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Dynorphins are synthesized directly from a precursor protein called proenkephalin.
Answer: False
Explanation: Dynorphins are derived from the precursor protein prodynorphin, not proenkephalin. Proenkephalin is the precursor for enkephalins.
The processing of prodynorphin by proprotein convertase 2 (PC2) yields dynorphin A, dynorphin B, and alpha/beta-neoendorphin.
Answer: True
Explanation: The enzymatic cleavage of the precursor protein prodynorphin by proprotein convertase 2 (PC2) generates several active peptides, including dynorphin A, dynorphin B, and alpha/beta-neoendorphin.
Big dynorphin is a shorter peptide than dynorphin A or dynorphin B, consisting of only 15 amino acids.
Answer: False
Explanation: Big dynorphin is a larger molecule, comprising 32 amino acids, and contains both dynorphin A and dynorphin B sequences. It is formed from incomplete processing of prodynorphin.
Dynorphin A and dynorphin B are characterized by a low proportion of basic and hydrophobic amino acid residues.
Answer: False
Explanation: Dynorphin A and dynorphin B, along with big dynorphin, are characterized by a high proportion of basic (lysine, arginine) and hydrophobic amino acid residues.
What is the precursor protein for dynorphins, and which enzyme processes it?
Answer: Prodynorphin, processed by proprotein convertase 2 (PC2)
Explanation: Dynorphins are derived from the precursor protein prodynorphin, which is proteolytically cleaved by proprotein convertase 2 (PC2) to yield active dynorphin peptides.
Which of the following peptides are released when prodynorphin is processed by PC2?
Answer: Dynorphin A, dynorphin B, and alpha/beta-neoendorphin
Explanation: The enzymatic processing of prodynorphin by PC2 generates dynorphin A, dynorphin B, and alpha/beta-neoendorphin as the primary active opioid peptides.
What distinguishes "big dynorphin" from other dynorphin peptides?
Answer: It is a 32-amino acid molecule containing both dynorphin A and dynorphin B.
Explanation: Big dynorphin is a larger peptide, consisting of 32 amino acids, which encompasses the sequences of both dynorphin A and dynorphin B. It arises from incomplete processing of the prodynorphin precursor.
Dynorphin peptides are characterized by a high proportion of which types of amino acid residues?
Answer: Basic (lysine, arginine) and hydrophobic residues
Explanation: Dynorphin peptides, including dynorphin A, dynorphin B, and big dynorphin, possess a high content of basic amino acid residues (such as lysine and arginine) and hydrophobic residues.
The highest concentrations of dynorphins in the central nervous system are found in the hypothalamus, medulla oblongata, and spinal cord.
Answer: True
Explanation: While dynorphins are widely distributed, their highest concentrations in the CNS are observed in regions such as the hypothalamus, medulla oblongata, pons, midbrain, and spinal cord.
Dynorphins are stored in large, dense-core vesicles, requiring a less intense stimulus for release compared to neurotransmitters.
Answer: False
Explanation: Dynorphins are stored in large, dense-core vesicles, which necessitates a more intense and prolonged stimulus for release compared to the small synaptic vesicles typically used by classical neurotransmitters.
Dynorphin is produced in various parts of the nervous system, including the hypothalamus, striatum, and hippocampus.
Answer: True
Explanation: Dynorphin exhibits a broad distribution within the nervous system, with significant production noted in areas such as the hypothalamus, striatum, hippocampus, and spinal cord.
In the CNS, which brain regions exhibit the highest concentrations of dynorphins?
Answer: Hypothalamus, medulla oblongata, pons, midbrain, and spinal cord
Explanation: The highest concentrations of dynorphins within the central nervous system are typically found in the hypothalamus, medulla oblongata, pons, midbrain, and spinal cord.
How does the storage mechanism of dynorphins differ from that of typical neurotransmitters?
Answer: Dynorphins are stored in large, dense-core vesicles, requiring a more intense stimulus for release.
Explanation: Unlike classical neurotransmitters stored in small synaptic vesicles, dynorphins are sequestered within large, dense-core vesicles. This storage modality necessitates a stronger and more sustained stimulus for their release into the synaptic cleft.
Goldstein and his colleagues named the first endogenous opioid peptide related to dynorphin "dynorphin" to signify its immense potency.
Answer: True
Explanation: The name 'dynorphin' was indeed chosen by Goldstein and his research group from the Greek word 'dynamis,' meaning power, to reflect the peptide's extraordinary potency.
Why did Goldstein et al. choose the name "dynorphin"?
Answer: From the Greek word "dynamis," signifying its great power or potency.
Explanation: The name 'dynorphin' was derived from the Greek word 'dynamis,' meaning power, chosen by its discoverers, Goldstein and colleagues, to emphasize the peptide's remarkable potency as an opioid.
Which receptor subtype is specifically responsible for the hypothermic effects of KOR agonists like dynorphin?
Answer: Kappa-opioid receptor 1 (K1)
Explanation: Research indicates that the hypothermic effects mediated by kappa opioid receptor (KOR) agonists, including dynorphin, are specifically associated with activation of the kappa-opioid receptor 1 (K1) subtype.
Injecting dynorphin into the rat spinal cord produced analgesia that could be completely blocked by the opioid antagonist naloxone.
Answer: False
Explanation: Studies involving the rat spinal cord demonstrated that dynorphin-induced analgesia was dose-dependent and only partially blocked by the opioid antagonist naloxone, not completely.
In rat spinal cord studies, dynorphin was found to be less potent than morphine in inducing analgesia.
Answer: False
Explanation: Research indicated that dynorphin was significantly more potent than morphine, approximately 6 to 10 times more potent on a per mole basis, in inducing analgesia when administered into the rat spinal cord.
Studies showed that morphine tolerance significantly reduced the analgesic effects of dynorphin.
Answer: False
Explanation: Contrary to this statement, studies by Han and Xie found that morphine tolerance did not significantly diminish the analgesic effects induced by dynorphin.
When injected into the intracerebroventricular (ICV) region of the brain, dynorphin A1-13 enhanced morphine-induced analgesia.
Answer: False
Explanation: When administered intracerebroventricularly (ICV), dynorphin A1-13 exhibited an antagonist effect on morphine-induced analgesia, contrasting with its additive effect when injected into the spinal cord.
The dynorphin-kappa opioid receptor (KOR) system is implicated in mediating neuropathic pain and astrocyte proliferation.
Answer: True
Explanation: Evidence suggests that the dynorphin-kappa opioid receptor (KOR) system plays a role in the development of neuropathic pain and is involved in the process of astrocyte proliferation.
Land et al. described a mechanism where corticotropin-releasing factor (CRF) inhibits dynorphin release, reducing aversive behaviors.
Answer: False
Explanation: Land et al. proposed that corticotropin-releasing factor (CRF) stimulates dynorphin release, which in turn contributes to aversive behaviors and dysphoria, rather than inhibiting it.
Mice lacking dynorphin displayed stress-induced aversive behaviors similar to control mice.
Answer: False
Explanation: Mice genetically engineered to lack dynorphin did not exhibit the stress-induced aversive behaviors observed in control animals, highlighting dynorphin's critical role in mediating these responses.
The pathway involving CRF2, dynorphin release, and KOR activation is linked to stress-induced dysphoria.
Answer: True
Explanation: Research suggests that activation of the CRF2 receptor leads to dynorphin release and subsequent kappa opioid receptor (KOR) activation, a pathway implicated in the generation of stress-induced dysphoria.
Overexpressing wild-type CREB in transgenic mice resulted in an antidepressant-like effect.
Answer: False
Explanation: Conversely, overexpressing wild-type CREB was associated with increased depression-like symptoms, whereas overexpressing a dominant-negative form of CREB (mCREB) produced an antidepressant-like effect, linked to reduced dynorphin expression.
Studies involving the rat spinal cord showed that dynorphin injection produced analgesia that was:
Answer: Dose-dependent and partially blocked by naloxone.
Explanation: In rat spinal cord studies, dynorphin administration induced analgesia in a dose-dependent manner, and this effect was only partially antagonized by naloxone.
Compared to morphine on a per mole basis, dynorphin was observed to be how much more potent in inducing analgesia in rat spinal cord studies?
Answer: 6 to 10 times as potent
Explanation: Research indicated that dynorphin was considerably more potent than morphine in producing analgesia in the rat spinal cord, estimated to be 6 to 10 times more potent on a molar basis.
How did morphine tolerance affect dynorphin-induced analgesia in the Han and Xie studies?
Answer: It had no significant effect on dynorphin-induced analgesia.
Explanation: The studies conducted by Han and Xie found that the development of morphine tolerance did not attenuate the analgesic effects produced by dynorphin.
What was the effect of injecting dynorphin A1-13 into the intracerebroventricular (ICV) region of the brain?
Answer: It had an antagonist effect on morphine-induced analgesia.
Explanation: Intracerebroventricular administration of dynorphin A1-13 resulted in an antagonistic interaction with morphine-induced analgesia, whereas spinal administration showed an additive effect.
In the context of stress and dysphoria, what pathway did Land et al. identify?
Answer: CRF2 receptor stimulation -> dynorphin release -> KOR activation -> dysphoria.
Explanation: Land et al. identified a pathway where CRF2 receptor stimulation leads to dynorphin release, which subsequently activates the kappa opioid receptor (KOR), contributing to stress-induced dysphoria.
How did mice lacking dynorphin respond to stress-induced aversive behaviors compared to controls?
Answer: They did not display the aversive behaviors seen in controls.
Explanation: Mice genetically deficient in dynorphin did not exhibit the characteristic aversive behaviors typically elicited by stress paradigms, unlike their control counterparts.
What did Shirayama et al. find regarding dynorphin levels in rats subjected to learned helplessness or immobilization stress?
Answer: Dynorphin levels increased in the hippocampus and nucleus accumbens.
Explanation: Shirayama et al. reported that both learned helplessness and immobilization stress led to elevated levels of dynorphins A and B within the hippocampus and nucleus accumbens of rats.
Dynorphin produced in magnocellular oxytocin neurons enhances oxytocin secretion.
Answer: False
Explanation: Dynorphin produced in magnocellular oxytocin neurons functions as a negative feedback inhibitor, thereby reducing oxytocin secretion, rather than enhancing it.
Dynorphin plays a role in appetite control, particularly when produced in the arcuate nucleus and lateral hypothalamus.
Answer: True
Explanation: Dynorphin synthesized in neurons of the arcuate nucleus and the lateral hypothalamus is implicated in the regulation of appetite.
Repeated cocaine exposure decreases dynorphin concentrations in the striatum and substantia nigra in rats.
Answer: False
Explanation: Conversely, repeated cocaine exposure has been shown to increase dynorphin concentrations in the striatum and substantia nigra of rats, indicating a role in addiction-related neuroadaptations.
Dynorphin enhances dopamine release by binding to kappa opioid receptors (KORs) on dopamine terminals.
Answer: False
Explanation: Dynorphin typically inhibits dopamine release by acting on kappa opioid receptors (KORs) located on dopamine nerve terminals, a mechanism thought to be involved in the negative affective states associated with withdrawal.
Dynorphin produced in magnocellular vasopressin neurons is involved in:
Answer: Patterning the electrical activity of these neurons.
Explanation: Within the magnocellular vasopressin neurons of the supraoptic nucleus, dynorphin plays a role in modulating and patterning the electrical firing activity of these cells.
What is the function of dynorphin produced in magnocellular oxytocin neurons?
Answer: To act as a negative feedback inhibitor of oxytocin secretion.
Explanation: Dynorphin synthesized within magnocellular oxytocin neurons serves to inhibit oxytocin secretion, acting as a negative feedback mechanism.
How does dynorphin typically affect dopamine release?
Answer: It inhibits dopamine release by acting on KORs.
Explanation: Dynorphin generally exerts an inhibitory effect on dopamine release through its action on kappa opioid receptors (KORs) located on dopaminergic nerve terminals.
What effect do KOR agonists, such as dynorphin, typically have on body temperature?
Answer: Hypothermia (decrease in body temperature)
Explanation: Kappa opioid receptor (KOR) agonists, including dynorphin, are known to induce hypothermia, a decrease in core body temperature.
Lai et al. proposed that dynorphin might stimulate pain by activating the bradykinin receptor in addition to the kappa opioid receptor (KOR).
Answer: True
Explanation: Research by Lai and colleagues suggested that dynorphin could contribute to pain stimulation not only via kappa opioid receptor (KOR) activation but also through interaction with the bradykinin receptor.
Svensson et al. found that a truncated dynorphin A2-17, which does not bind opioid receptors, increased p38 MAPK activation in spinal cord microglia.
Answer: True
Explanation: Svensson and colleagues demonstrated that dynorphin A2-17, a fragment incapable of binding opioid receptors, could still induce p38 mitogen-activated protein kinase (MAPK) phosphorylation in spinal cord microglia, suggesting a non-opioid mechanism for pain signaling.
The proposed mechanism for increased dynorphin after cocaine involves PKA activating CREB, leading to decreased dynorphin expression.
Answer: False
Explanation: The proposed mechanism involves PKA activating CREB, which subsequently leads to *increased* dynorphin expression, contributing to the neurobiological changes associated with cocaine use.
Mice overexpressing CREB showed place aversion to cocaine, reversing the typical place preference seen in control mice.
Answer: True
Explanation: Experimental findings by Carlezon et al. indicated that mice with enhanced CREB activity exhibited place aversion to cocaine, counteracting the rewarding effects observed in control animals, and this was associated with increased dynorphin expression.
Besides KOR, what other receptor did Lai et al. propose dynorphin might activate to stimulate pain?
Answer: Bradykinin receptor
Explanation: Lai et al. hypothesized that dynorphin might also stimulate pain by activating the bradykinin receptor, in addition to its primary interaction with the kappa opioid receptor (KOR).
According to Lai et al.'s proposed mechanism, how does dynorphin activate bradykinin receptors to stimulate pain?
Answer: By triggering calcium ion release via voltage-sensitive channels.
Explanation: Lai et al.'s proposed mechanism suggests that dynorphin activation of bradykinin receptors leads to pain stimulation by triggering intracellular calcium ion release through voltage-sensitive channels.
What did Svensson et al. find regarding the effect of truncated dynorphin A2-17 on spinal cord microglia?
Answer: It increased phosphorylated p38 MAPK.
Explanation: Svensson et al. observed that dynorphin A2-17, a fragment that does not bind opioid receptors, induced an increase in phosphorylated p38 MAPK levels within spinal cord microglia.
The molecular mechanism linking cocaine exposure to increased dynorphin involves PKA activating which transcription factor?
Answer: CREB (3',5'-monophosphate response element binding protein)
Explanation: The proposed molecular pathway suggests that cocaine elevates cAMP levels, activating PKA, which in turn phosphorylates and activates the transcription factor CREB, leading to increased dynorphin gene expression.
Why are dynorphin derivatives generally considered to have limited clinical utility?
Answer: They have a very short duration of action.
Explanation: The primary limitation for the clinical application of dynorphin derivatives is their exceedingly short duration of action, which hinders their utility for sustained therapeutic effects.