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brightlotusmoon***
The landmark discovery of the endogenous pain-suppressing chemicals came about because researchers in Aberdeen, Scotland, and at the Johns Hopkins University Hospital in Baltimore were curious about how exogenous morphine and other opium-derived painkillers works (Cooks 1998). When scientists in Scotland and at John Hopkins injected morphine into experimental animals, they found that the morphine molecules fitted perfectly into receptors on certain brain and spinal cord neurons. This prompted to researchers to speculate that perhaps there were naturally occurring brain chemicals that behaved analogous to morphine.
With further research, the two groups of scientists found not one but a whole family of these endogenous pain-killing chemicals. The Aberdeen investigators called the smaller members of the family enkephalins, which translates into "in the head" (Cook, 1998). In time the larger molecules were also discovered and it was called endorphins, meaning the "morphine within". Nowadays, the word endorphins is often used to refer to the groups as a whole. Now, that we have a clear picture of how these endogenous were discovered, the following will be a brief overview of opioids and its analgesic properties. Opioid analgesics, like other drugs, exert significant effects on mood and motivation (for review, see Wise, 1987; Herz & Shippenberg, 1989). They have been shown to produce euphoria in humans and are self-administered in animals. Repeated administration of opioids can result in development of tolerance and physical dependence (Bromm & Desmedt, 1995).
Opioidergic neurotransmission is found throughout the brain and appears to influence many central nervous system functions, including nociception (Bromm & Desmedt, 1995). The opioid peptides that have been cloned and characterized in mammalian central and peripheral nervous systems are derived from three precursors: proopiomelanocortin, proenkephalin, and prodynorphin. There are three opioid receptors that are well known and characterized at the present: these are mu-, delta-, and kappa opioid receptors. As of today the enkephalins are considered to be the putative ligands for the delta-receptors, beta-endorphins for the mu-receptors, and dynorphins for the kappa-receptors (Bromm & Desmedt, 1995).
At analgesic doses, systematically administered opioids activate spinal and supraspinal mechanisms via mu-, delta, and kappa-opioid receptors (Bromm & Desmedt, 1995). Opioids generally exert and inhibitory effect of spontaneous, chemically, or synaptically induced neuronally discharged. These effects is believe to occur via the inhibition of inhibitory gamma-butyratergiv (GABAergic) interneurons, opioid excite hippocampal pyramidal neurons and neurons in the rostral ventromedial medulla (Gershon, 1986, Bromm & Desmedt, 1995). Studies have found GABA and it synthesizing enzyme glutamate decarbosylase (GAD) in the superficial dorsal horn (for review, see Clarton & Hayes, 1990), and GABA binding sites and GABA containing neurons have been characterized in almost all pain-related pathways (Bromm & Desmedt, 1995). Recent studies found an increase in GABA-immunoreactive neurons and GABA levels in the spinal cord of rats with unilateral peripheral inflammation (for review, see Castro-Lopes et al., 1992). This effect is proposed to occur in parallel with increase in enkaphalin and dynorphin in response to increase nociceptive input (Bromm & Desmedt, 1995). The following section is a correlation of opioids and other neurotransmitter in the possible roles in which they interact with one another in eliciting pain responses.
Neurotransmitters that are involved in pain response are norepinephrine, dopamine, L-dopa, serotonin, and enkephalines. These neurotransmitters are found mainly in the limbic system and is therefore, thought to play a crucial role in mediation of both pain and emotion.
Animal studies have shown that when serotonin is added directly to the central nervous system, it accumulates in the periventricular areas and enhances the effectiveness of analgesia produced by electrical stimulation and decreased pain perception (Gershon, 1987). Furthermore, studies have shown that blocking presynaptic reuptake of serotonin, increases the level of serotonin in the presynaptic cleft, and consequently raises the pain threshold. The opposite is true when serotonin levels is decreased (Gershon, 1987). In contrast, norepinephrine, on the other hand, is thought to exert its effect by blocking morphine activity; it is also suggested that drugs that increases norepinephrine levels potentially lower pain threshold and increase pain.
Enkephalins are the morphine-like neurotransmitters as mention previously, are found in known nociceptive pathways in the brain (the limbic system) and spinal cord (for review, see Hendler, N., 1982). SInce their discovery, the importance of enkephalins as inhibitory neurotransmitters of pain has been recognized. Since both serotonin and norepinephrine share pathways with enkephalin, the overlap indicates a system of mutually interacting feedback loops.
Copied in full from: http://www.macalester.edu/psychology/whathap/UBNRP/Audition/site/endogenous%20painkillers.htm
***
I suppose, then, that the next time someone tells me that my fibromyalgia pain is all in my head, I can grin and say, "Why, yes! That's what the enkephalins are for!"
The landmark discovery of the endogenous pain-suppressing chemicals came about because researchers in Aberdeen, Scotland, and at the Johns Hopkins University Hospital in Baltimore were curious about how exogenous morphine and other opium-derived painkillers works (Cooks 1998). When scientists in Scotland and at John Hopkins injected morphine into experimental animals, they found that the morphine molecules fitted perfectly into receptors on certain brain and spinal cord neurons. This prompted to researchers to speculate that perhaps there were naturally occurring brain chemicals that behaved analogous to morphine.
With further research, the two groups of scientists found not one but a whole family of these endogenous pain-killing chemicals. The Aberdeen investigators called the smaller members of the family enkephalins, which translates into "in the head" (Cook, 1998). In time the larger molecules were also discovered and it was called endorphins, meaning the "morphine within". Nowadays, the word endorphins is often used to refer to the groups as a whole. Now, that we have a clear picture of how these endogenous were discovered, the following will be a brief overview of opioids and its analgesic properties. Opioid analgesics, like other drugs, exert significant effects on mood and motivation (for review, see Wise, 1987; Herz & Shippenberg, 1989). They have been shown to produce euphoria in humans and are self-administered in animals. Repeated administration of opioids can result in development of tolerance and physical dependence (Bromm & Desmedt, 1995).
Opioidergic neurotransmission is found throughout the brain and appears to influence many central nervous system functions, including nociception (Bromm & Desmedt, 1995). The opioid peptides that have been cloned and characterized in mammalian central and peripheral nervous systems are derived from three precursors: proopiomelanocortin, proenkephalin, and prodynorphin. There are three opioid receptors that are well known and characterized at the present: these are mu-, delta-, and kappa opioid receptors. As of today the enkephalins are considered to be the putative ligands for the delta-receptors, beta-endorphins for the mu-receptors, and dynorphins for the kappa-receptors (Bromm & Desmedt, 1995).
At analgesic doses, systematically administered opioids activate spinal and supraspinal mechanisms via mu-, delta, and kappa-opioid receptors (Bromm & Desmedt, 1995). Opioids generally exert and inhibitory effect of spontaneous, chemically, or synaptically induced neuronally discharged. These effects is believe to occur via the inhibition of inhibitory gamma-butyratergiv (GABAergic) interneurons, opioid excite hippocampal pyramidal neurons and neurons in the rostral ventromedial medulla (Gershon, 1986, Bromm & Desmedt, 1995). Studies have found GABA and it synthesizing enzyme glutamate decarbosylase (GAD) in the superficial dorsal horn (for review, see Clarton & Hayes, 1990), and GABA binding sites and GABA containing neurons have been characterized in almost all pain-related pathways (Bromm & Desmedt, 1995). Recent studies found an increase in GABA-immunoreactive neurons and GABA levels in the spinal cord of rats with unilateral peripheral inflammation (for review, see Castro-Lopes et al., 1992). This effect is proposed to occur in parallel with increase in enkaphalin and dynorphin in response to increase nociceptive input (Bromm & Desmedt, 1995). The following section is a correlation of opioids and other neurotransmitter in the possible roles in which they interact with one another in eliciting pain responses.
Neurotransmitters that are involved in pain response are norepinephrine, dopamine, L-dopa, serotonin, and enkephalines. These neurotransmitters are found mainly in the limbic system and is therefore, thought to play a crucial role in mediation of both pain and emotion.
Animal studies have shown that when serotonin is added directly to the central nervous system, it accumulates in the periventricular areas and enhances the effectiveness of analgesia produced by electrical stimulation and decreased pain perception (Gershon, 1987). Furthermore, studies have shown that blocking presynaptic reuptake of serotonin, increases the level of serotonin in the presynaptic cleft, and consequently raises the pain threshold. The opposite is true when serotonin levels is decreased (Gershon, 1987). In contrast, norepinephrine, on the other hand, is thought to exert its effect by blocking morphine activity; it is also suggested that drugs that increases norepinephrine levels potentially lower pain threshold and increase pain.
Enkephalins are the morphine-like neurotransmitters as mention previously, are found in known nociceptive pathways in the brain (the limbic system) and spinal cord (for review, see Hendler, N., 1982). SInce their discovery, the importance of enkephalins as inhibitory neurotransmitters of pain has been recognized. Since both serotonin and norepinephrine share pathways with enkephalin, the overlap indicates a system of mutually interacting feedback loops.
Copied in full from: http://www.macalester.edu/psychology/whathap/UBNRP/Audition/site/endogenous%20painkillers.htm
***
I suppose, then, that the next time someone tells me that my fibromyalgia pain is all in my head, I can grin and say, "Why, yes! That's what the enkephalins are for!"
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no subject
Date: 2009-09-12 12:17 am (UTC)I HATE HATE HATE HATE PAINDOUBTERS. My best friend used to doubt the tooth pain that I was in -all the fucking time-. In fact, my pain was one of the reasons she didn't want to hang out with me anymore. When we became friends again, I thoroughly bitched her out for it. I remember crying and telling her that doubting someone's pain is one of the worst things you can do as a friend or a loved one. We already endure being treated like drug addicts by nurses and doctors; we shouldn't have to put up with it from anyone else.
no subject
Date: 2009-09-12 02:10 am (UTC)Doubting someone's pain is an atrocity, especially in a friendship!
*nods*
Date: 2009-09-12 08:00 pm (UTC)no subject
Date: 2009-09-24 07:10 am (UTC)no subject
Date: 2009-09-24 06:22 pm (UTC)