of oxygen fatal to cells?, although the top answer there does not address why damage starts to pop in.

The answer says this:

Neurons are also highly metabolically active, which means they generate more waste products. A buildup of nitrogenous waste products in the cell (and bloodstream) can be potentially fatal due to it's effects on pH (screws up enzymes and a whole slew of biochemical reactions)

But when the brain is deprived of oxygen, metabolism shuts down. So waste products aren't being generated anymore.

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Basically I'm wondering - what causes neurons, in particular, to die so quickly (relative to other cells, like kidney cells) after they're depleted of energy?


There is a good review in the Journal of Experimental Biology (Bickler and Donohoe 2002, JEB 205, 3579-3585) I will just summarize for those that do not have access to the review.

Neurons use lot of energy to maintain their polarized state, this is not required to other cells. When O2 or blood flow is reduced, the neuronal ATP levels breaks down very fast, with 90% ATP depleted in less than 5 minutes. Without ATP, the neuron can not maintain the correct ion flux, so depolarization occurs causing glutamate excitotoxicity, cell swelling and finally cell death.


A &P 2 Module 1

Bipolar neurons have 2 extensions, 1 axon and 1 dendrite and are found as receptors cells in the visual and olfactory systems.

Motor neurons are multipolar and carry impulses from the central nervous system to muscle fibers or glands.

2nd - Optic - Sensory - Sense of sight

3rd - Oculomotor - Motor Eye movement

4th - Trochlear - Motor Eye movement

5th - Trigeminal - Motor and sensory Chewing and sensation of face, nose, and mouth

6th - Abducens - Motor Eye movement

7th - Facial Motor and sensory - Facial expressions and sensation of tongue

8th - Vestibulocochlear Sensory - Hearing and balance

9th - Glossopharyngeal Motor and sensory - Swallowing and taste

10th - Vagus Motor and sensory - Digestion, regulation of heart rate, sensation of digestive tract

11th - Accessory Motor - Rotation of the head and shrugging of the shoulders


Test 2


2.Metencephalon
- Pons (bridge): Works in conjunction to increase arousal and readiness of
other parts of the brain.

-cerebellum: ▪ Fine detailed motor control, balance, coordination
▪ Shifting attention between auditory and visual stimuli

Midbrain:
3. Mesencephalon
Midbrain, Superior and Inferior
Colliculus
§ Tectum (roof) contains:
▪ Superior and inferior colliculli
▪ Superior (vision) and Inferior (hearing)
§ Tegmentum contains
▪ Periaqueductal gray (surrounds cerebral aqueduct and
plays a rold in pain and analgesia)
▪ enkephalins, and endorphins
▪ Substantia nigra (black substance) - voluntary movement
▪ dopamine
Red Nucleus
¡ primary motor cortex synapses and output to cranial nerves
controlling facial muscles
¡ Serotonin and perhaps GABA
- Locus Coeruleus (local blue) - innervates many structures, including hypothalamus, cerebral
cortex, and hippocampus, and is thought to be involved in general
arousal
norepinephrine

Forebrain: Most anterior and prominent part of the
mammalian brain
¡ 2 hemispheres
¡ Consists of the outer cortex and subcortical
regions
¡ Each side receives sensory info and controls
motor movement from the contralateral side
of the body
4. Diencephalon
-Hypothalamus, Pituitary Gland,
Thalamus, and Pineal Gland
Thalamus
Hypothalamus
Pituitary gland: "Master gland", Controlled by hypothalamus, Regulates
growth hormone

5. Telencephalon
-Cortex /Lobes, Cingulate gyrus, and
Corpus Callosum
Basal ganglia: Caudate nucleus
▪ Putamen
▪ Globus pallidus
Parkinson's and Huntington's disease


Brain oxygen levels can sometimes suddenly drop, such that your nonessential body processes shut down, allowing the vital functions of the brain to continue. Fainting is the result. Symptoms such as light-headedness, nausea and a feeling of warmth may precede fainting, according to the Mayo Clinic. If you faint regularly, see your doctor to determine if there is a serious underlying cause.

  • Brain oxygen levels can sometimes suddenly drop, such that your nonessential body processes shut down, allowing the vital functions of the brain to continue.
  • If you faint regularly, see your doctor to determine if there is a serious underlying cause.

Introduction

For many cells, the balance between life and death is regulated by the BCL-2 family of proteins. As reviewed previously, a dance occurs within the BCL-2 family on the mitochondrial outer membrane (MOM) dance floor [1]—with the outcome of this dance ultimately deciding whether a cell will live or die. But what if the dance floor were extended unimaginably? Neurons are morphologically unique cells with long cytoplasmic extensions called axons. The vast distance axons span results in a separation of mitochondrial populations within a single cell—one population within the cell body, and another that extends down the length of the axon. The integrity of both mitochondrial populations is vital to neuronal health [2]. The same BCL-2 family dance-of-death occurs within neurons but now the dance floor has been extended and as a result, the BCL-2 family can regulate axonal degeneration in addition to life and death. Mitochondria are the “power-house” organelle of the cell, but ironically, the MOM is also the platform to initiate BCL-2-protein regulated cell death [1]. MOM permeabilization (MOMP) results in the release of pro-apoptotic factors into the cytoplasm thereby committing a neuron to die through apoptosis or degenerate only the axon. It remains unclear how the BCL-2 family of proteins regulates this dichotomy of programmed cell death and degeneration, yet it is widespread in the nervous system during development [3] and disease.


What Happens During Cardiac Arrest

During cardiac arrest, unconsciousness will occur rapidly once the heart stops beating, typically within 20 seconds. Deprived of the oxygen and sugars it needs to function, the brain will be unable to deliver the electrical signals needed to sustain organ function, including breathing.

This can lead to a hypoxic-anoxic injury (HAI). Hypoxia refers to a partial lack of oxygen, while anoxia indicates a total lack of oxygen. In general, the more complete the deprivation, the more severe the harm to the brain.

With cardiac arrest, the lack of circulation affects not just one part of the brain but everywhere in the brain where blood flows. An injury caused by apoxia is referred to as diffuse brain damage. Among the parts of the brain most vulnerable to injury is the temporal lobe where memories are stored.

Timeline

When cardiac arrest occurs, it is essential to start cardiopulmonary resuscitation (CPR) within two minutes. After three minutes, global cerebral ischemia (the lack of blood flow to the entire brain) can lead to progressively worsening brain injury.

By nine minutes, severe and irreversible brain damage is likely. After 10 minutes, the chances of survival are low.

Even if a person is resuscitated, eight out of every 10 will be comatose and sustain some level of brain damage. Simply put, the longer the brain is deprived of oxygen, the worse the damage will be.

If you haven't learned CPR recently, things have changed. You can usually find a two- to three-hour training course at a local community health center or by contacting a Red Cross or American Heart Association office in your area.


Peripheral Receptive Fields

The autonomic reflexes of the mammalian DR can be induced with only snout immersion, suggesting that primary afferent fibers innervating paranasal areas may be important. Paranasal areas ( FIGURE 3 ), including the anterior nasal mucosa, are innervated by branches of the infraorbital nerve as well as the anterior ethmoidal nerve (AEN) from maxillary and ophthalmic divisions of the trigeminal, respectively (250). Innervation of the nasal mucosa is via free nerve endings from small-diameter fibers (39), many of which contain peptides, notably calcitonin gene-related peptide and substance P (76, 150, 151, 197, 228, 230, 237, 238), derived from trigeminal ganglion neurons (104, 151, 211, 230). Most of these fibers are sensory in function, and many respond as chemoreceptors to local chemical changes induced by inhalation of noxious gases or inflammatory processes (43, 44, 45, 89, 101).

Work on diving rodents suggest paranasal areas (shaded blue) innervated by the anterior ethmoidal and infraorbital nerves are important for initiating the diving response

These nerves project [A1 and A2 show transport of an HRP cocktail (colored gold) transported transganglionically from the anterior ethmoidal and infraorbital nerves, respectively] into the rostral medullary dorsal horn (MDH) overlapping the caudal subnucleus interpolaris (Sp5I). Note the band of neuropil just dorsal to the Sp5I (arrows) is labeled from either nerve. Neurons activated with cFos (A3 small black nuclei) induced by diving are found in similar neuropil. Moreover, small, bilateral injections of lidocaine (blue squares) or kynurenate (red circles) made into similar locations (A4) blocked the cardiorespiratory responses of nasal stimulation. The hallmark of the diving response is the dramatic bradycardia (see FIGURE 1A ) many neurons surrounding the rostral nucleus ambiguus are labeled with cFos after diving (B1), and some of these are preganglionic cardiac motoneurons (B2 arrows point to double-labeled neurons containing cFos and a retrograde tracer injected into the pericardial sac). There also is a massive but selective peripheral vasoconstriction during diving in rats mediated by neurons in the rostral ventrolateral medulla (C1 shows cFos-labeled neurons in the RVLM induced by diving) many such neurons are monoaminergic (C2 showing double labeled neurons with antibodies against cFos and tyrosine hydroxylase). The third neuronal reflex induced by underwater submergence is a profound apnea, which is maintained despite gross disruption of blood chemistry, suggesting inhibition of the respiratory chemoreceptor reflex. Few neurons were activated in the medullary ventral respiratory column (see C1, C2), but projections from the MDH to the ventral surface of the caudal medulla at the spinomedullary junction (D2 approximately �.6 mm from bregma) overlap where neurons/glia activated by diving are found (D1, arrows small black profiles show cFos activation). Arrows in D2 point to presumptive neurons with juxtaposed BDA fibers. Injection of a retrograde tracer, which included the retrotrapezoid nucleus labeled small neurons in neuropil similar to that labeled by paranasal primary afferent fibers (D3, arrow). Anterograde transport of tracers injected into these areas of the MDH resulted in extremely small labeled fibers with swellings (D4, arrows) in the retrotrapzoid nucleus ventral to the facial motor nucleus. Similar neurons/glia have long been suspected to be chemoreceptors sensitive to high P co 2, but details of how they interact with central respiratory neurons is lacking. Other studies (188) have shown the neuronal circuitry driving the diving response is contained within the medulla and spinal cord.

The AEN is considered the “gatekeeper” nerve by us since it is the first to sense noxious gases or water entering the nasal passages. Indeed, transection of the AEN eliminates the bradycardia and attenuates the apnea and ABP changes to nasal stimulation (210). This nerve contains both mechanoreceptors and chemoreceptors (136, 165, 221, 222, 223, 224, 229, 248) responsive to a variety of stimuli, with fibers of small diameter in the Aγ or C range (7, 161) that reach between the epithelial cells toward tight junctions (76, 237). The central fibers of the AEN descend in the ventral third of the spinal trigeminal tract (178, 184) and send fibers into the trigeminal sensory complex. The infra-orbital nerve also sends central fibers to all trigeminal sensory nuclei (190), but its distribution is much wider than the AEN. Although currently unknown, it is probable that similar distributions exist in aquatic mammals.


The Pain of Dying: An Examination of Whether Dead Bodies Feel Pain

The question “can dead bodies feel pain” is a complex one to answer.

Current research suggests that our bodies no longer feel pain once we die. Once the heart stops beating, blood is no longer transported through the body, and the brain soon dies.

A person’s brain may be active for a short time after they are clinically dead, but there is evidence that our brain and biology protect us from pain.

Even though death is a universal experience, there is still a lot of mystery surrounding what death feels like and what actually happens when we die. The mysteries of death have been the focus of science, religion, and psychology for thousands of years. Every year, new research examining death from a biological or neurological standpoint is published.

The aura of mystery around death is understandable. The human body is indescribably complex and, as a result, so is death. Every person’s experience of death, both biologically and psychologically, is unique.

  1. Death and the Brain
  2. Definition of Death
  3. The Stages of Death
  4. How the Body Feels Pain
  5. Near-Death Experiences (NDEs)

Death and the Brain

The question “can dead bodies feel pain” is a complex one to answer. The short answer is that, based on our current understanding of death, we do not believe that dead bodies feel pain. However, the long answer is slightly more complex.

Most doctors believe that dying is not a painful process, even if the time leading up to death can be. Whether due to pain management or loss of biological senses, by the time you die, most people are past the point of being able to process pain.

Though we typically discuss and depict death as a single moment in time, in actuality, death is a multi-step process that occurs when the various components of your body shut down.

When your heart stops beating, oxygen-rich blood is no longer transported through the body. Without oxygen, our brain quickly dies.

However, the brain does not shut down instantaneously when the heart stops beating. In fact, current research indicates that though your brain shuts down after 20-30 seconds, conscious awareness may continue for up to 10 minutes once you are declared clinically dead.

This means that it is possible that your brain may still be aware for a brief period of time after you die. In fact, some people who are resuscitated are able to recount specific details about what happened around them between when their heart stopped and when it was restarted.

During the brief period of time between clinical death and your brain shutting down, your brain is still able to receive messages from your body. As we discuss in “How Your Body Feels Pain” below, pain is felt when the electrical signals from your nerves are processed in your brain. Therefore, until your brain shuts down, it is still able to receive and send “pain” messages to other living components of your body.

  • People who have had near-death experiences tend to report feelings of “relaxation” or “peace.” More information is provided in the “Near-Death Experiences” section below. of animals and humans at the point of death have revealed evidence that our brain activity is actually heightened right before death. However, it appears that the brain’s processes begin to change, and the brain begins to focus inward, instead of on the outward pain that the body is reporting.
  • When blood stops reaching the brain, the brain will begin to die from the top (farthest from the blood) downward. The first portions of the brain to die are our sense of self and our ability to think critically. Therefore, while the base of our brain may still be receiving messages, it is unlikely that we are conscious enough to hear them.

However, the fact remains that we cannot talk to people once they die. As such, we cannot answer with absolute certainty whether or not we feel pain after we die.

Definition of Death

When you die, your body does not die all at once. In fact, various components of your body will continue to shut down for about 24 hours after you are declared “dead.” In general, death is defined in one of two ways:

1. Brain Dead:

The brain stem, the most rudimentary portion of the brain, controls the flow of messages between the brain and the rest of the body. You are considered brain dead when you no longer have any neurological activity in your brain stem.

Though brain dead is considered death, the remainder of your organs can still be kept alive “artificially” for long periods of time.

2. Clinically Dead:

Most people are considered clinically dead before they are brain dead. You are considered clinically dead when your heart, breathing, and blood circulation stops. When your blood circulation stops, oxygen is no longer transported throughout your body, which causes the rest of your body to slowly shut down.

Though clinical death is considered death, cardiopulmonary resuscitation (also known as CPR) is still possible and successful in many cases.

Stages of Death

In our discussions and depictions of death, we tend to think of death as a single moment in time. However, once we are clinically dead, it takes about 24 hours for all of the various components of our body to shut down. For example, live skin cells can be harvested up to 24 hours after death.

Death can be broken down into a number of stages:

1. Pallor Mortis

Pallor mortis occurs immediately after death. As soon as capillary circulation (also known as blood circulation) stops, the body begins to pale as the blood sinks away from the skin. Pallor mortis is noticeable 15-30 minutes after death.

During pallor mortis, the brain also stops functioning because it is no longer being supplied with oxygen-rich blood. Like-wise, oxygen-deprived cells throughout the body begin to die.

2. Algor Mortis

Algor mortis, also known as the death chill, begins immediately after death. Once the heart stops beating, and blood stops circulating, body temperature begins to drop. The body’s temperature will fall approximately 1.5 degrees Fahrenheit every hour until it reaches room temperature.

3. Rigor Mortis

When the blood stops circulating, the body is no longer able to produce the energy it needs to function. Without energy, also known as ATP (adenosine and triphosphate), the muscles of the body will stiffen. Rigor mortis sets in 2-6 hours after death and will last anywhere from 18 hours to 2 days.

4. Livor Mortis

Livor mortis is the final stage of active death. Thanks to gravity, the blood that is no longer circulating through the body collects in the lowest portions of the body.

Within 12 hours of death, the pooling blood begins to discolor the nearby tissue, turning the skin blue.

5. Decomposition

The true final stage of death is decomposition. As your body dies, microorganisms that were previously contained to certain sections of the body, or repressed by your immune system, are now given free reign of your body.

Decomposition typically starts in the intestinal tract, where gut bacteria will begin to break down intestinal walls and move into other sections of the body.

As you can see, death is a gradual process. When we ask whether a dead body can feel pain, we must consider where the body is within the death process.

For more information on the biology behind what happens to your body when you die, Death and Poop: The Dirty Truth about What Happens When You Die.

How the Body Feels Pain

Just like we have to understand death to answer the question “can a dead body feel pain,” we also need to understand how pain is processed in our bodies.

The body feels pain, thanks to electrical communication between the brain and nerve cells throughout the body. When your body experiences bodily harm, the following process occurs:

1. Bodily Harm:

You do something to cause yourself bodily harm, such as pricking your finger on something sharp.

2. Nerves Send Messages to Your Brain:

When you experience bodily harm, microscopic pain receptors (the end of your nerve cells) send electric shocks to your brain via the spinal cord.

3.Your Brain Alerts Your Body:

Once the brain receives the electrical shock from your nerve cells, it transfers the message to various parts of your brain, which in turn transfers the message to your body.

For example, for pain messages, alerts are sent to the somatosensory cortex (responsible for physical sensation), the frontal cortex (responsible for critical thinking), and the limbic system (responsible for emotional responses).

4. Your Body Reacts:

Based on the messages from your brain, your body will react to minimize the pain. For example, if you prick your finger, your brain will tell your finger to pull away from the sharp object.

In the same way, when you touch something hot, it takes a moment for you to register that it is a hot object. That’s because you have to wait for the message to get to your brain!

When determining if a dead body feels pain, it is important to understand what pain is and how our body processes it.

Near-Death Experiences

A study completed by Jimo Borjigin at the University of Michigan found that rats actually experienced higher rates of consciousness at the time of death than they did in a healthy, wakeful state.

Similar to the point above, encounters during near-death experiences are also used as proof of an afterlife. People who have near-death experiences are known to see deceased loved ones or a divine being. However, whether the encounter is real or a product of their imagination is open to debate.

Near-death experiences are hard to measure in real time, as neurological monitoring must be completed at the time of death. Therefore, the research on near-death experiences is still in its infancy.

Jimo Borjigin, a neuroscientist at the University of Michigan performed a study in which they showed that immediately following cardiac arrest, the brains of rodents showed heightened activity, specifically in the consciousness portion of the brain, for at least 30 seconds after the rats were clinically dead.

Dr. Borjigin believed that this heightened activity was likely linked to near-death experiences. However, the research has not been supported by other research, and there are still other potential explanations.

For example, Sam Parnia, a cardiologist from Stony Brook University Hospital, stipulates that electroencephalography (EEG) activity could be caused by an influx of calcium inside the brain cells when blood flow to the brain ceases.

Still other researchers, such as Cameron Shaw from Deakin University, are skeptical about whether near-death experiences happen after clinical death at all. He, and many other scientists in the field, believes that near-death experiences likely happen before, not after, clinical death.

Until research is completed on a wider scale, near-death experiences will continue to be an occurrence that mystifies the scientific and medical communities.

Final Thoughts

Understanding what a body feels after death is incredibly challenging. While there are many variables to consider, current research suggests that once we die, our bodies no longer feel pain. We can therefore take comfort in knowing that our loved ones are no longer suffering when they die.


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1. Central Nervous System
Brain and spinal cord
Peripheral nervous system
Somatic and visceral nervous system
This means that it controls involuntary functions and that conducts impulses DOWNWARDS to smooth muscles, cardiac muscle, etc.
2. Oligodendotrcyte- b, e, i
Satelite cell- a, d, g
Microglial.

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