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== CNS effects ==
== CNS effects ==
[[Cholecystokinin|CCK]] receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B receptors possess a complex regulation of [[dopamine]] activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the DA-enhancing effects of [[cholecystokinin A receptor|CCK-A]]. However, the effects of CCK-B on [[dopamine]] activity vary depending on location.<ref name="pmid2706523">{{cite journal |author=Altar CA, Boyar WC |title=Brain CCK-B receptors mediate the suppression of dopamine release by cholecystokinin |journal=Brain Res. |volume=483 |issue=2 |pages=321–6 |year=1989 |month=April |pmid=2706523 |doi= |url=}}</ref> CCK-B antagonism enhances dopamine release in rat striatum.<ref name="Loonam_2003">{{cite journal | author = Loonam TM, Noailles PA, Yu J, Zhu JP, Angulo JA | title = Substance P and cholecystokinin regulate neurochemical responses to cocaine and methamphetamine in the striatum | journal = Life Sci. | volume = 73 | issue = 6 | pages = 727–39 | year = 2003 | month = June | pmid = 12801594 | doi = 10.1016/S0024-3205(03)00393-X | url = | issn = }}</ref> CCK-B activation enhances [[GABA]] release in rat anterior [[nucleus accumbens]]. <ref name="urlSpringerLink - Journal Article">{{cite web |url=http://www.springerlink.com/content/yxt7tddfjvgx194k/ |title=SpringerLink - Journal Article |format= |work= |accessdate=}}</ref>CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.<ref name="pmid2311658">{{cite journal | author = Dourish CT, O'Neill MF, Coughlan J, Kitchener SJ, Hawley D, Iversen SD | title = The selective CCK-B receptor antagonist L-365,260 enhances morphine analgesia and prevents morphine tolerance in the rat | journal = Eur. J. Pharmacol. | volume = 176 | issue = 1 | pages = 35–44 | year = 1990 | month = January | pmid = 2311658 | doi = | url = | issn = }}</ref> CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.<ref name="pmid7972279">{{cite journal | author = Higgins GA, Sills TL, Tomkins DM, Sellers EM, Vaccarino FJ | title = Evidence for the contribution of CCKB receptor mechanisms to individual differences in amphetamine-induced locomotion | journal = Pharmacol. Biochem. Behav. | volume = 48 | issue = 4 | pages = 1019–24 | year = 1994 | month = August | pmid = 7972279 | doi = 10.1016/0091-3057(94)90214-3 | url = | issn = }}</ref>
[[Cholecystokinin|CCK]] receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B receptors possess a complex regulation of [[dopamine]] activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the DA-enhancing effects of [[cholecystokinin A receptor|CCK-A]]. However, the effects of CCK-B on [[dopamine]] activity vary depending on location.<ref name="pmid2706523">{{cite journal |author=Altar CA, Boyar WC |title=Brain CCK-B receptors mediate the suppression of dopamine release by cholecystokinin |journal=Brain Res. |volume=483 |issue=2 |pages=321–6 |year=1989 |month=April |pmid=2706523 |doi= |url=}}</ref> CCK-B antagonism enhances dopamine release in rat striatum.<ref name="Loonam_2003">{{cite journal | author = Loonam TM, Noailles PA, Yu J, Zhu JP, Angulo JA | title = Substance P and cholecystokinin regulate neurochemical responses to cocaine and methamphetamine in the striatum | journal = Life Sci. | volume = 73 | issue = 6 | pages = 727–39 | year = 2003 | month = June | pmid = 12801594 | doi = 10.1016/S0024-3205(03)00393-X | url = | issn = }}</ref> CCK-B activation enhances [[GABA]] release in rat anterior [[nucleus accumbens]].<ref name="pmid10651144">{{cite journal | author = Lanza M, Makovec F | title = Cholecystokinin (CCK) increases GABA release in the rat anterior nucleus accumbens via CCK(B) receptors located on glutamatergic interneurons | journal = Naunyn Schmiedebergs Arch. Pharmacol. | volume = 361 | issue = 1 | pages = 33–8 | year = 2000 | month = January | pmid = 10651144 | doi = 10.1007/s002109900161 | url = | issn = }}</ref> CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.<ref name="pmid2311658">{{cite journal | author = Dourish CT, O'Neill MF, Coughlan J, Kitchener SJ, Hawley D, Iversen SD | title = The selective CCK-B receptor antagonist L-365,260 enhances morphine analgesia and prevents morphine tolerance in the rat | journal = Eur. J. Pharmacol. | volume = 176 | issue = 1 | pages = 35–44 | year = 1990 | month = January | pmid = 2311658 | doi = | url = | issn = }}</ref> CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.<ref name="pmid7972279">{{cite journal | author = Higgins GA, Sills TL, Tomkins DM, Sellers EM, Vaccarino FJ | title = Evidence for the contribution of CCKB receptor mechanisms to individual differences in amphetamine-induced locomotion | journal = Pharmacol. Biochem. Behav. | volume = 48 | issue = 4 | pages = 1019–24 | year = 1994 | month = August | pmid = 7972279 | doi = 10.1016/0091-3057(94)90214-3 | url = | issn = }}</ref>


In rats, CCK-B antagonism prevents the stress-induced reactivation of [[cocaine]]-induced [[conditioned place preference]], and prevents the long-term maintenance and reinstatement of [[morphine]]-induced CPP.<ref name="pmid11173090">{{cite journal | author = Lu L, Huang M, Ma L, Li J | title = Different role of cholecystokinin (CCK)-A and CCK-B receptors in relapse to morphine dependence in rats | journal = Behav. Brain Res. | volume = 120 | issue = 1 | pages = 105–10 | year = 2001 | month = April | pmid = 11173090 | doi = 10.1016/S0166-4328(00)00361-2 | url = | issn = }}</ref> Blockade of CCK-B potentiates cocaine-induced dopamine overflow in rat striatum.<ref name="Loonam_2003"/> CCK-B may pose a modulatory role in parkinson's disease. Blockade of CCK-B in dopamine-depleted [[squirrel monkeys]] induces significant enhancement of [[locomotor]] response to [[L-DOPA]].<ref name="pmid1976438">{{cite journal | author = Boyce S, Rupniak NM, Tye S, Steventon MJ, Iversen SD | title = Modulatory role for CCK-B antagonists in Parkinson's disease | journal = Clin Neuropharmacol | volume = 13 | issue = 4 | pages = 339–47 | year = 1990 | month = August | pmid = 1976438 | doi = | url = http://journals.lww.com/clinicalneuropharm/Abstract/1990/08000/Modulatory_Role_for_CCK_B_Antagonists_in.9.aspx | issn = }}</ref>
In rats, CCK-B antagonism prevents the stress-induced reactivation of [[cocaine]]-induced [[conditioned place preference]], and prevents the long-term maintenance and reinstatement of [[morphine]]-induced CPP.<ref name="pmid11173090">{{cite journal | author = Lu L, Huang M, Ma L, Li J | title = Different role of cholecystokinin (CCK)-A and CCK-B receptors in relapse to morphine dependence in rats | journal = Behav. Brain Res. | volume = 120 | issue = 1 | pages = 105–10 | year = 2001 | month = April | pmid = 11173090 | doi = 10.1016/S0166-4328(00)00361-2 | url = | issn = }}</ref> Blockade of CCK-B potentiates cocaine-induced dopamine overflow in rat striatum.<ref name="Loonam_2003"/> CCK-B may pose a modulatory role in parkinson's disease. Blockade of CCK-B in dopamine-depleted [[squirrel monkeys]] induces significant enhancement of [[locomotor]] response to [[L-DOPA]].<ref name="pmid1976438">{{cite journal | author = Boyce S, Rupniak NM, Tye S, Steventon MJ, Iversen SD | title = Modulatory role for CCK-B antagonists in Parkinson's disease | journal = Clin Neuropharmacol | volume = 13 | issue = 4 | pages = 339–47 | year = 1990 | month = August | pmid = 1976438 | doi = | url = http://journals.lww.com/clinicalneuropharm/Abstract/1990/08000/Modulatory_Role_for_CCK_B_Antagonists_in.9.aspx | issn = }}</ref>

Revision as of 13:24, 6 March 2010

Template:PBB The cholecystokinin B receptor also known as CCKBR or CCK2 is a protein[1] that in humans is encoded by the CCKBR gene.[2]

This gene encodes a G-protein coupled receptor for gastrin and cholecystokinin (CCK), regulatory peptides of the brain and gastrointestinal tract. This protein is a type B gastrin receptor, which has a high affinity for both sulfated and nonsulfated CCK analogs and is found principally in the central nervous system and the gastrointestinal tract. A misspliced transcript variant including an intron has been observed in cells from colorectal and pancreatic tumors.[3]

CNS effects

CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the DA-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location.[4] CCK-B antagonism enhances dopamine release in rat striatum.[5] CCK-B activation enhances GABA release in rat anterior nucleus accumbens.[6] CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.[7] CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.[8]

In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and prevents the long-term maintenance and reinstatement of morphine-induced CPP.[9] Blockade of CCK-B potentiates cocaine-induced dopamine overflow in rat striatum.[5] CCK-B may pose a modulatory role in parkinson's disease. Blockade of CCK-B in dopamine-depleted squirrel monkeys induces significant enhancement of locomotor response to L-DOPA.[10]

Selective Ligands

Agonists

Antagonists

  • Proglumide
  • CI-988
  • CI-1015
  • L-365,260
  • L-369,293
  • YF-476
  • YM-022
  • RP-69758
  • LY-225,910
  • LY-288,513
  • PD-135,158
  • PD-145,942

Inverse agonists

  • L-740,093

Interactions

Cholecystokinin B receptor has been shown to interact with cholecystokinin.[11][12][13]

See also

References

  1. ^ Noble F, Roques BP (1999). "CCK-B receptor: chemistry, molecular biology, biochemistry and pharmacology". Prog. Neurobiol. 58 (4): 349–79. PMID 10368033. {{cite journal}}: Unknown parameter |month= ignored (help)
  2. ^ Pisegna JR, de Weerth A, Huppi K, Wank SA (1992). "Molecular cloning of the human brain and gastric cholecystokinin receptor: structure, functional expression and chromosomal localization". Biochem. Biophys. Res. Commun. 189 (1): 296–303. PMID 1280419. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. ^ "Entrez Gene: CCKBR cholecystokinin B receptor".
  4. ^ Altar CA, Boyar WC (1989). "Brain CCK-B receptors mediate the suppression of dopamine release by cholecystokinin". Brain Res. 483 (2): 321–6. PMID 2706523. {{cite journal}}: Unknown parameter |month= ignored (help)
  5. ^ a b Loonam TM, Noailles PA, Yu J, Zhu JP, Angulo JA (2003). "Substance P and cholecystokinin regulate neurochemical responses to cocaine and methamphetamine in the striatum". Life Sci. 73 (6): 727–39. doi:10.1016/S0024-3205(03)00393-X. PMID 12801594. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. ^ Lanza M, Makovec F (2000). "Cholecystokinin (CCK) increases GABA release in the rat anterior nucleus accumbens via CCK(B) receptors located on glutamatergic interneurons". Naunyn Schmiedebergs Arch. Pharmacol. 361 (1): 33–8. doi:10.1007/s002109900161. PMID 10651144. {{cite journal}}: Unknown parameter |month= ignored (help)
  7. ^ Dourish CT, O'Neill MF, Coughlan J, Kitchener SJ, Hawley D, Iversen SD (1990). "The selective CCK-B receptor antagonist L-365,260 enhances morphine analgesia and prevents morphine tolerance in the rat". Eur. J. Pharmacol. 176 (1): 35–44. PMID 2311658. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Higgins GA, Sills TL, Tomkins DM, Sellers EM, Vaccarino FJ (1994). "Evidence for the contribution of CCKB receptor mechanisms to individual differences in amphetamine-induced locomotion". Pharmacol. Biochem. Behav. 48 (4): 1019–24. doi:10.1016/0091-3057(94)90214-3. PMID 7972279. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Lu L, Huang M, Ma L, Li J (2001). "Different role of cholecystokinin (CCK)-A and CCK-B receptors in relapse to morphine dependence in rats". Behav. Brain Res. 120 (1): 105–10. doi:10.1016/S0166-4328(00)00361-2. PMID 11173090. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ Boyce S, Rupniak NM, Tye S, Steventon MJ, Iversen SD (1990). "Modulatory role for CCK-B antagonists in Parkinson's disease". Clin Neuropharmacol. 13 (4): 339–47. PMID 1976438. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ Harikumar KG, Clain J, Pinon DI, Dong M, Miller LJ (2005). "Distinct molecular mechanisms for agonist peptide binding to types A and B cholecystokinin receptors demonstrated using fluorescence spectroscopy". J. Biol. Chem. 280 (2): 1044–50. doi:10.1074/jbc.M409480200. PMID 15520004. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  12. ^ Aloj L, Caracò C, Panico M, Zannetti A, Del Vecchio S, Tesauro D, De Luca S, Arra C, Pedone C, Morelli G, Salvatore M (2004). "In vitro and in vivo evaluation of 111In-DTPAGlu-G-CCK8 for cholecystokinin-B receptor imaging". J. Nucl. Med. 45 (3): 485–94. PMID 15001692. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ Galés C, Poirot M, Taillefer J, Maigret B, Martinez J, Moroder L, Escrieut C, Pradayrol L, Fourmy D, Silvente-Poirot S (2003). "Identification of tyrosine 189 and asparagine 358 of the cholecystokinin 2 receptor in direct interaction with the crucial C-terminal amide of cholecystokinin by molecular modeling, site-directed mutagenesis, and structure/affinity studies". Mol. Pharmacol. 63 (5): 973–82. PMID 12695525. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

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