What are dynorphins, and what is their precursor protein?

Dynorphins are a class of opioid peptides that originate from the precursor protein prodynorphin. Prodynorphin is processed by proprotein convertase 2 (PC2) to release active peptides such as dynorphin A, dynorphin B, and alpha/beta-neoendorphin.

What opioid peptides are released when prodynorphin is processed by proprotein convertase 2 (PC2)?

When prodynorphin is processed by proprotein convertase 2 (PC2), the active peptides released include dynorphin A, dynorphin B, and alpha/beta-neoendorphin.

What is "big dynorphin," and how is it formed?

Big dynorphin is a 32-amino acid molecule that consists of both dynorphin A and dynorphin B. It is formed when prodynorphin is not fully processed during its conversion into smaller active peptides.

What are the key compositional characteristics of dynorphin A, dynorphin B, and big dynorphin in terms of amino acid residues?

Dynorphin A, dynorphin B, and big dynorphin are characterized by a high proportion of basic amino acid residues, specifically lysine and arginine, and also contain many hydrophobic residues. For instance, dynorphin A contains 29.4% basic residues and 41.2% hydrophobic residues, while dynorphin B has 23.1% basic and 30.8% hydrophobic residues, and big dynorphin has 31.2% basic and 34.4% hydrophobic residues.

In the central nervous system (CNS), where are the highest concentrations of dynorphins found?

Dynorphins are widely distributed throughout the CNS, but they are found in the highest concentrations in the hypothalamus, medulla oblongata, pons, midbrain, and spinal cord.

How do the vesicles that store dynorphins differ from those storing neurotransmitters, and what does this imply about their release?

Dynorphins are stored in large, dense-core vesicles (80-120 nm diameter), which are significantly larger than the small synaptic vesicles typically used for neurotransmitters. This difference in storage mechanism means that a more intense and prolonged stimulus is required to trigger the release of dynorphins into the synaptic cleft, a characteristic storage method for opioid peptides.

Who discovered the first endogenous opioid peptide related to dynorphin, and what was the peptide named?

The first endogenous opioid peptide related to dynorphin was discovered by Goldstein and his group. They named the peptide dynorphin, derived from the Greek word dynamis, meaning power, to reflect its extraordinary potency.

What does the name "dynorphin" signify, and why was it chosen?

The name "dynorphin" was chosen by its discoverers, Goldstein et al., from the Greek word dynamis, meaning power. This name was selected to describe the peptide's exceptionally high potency as an opioid peptide.

In which regions of the nervous system is dynorphin produced?

Dynorphin is produced in various parts of the nervous system, including the hypothalamus, striatum, hippocampus, and spinal cord.

What is the role of dynorphin produced in magnocellular vasopressin neurons of the supraoptic nucleus?

Dynorphin produced in the magnocellular vasopressin neurons of the supraoptic nucleus plays a role in the patterning of electrical activity within these neurons.

How does dynorphin influence pain response, according to studies involving the rat spinal cord?

Dynorphin has been shown to modulate pain response. Injecting dynorphin into the subarachnoid space of the rat spinal cord produced dose-dependent analgesia, which was measured by the tail-flick latency and could be partially blocked by the opioid antagonist naloxone.

What was the observed potency of dynorphin compared to morphine in inducing analgesia in rats?

Studies by Han and Xie indicated that dynorphin was 6 to 10 times more potent than morphine on a per mole basis when injected into the subarachnoid space of the rat spinal cord to produce analgesia.

Did morphine tolerance affect dynorphin-induced analgesia in the studies mentioned?

No, the studies by Han and Xie found that morphine tolerance did not reduce the analgesia induced by dynorphin.

What were the differing effects of dynorphin A1-13 when injected into the rat spinal cord versus the intracerebroventricular (ICV) region?

When dynorphin A1-13 was injected into the rat spinal cord, it had additive effects when combined with morphine. However, when injected into the intracerebroventricular (ICV) region of the brain, it had an antagonist effect on morphine-induced analgesia.

What alternative mechanism did Lai et al. propose for dynorphin's effect on pain, involving bradykinin receptors?

Lai et al. proposed that dynorphin might stimulate pain by acting on the bradykinin receptor in addition to the kappa opioid receptor (KOR). They found that the N-terminal tyrosine of dynorphin A is necessary for activating opioid receptors but not for binding to bradykinin receptors.

According to Lai et al.'s proposed mechanism, how does dynorphin activate bradykinin receptors to stimulate pain?

According to Lai et al.'s proposed mechanism, dynorphin activates bradykinin receptors, which in turn triggers the release of calcium ions into the cell through voltage-sensitive channels in the cell membrane, thereby stimulating the pain response. Blocking these bradykinin receptors in the lumbar spinal cord reversed persistent pain.

What did Svensson et al. find regarding the effect of truncated dynorphin A2-17 on microglia in the spinal cord, and how might this relate to pain?

Svensson et al. found that administering truncated dynorphin A2-17, which does not bind to opioid receptors, increased phosphorylated p38 mitogen-activated protein kinase (MAPK) in microglia in the dorsal horn of the spinal cord. Since activated p38 is linked to prostaglandin release that causes pain, this suggests dynorphin might induce pain via a non-opioid p38 pathway.

What role has the dynorphin-kappa opioid receptor (KOR) system been identified to play in neuropathic pain?

Studies have identified a role for the dynorphin and kappa opioid receptor (KOR) system in mediating neuropathic pain.

How does the dynorphin-KOR system mediate astrocyte proliferation in the context of neuropathic pain?

The dynorphin-KOR system mediates astrocyte proliferation through the activation of p38 MAPK, which was found to be necessary for the effects of neuropathic pain on analgesic responses.

How does cocaine addiction relate to changes in brain dynorphin levels?

Repeated exposure to cocaine increases dynorphin concentrations in specific brain regions, such as the striatum and substantia nigra, in rats. This suggests dynorphins play a role in the molecular changes associated with cocaine addiction.

What is the proposed molecular mechanism for increased dynorphin levels following repeated cocaine exposure, involving CREB?

The proposed mechanism involves cocaine increasing cyclic adenosine monophosphate (cAMP) and cAMP-dependent protein kinase (PKA). PKA then activates CREB (3',5'-monophosphate response element binding protein), which leads to increased expression of dynorphin in brain areas crucial for addiction, like the nucleus accumbens and dorsal striatum.

How does dynorphin affect dopamine release, and what is the significance of this interaction in addiction?

Dynorphin decreases dopamine release by binding to kappa opioid receptors (KORs) located on dopamine nerve terminals. This reduction in dopamine signaling is thought to contribute to the reinforcing properties of drugs like cocaine.

What experimental findings by Carlezon et al. supported the model linking CREB, dynorphin, and cocaine reward?

Carlezon et al. found that mice injected with cocaine showed a stronger place preference for the injection location compared to control mice. However, mice overexpressing CREB exhibited place aversion, suggesting that increased CREB activity reverses the positive effects of cocaine. Northern blot analysis confirmed a marked increase in dynorphin mRNA in the nucleus accumbens of these mice.

How might different functional variations of the dynorphin gene potentially protect individuals from cocaine addiction?

Research suggests that a "high output" functional variation of the dynorphin gene, containing specific promoter polymorphisms, may produce more dynorphin mRNA. This could provide individuals carrying this variation with a "built-in defense system" against developing drug addiction.

What mechanism did Land et al. describe for dysphoria involving corticotropin-releasing factor (CRF) and dynorphin release?

Land et al. described a mechanism where corticotropin-releasing factor (CRF) provokes dynorphin release. They observed that injecting CRF induced aversive behaviors in mice with functional dynorphin genes, even without stress, and that blocking the CRF2 receptor with an antagonist eliminated this place aversion, suggesting this pathway is linked to stress-induced dysphoria.

How did mice lacking dynorphin respond differently to stress-induced aversive behaviors compared to control mice?

Mice lacking dynorphin did not display the aversive behaviors typically seen in control mice when subjected to stress, such as forced swim tests and foot shocks, indicating dynorphin's role in mediating these stress-related negative emotional responses.

What did Land et al. conclude about the pathway involving CRF2, dynorphin release, and KOR activation in relation to stress and dysphoria?

Land et al. concluded that the dysphoric aspects of stress occur when CRF2 stimulates dynorphin release, which then activates the kappa opioid receptor (KOR). This pathway was also postulated to be involved in drug-seeking behavior.

How has the dynorphin system been implicated in stress-induced reinstatement of cocaine-seeking behavior?

The dynorphin system has been shown to be required for the reinstatement of cocaine-seeking behavior that is induced by stress, although it is not required for prime-induced reinstatement.

What role does p38, a mitogen-activated protein kinase (MAPK) family member, play in KOR-dependent behaviors related to stress?

Bruchas et al. found that the kappa opioid receptor (KOR) activates p38, a member of the mitogen-activated protein kinase (MAPK) family, through phosphorylation. This activation of p38 is necessary for producing behaviors dependent on KOR signaling, including those related to stress.

How did manipulating CREB expression affect antidepressant-like behavior and dynorphin expression in mice, according to Newton et al.?

Newton et al. found that overexpressing a dominant-negative form of CREB (mCREB) in transgenic mice resulted in an antidepressant-like effect behaviorally. Conversely, overexpressing wild-type CREB led to an increase in depression-like symptoms. This was linked to mCREB being colocalized with decreased prodynorphin expression, suggesting the CREB-dynorphin pathway regulates mood.

What did Shirayama et al. find regarding dynorphin levels in the hippocampus and nucleus accumbens in response to stress and learned helplessness?

Shirayama et al. observed that learned helplessness and immobilization stress increased the levels of both dynorphins A and B in the hippocampus and nucleus accumbens of rats. Forced swim stress also increased dynorphin A levels in the hippocampus.

What potential mechanisms did Shirayama et al. propose for how KOR antagonists might reverse learned helplessness?

Shirayama et al. proposed that increased dynorphin levels might block the release of glutamate, a neurotransmitter vital for plasticity in the hippocampus, thereby inhibiting new learning. Blocking dynorphin effects would allow glutamate release, restoring hippocampal plasticity and reversing learned helplessness. Additionally, blocking dynorphin could enhance dopamine signaling, reducing stress-related depressive symptoms.

How might blocking dynorphin signaling potentially reduce depressive symptoms associated with stress?

By blocking dynorphin's effects, it is hypothesized that dopamine signaling could be enhanced. This enhancement in dopamine signaling may help to reduce depressive symptoms that are often associated with stress.

What is the role of dynorphins in maintaining homeostasis through appetite control and circadian rhythms?

Dynorphins play a role in maintaining homeostasis by influencing appetite control and circadian rhythms, suggesting they are important regulators of basic physiological functions.

How do dynorphin levels in the neurointermediate lobe of the pituitary and hypothalamus change between day and night?

During the day, dynorphin levels are naturally elevated in the neurointermediate lobe of the pituitary and depressed in the hypothalamus. This pattern reverses at night, with dynorphin levels being depressed in the pituitary and elevated in the hypothalamus.

What effect did food and water deprivation have on dynorphin levels in the hypothalamus and neurointermediate lobe of the pituitary?

Mice deprived of food and water, or just water, showed increased levels of dynorphin in the hypothalamus during the day. Water deprivation alone also led to decreased dynorphin levels in the neurointermediate lobe of the pituitary.

What evidence suggests dynorphin acts as an appetite stimulant?

Several studies in rats have shown that increasing dynorphin levels stimulates eating behavior. Conversely, opioid antagonists like naloxone can reverse these effects, particularly in obese animals or those presented with highly palatable food.

How do opioid antagonists like naloxone affect dynorphin-induced eating, particularly in obese animals?

Opioid antagonists, such as naloxone, can reverse the appetite-stimulating effects of elevated dynorphin. This inhibitory effect is noted to be particularly strong in obese animals or those consuming highly appealing food.

What role has dynorphin been observed to play in the eating behavior of hibernating animals?

Dynorphin levels were found to increase during starvation periods in ground squirrels, which undergo cycles of excessive eating and starvation before winter, suggesting a role in regulating feeding behavior during these physiological states.

How did food restriction affect dynorphin A and dynorphin B levels in different rat brain regions?

While food restriction did not alter dynorphin B expression, it increased dynorphin A levels in several brain regions of rats, including the hypothalamus, nucleus accumbens, and the bed nucleus of the stria terminalis.

What differences were observed in fat storage and fatty acid oxidation in dynorphin knockout mice compared to control mice?

Dynorphin knockout mice showed reduced fat storage, particularly in males, and oxidized fatty acids more quickly compared to control mice. However, no differences in food intake were observed between the knockout and control groups.

How does ingesting a high-fat diet influence dynorphin gene expression in the hypothalamus?

Ingesting a high-fat diet has been shown to increase the gene expression of dynorphin in the hypothalamus, suggesting a link between dietary fat intake and dynorphin signaling in appetite regulation.

What evolutionary mechanism is suggested by the observation that during stress, more food is eaten, nutrients are stored, and energy expenditure is reduced, potentially involving dynorphins?

Studies suggest an evolutionary mechanism where, during times of stress, endogenous opioids like dynorphin stimulate appetite, promote nutrient storage, and decrease energy expenditure. This coordinated response would help an organism survive periods of scarcity or high demand.

How do MOR agonists and KOR agonists differ in their effects on body temperature?

While mu-opioid receptor (MOR) agonists have been found to stimulate hyperthermia (an increase in body temperature), kappa-opioid receptor (KOR) agonists, such as dynorphin, have been shown to mediate hypothermia (a decrease in body temperature).

What effect did dynorphin A1-17 have when administered into the periaqueductal gray (PAG) region of the rat brain?

When dynorphin A1-17, a KOR agonist, was administered into the periaqueductal gray (PAG) region of the rat brain via microdialysis, it induced hypothermia. The severity of the hypothermia was proportional to the dose administered and could be prevented by co-administering a KOR antagonist.

What did Ansonoff et al. discover about the role of K1 versus K2 receptors in the hypothermic effects mediated by KOR agonists?

Ansonoff et al. discovered that the hypothermic effects of KOR agonists are mediated specifically through the kappa-opioid receptor 1 (K1) subtype, not K2. Applying a KOR agonist to K1 knockout mice eliminated the hypothermic response, indicating K2 receptors do not play a role in this mechanism.

Why are dynorphin derivatives generally considered to have limited clinical use?

Dynorphin derivatives are generally considered to have limited clinical utility primarily because of their very short duration of action, which makes them less practical for sustained therapeutic effects.

What are the primary identifiers listed for prodynorphin (PDYN) in the infobox?

The primary identifiers listed for prodynorphin (PDYN) include its symbol PDYN, NCBI gene ID 5173, HGNC ID 8820, OMIM ID 131340, RefSeq NM_024411, and UniProt ID P01213.

Dynorphin Wiki: Dynorphins: The Body's Potent Peptides

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Introduction

Opioid Peptide Family

Dynorphins constitute a class of opioid peptides derived from the precursor protein prodynorphin. Upon enzymatic cleavage by proprotein convertase 2 (PC2), multiple biologically active peptides are generated, including dynorphin A, dynorphin B, and the neoendorphins (\u03b1/\u03b2-neoendorphin).¹ These peptides are synthesized and stored within synaptic vesicles in presynaptic terminals, released upon neuronal depolarization.²

Distribution and Storage

Dynorphins are widely distributed throughout the central nervous system (CNS), with particularly high concentrations observed in the hypothalamus, medulla, pons, midbrain, and spinal cord.⁵ They are stored in large, dense-core vesicles (80-120 nm diameter), distinguishing them from smaller neurotransmitter vesicles. This storage mechanism necessitates a more intense and prolonged stimulus for release into the synaptic cleft, characteristic of peptide neuromodulators.⁶

Potency and Discovery

The term "dynorphin" originates from the Greek word for power, reflecting its remarkable potency as an opioid peptide. Initial research by Goldstein and colleagues identified an endogenous opioid peptide in porcine pituitary that exhibited exceptionally high opioid activity, leading to its characterization and naming.⁷

Production and Processing

Synthesis Pathway

Prodynorphin serves as the precursor protein for all dynorphin peptides. Its processing involves cleavage by the enzyme proprotein convertase 2 (PC2), primarily occurring within synaptic vesicles in the presynaptic terminal.¹ This process yields multiple distinct peptides, including dynorphin A, dynorphin B, and \u03b1/\u03b2-neoendorphin. In some instances, incomplete processing results in the release of "big dynorphin," a larger molecule comprising both dynorphin A and B sequences.³

Regional Expression

Dynorphin synthesis is observed across various neural regions, including the hypothalamus, striatum, hippocampus, and spinal cord. Gene expression patterns can be visualized using resources like the Allen Brain Atlases, offering insights into dynorphin's anatomical localization in different species.^{Allen Brain Atlas}

Physiological Actions

Dynorphins exert diverse physiological effects contingent on their site of synthesis and release. For example, dynorphin within magnocellular vasopressin neurons influences electrical activity patterning, while its presence in oxytocin neurons acts as a negative feedback inhibitor of oxytocin secretion.^{citation needed} Dynorphins produced in the arcuate nucleus and lateral hypothalamus are implicated in appetite regulation.^{citation needed}

Analgesia: Pain Modulation

Potent Pain Relief

Dynorphin administration into the rat spinal cord has been shown to produce dose-dependent analgesia, as measured by the tail-flick latency test. This effect is partially reversible by the opioid antagonist naloxone, confirming its opioid-mediated mechanism.¹⁰ Notably, dynorphin demonstrated significantly higher potency than morphine on a molar basis, and tolerance to morphine did not diminish dynorphin-induced analgesia.¹⁰

Complex Mechanisms

The interaction between dynorphin and other analgesics, like morphine, is complex. While synergistic effects were observed when co-administered in the rat spinal cord, dynorphin exhibited an antagonistic effect on morphine-induced analgesia when delivered intracerebroventricularly (ICV), suggesting distinct central nervous system pathways.¹¹

Paradoxical Pain Stimulation

Intriguingly, some research suggests dynorphin may also stimulate pain. It appears to interact with bradykinin receptors, in addition to the kappa opioid receptor (KOR). The N-terminal tyrosine residue of dynorphin A is crucial for opioid receptor activation but not for bradykinin receptor binding. This dual action may contribute to dynorphin's complex role in pain perception.⁸ Furthermore, dynorphin can activate p38 mitogen-activated protein kinase (MAPK) in spinal microglia via a non-opioid pathway, potentially contributing to pain sensitization.¹² Dynorphin and KOR stimulation are implicated in neuropathic pain, potentially involving astrocyte proliferation and p38 MAPK activation.¹⁴¹⁵

Addiction and Reward Pathways

Cocaine Addiction Link

Dynorphins play a significant role in the neurobiological adaptations underlying cocaine addiction. While acute cocaine exposure does not alter brain dynorphin levels, repeated administration increases dynorphin concentrations in the striatum and substantia nigra in rats.¹⁷

Molecular Mechanisms

A proposed mechanism involves the cAMP response element-binding protein (CREB) pathway. Cocaine increases intracellular cAMP and activates protein kinase A (PKA), leading to CREB activation. Activated CREB enhances prodynorphin gene expression in key addiction-related brain areas like the nucleus accumbens and dorsal striatum. This results in increased dynorphin, which subsequently inhibits dopamine release by acting on KORs located on dopamine terminals.¹⁸¹⁹

Protective Variations

Interestingly, genetic variations in dynorphin production may influence susceptibility to addiction. Individuals with a "high output" functional variation of the dynorphin gene, potentially leading to higher dynorphin levels, might possess a natural defense against developing cocaine addiction.²¹ Conversely, experimental manipulation of CREB levels and KOR antagonism demonstrated that the dynorphin system is crucial for mediating cocaine reward and aversion.¹⁸

Stress, Depression, and Mood

CRF-Dynorphin Pathway

Corticotropin-releasing factor (CRF) stimulation can provoke dynorphin release, contributing to the dysphoric (unpleasant mood) effects associated with stress. Studies indicate that CRF-induced aversion behaviors in mice are dependent on dynorphin release and KOR activation.²² This pathway may also be involved in stress-induced drug-seeking behavior.²³

Mood Regulation

The CREB-dynorphin pathway is implicated in mood regulation. Overexpression of a dominant-negative CREB mutant, which reduces prodynorphin expression, produced antidepressant-like effects in mice. Conversely, overexpressing wild-type CREB exacerbated depression-like symptoms, correlating with increased dynorphin.²⁷ Direct antagonism of dynorphin activity also yielded antidepressant-like behavioral effects.²⁷

Therapeutic Potential

Research suggests that dynorphins A and B levels increase in limbic brain regions following stress. Administration of KOR antagonists has been shown to reverse learned helplessness (an animal model of depression) and potentially alleviate depressive symptoms by restoring hippocampal plasticity and enhancing dopamine signaling.²⁸ These findings highlight the potential of KOR antagonists as therapeutic agents for depression.

Appetite and Homeostasis

Appetite Stimulation

Dynorphins play a role in maintaining energy homeostasis, particularly in regulating appetite. Studies in rats and dogs demonstrate that elevated dynorphin levels stimulate food intake. This effect can be reversed by opioid antagonists like naloxone, especially in situations involving palatable foods or obesity.²⁹³⁰³³

Hibernation and Fasting

In hibernating animals like the ground squirrel, dynorphin levels increase during starvation periods, suggesting a role in managing energy reserves.³⁴ Food restriction studies in rats also show increased dynorphin A levels in brain regions associated with appetite control, such as the hypothalamus and nucleus accumbens.³⁵

Fat Storage and Metabolism

Research using dynorphin knockout mice revealed reduced fat mass and increased weight loss during fasting, alongside enhanced fatty acid oxidation. Conversely, high-fat diets increase dynorphin gene expression in the hypothalamus, potentially promoting overeating.³⁶³⁷ Endogenous opioids, including dynorphin, appear to be activated during stress, stimulating appetite and reducing energy expenditure, likely as an adaptive mechanism for survival.³²

Temperature Regulation

Hypothermia Induction

Dynorphins, acting primarily via the kappa opioid receptor (KOR), influence body temperature regulation. Microdialysis studies delivering dynorphin A_1-17 (a KOR agonist) into the periaqueductal gray (PAG) region of rats induced hypothermia, with the effect being dose-dependent and blocked by KOR antagonists.³⁹ This contrasts with mu-opioid receptor agonists, which typically induce hyperthermia.

Hyperthermia and Stress

Exposure to heat stress (38°C) increases dynorphin levels in various rat brain regions. Concurrently, nitric oxide synthase (NOS) inhibitors reduced dynorphin A levels and attenuated heat stress symptoms, suggesting a role for nitric oxide in this mechanism.⁴⁰

Receptor Specificity

Further research indicated that the hypothermic effects of KOR agonists are mediated specifically through the \u03ba-opioid receptor 1 (K1) subtype, as these effects were abolished in K1 knockout mice. The K2 subtype does not appear to be involved in this thermoregulatory mechanism.⁴¹

Clinical Significance

Limited Therapeutic Use

Despite their potent biological effects, dynorphin derivatives have found limited clinical application. Their primary limitation stems from a very short duration of action, making sustained therapeutic effects challenging to achieve.⁴² Research continues into developing stabilized derivatives or alternative strategies to harness their pharmacological potential.

References

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Dynorphins: The Body's Potent Peptides

💡 Dive in with Flashcard Learning! 💡

Introduction ℹ️

🧬 Opioid Peptide Family

📍 Distribution and Storage

💪 Potency and Discovery

Production and Processing ⚙️

🏭 Synthesis Pathway

🌐 Regional Expression

🔬 Physiological Actions

Analgesia: Pain Modulation ⚖️

🩹 Potent Pain Relief

🤔 Complex Mechanisms

❓ Paradoxical Pain Stimulation

Addiction and Reward Pathways 🔗

🌿 Cocaine Addiction Link

📈 Molecular Mechanisms

🛡️ Protective Variations

Stress, Depression, and Mood 😔

⚡ CRF-Dynorphin Pathway

🧠 Mood Regulation

💡 Therapeutic Potential

Appetite and Homeostasis 🍎

🍽️ Appetite Stimulation

❄️ Hibernation and Fasting

⚖️ Fat Storage and Metabolism

Temperature Regulation 🌡️

🥶 Hypothermia Induction

🔥 Hyperthermia and Stress

🔑 Receptor Specificity

Clinical Significance 🧑‍⚕️

⏳ Limited Therapeutic Use

References 📚

📜 Source Citations

Teacher's Corner 🧑‍🏫

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References

📜 References

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📜 Important Notice

Dive in with Flashcard Learning!

Introduction

Opioid Peptide Family

Distribution and Storage

Potency and Discovery

Production and Processing

Synthesis Pathway

Regional Expression

Physiological Actions

Analgesia: Pain Modulation

Potent Pain Relief

Complex Mechanisms

Paradoxical Pain Stimulation

Addiction and Reward Pathways

Cocaine Addiction Link

Molecular Mechanisms

Protective Variations

Stress, Depression, and Mood

CRF-Dynorphin Pathway

Mood Regulation

Therapeutic Potential

Appetite and Homeostasis

Appetite Stimulation

Hibernation and Fasting

Fat Storage and Metabolism

Temperature Regulation

Hypothermia Induction

Hyperthermia and Stress

Receptor Specificity

Clinical Significance

Limited Therapeutic Use

References

Source Citations

Teacher's Corner

True or False?

Test Your Knowledge!

Gamer's Corner

Discover other topics to study!

References

Feedback & Support

Disclaimer

Important Notice