PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2171716-0 1990 Inhibition of potassium-evoked release of cholecystokinin from rat caudate-putamen, cerebral cortex and hippocampus incubated in vitro by phencyclidine and related compounds. Potassium 14-23 cholecystokinin Rattus norvegicus 42-57 1762664-1 1991 Cholecystokinin (CCK) affects neuronal excitability in a variety of in vivo and in vitro preparations, apparently by modulating a resting potassium conductance. Potassium 138-147 cholecystokinin Rattus norvegicus 17-20 1762664-2 1991 The data presented here show that CCK (applied as CCK8-S) also affects the transient potassium current in hippocampal neurones, by changing the voltage dependence of the inactivation and activation of the current. Potassium 85-94 cholecystokinin Rattus norvegicus 34-37 2171716-1 1990 Potassium-evoked release of cholecystokinin (CCK) from slices of caudate-putamen, hippocampus, and cerebral cortex was inhibited in a dose-related fashion by phencyclidine (PCP). Potassium 0-9 cholecystokinin Rattus norvegicus 28-43 2171716-1 1990 Potassium-evoked release of cholecystokinin (CCK) from slices of caudate-putamen, hippocampus, and cerebral cortex was inhibited in a dose-related fashion by phencyclidine (PCP). Potassium 0-9 cholecystokinin Rattus norvegicus 45-48 2804664-4 1989 However, locally applied CCK-8S potentiated the potassium-evoked overflow of dopamine (DA) into the extracellular space in both the caudate and nucleus accumbens. Potassium 48-57 cholecystokinin Rattus norvegicus 25-28 2804664-6 1989 These data support a facilitatory effect of CCK-8S on potassium-evoked overflow from DA-containing nerve terminals in the urethane anesthetized rat that is likely mediated through a peripheral type CCK receptor. Potassium 54-63 cholecystokinin Rattus norvegicus 44-47 2804664-6 1989 These data support a facilitatory effect of CCK-8S on potassium-evoked overflow from DA-containing nerve terminals in the urethane anesthetized rat that is likely mediated through a peripheral type CCK receptor. Potassium 54-63 cholecystokinin Rattus norvegicus 198-201 17581850-4 2007 Under voltage clamp (V H -65 mV), 22/24 motoneurons displayed a CCK-8s-induced tetrodotoxin-resistant inward current [peak: -136 +/- 28 pA] with a similar time course, mediated via reduction in a potassium conductance. Potassium 196-205 cholecystokinin Rattus norvegicus 64-67 3032357-3 1987 The addition of potassium (40 mM) in excess, resulted in a highly significant elevation in the levels of CCK-LI in the cortical superfusate. Potassium 16-25 cholecystokinin Rattus norvegicus 105-108 6200866-5 1984 The potassium stimulated release of CCK from obese rat hypothalamic tissue was significantly higher than from lean rat hypothalamus (3.62 +/- 0.3 vs. 1.91 +/- 0.3 fmole equivalents CCK-8/mg tissue/10 min). Potassium 4-13 cholecystokinin Rattus norvegicus 36-39 6200866-5 1984 The potassium stimulated release of CCK from obese rat hypothalamic tissue was significantly higher than from lean rat hypothalamus (3.62 +/- 0.3 vs. 1.91 +/- 0.3 fmole equivalents CCK-8/mg tissue/10 min). Potassium 4-13 cholecystokinin Rattus norvegicus 181-184 6200866-7 1984 However, the potassium stimulated release of CCK and VIP from cortical tissue was the same in all three groups of rats. Potassium 13-22 cholecystokinin Rattus norvegicus 45-48 32490811-2 2020 We found two firing phenotypes of CCK+INs in rat hippocampal CA3 area; either possessing a previously undetected membrane potential-dependent firing or regular firing phenotype, due to different low-voltage-activated potassium currents. Potassium 217-226 cholecystokinin Rattus norvegicus 34-37 2884011-5 1987 The release of CCK from rat cp slices in vitro stimulated by potassium was quantitated with a specific CCK radioimmunoassay. Potassium 61-70 cholecystokinin Rattus norvegicus 15-18 2884011-6 1987 This potassium-stimulated release of CCK was Ca2+-dependent. Potassium 5-14 cholecystokinin Rattus norvegicus 37-40 2884011-7 1987 Maximal stimulation of CCK release was observed at 55 mM potassium. Potassium 57-66 cholecystokinin Rattus norvegicus 23-26 2948613-1 1986 The effect of specific D-2 dopamine (DA) receptor agonists and antagonists on potassium (55 mM)-evoked release of cholecystokinin-like immunoreactivity (CCK-LI) was studied in tissue slices of the rat posterior nucleus accumbens (NAc). Potassium 78-87 cholecystokinin Rattus norvegicus 153-156 3785588-0 1986 Vasoactive intestinal polypeptide (VIP) inhibits potassium-induced release of cholecystokinin (CCK) from rat caudato-putamen but not from cerebral cortex. Potassium 49-58 cholecystokinin Rattus norvegicus 78-93 3785588-0 1986 Vasoactive intestinal polypeptide (VIP) inhibits potassium-induced release of cholecystokinin (CCK) from rat caudato-putamen but not from cerebral cortex. Potassium 49-58 cholecystokinin Rattus norvegicus 95-98 3785588-1 1986 CCK release elicited by 40 mM potassium from slices of rat caudato-putamen (cp) was inhibited by VIP. Potassium 30-39 cholecystokinin Rattus norvegicus 0-3 4045551-2 1985 In this study, we have examined the action of CCK-peptides on the basal and potassium-evoked release of [3H]DA within this structure. Potassium 76-85 cholecystokinin Rattus norvegicus 46-49 4045551-8 1985 In contrast to its effects on the basal release of [3H]DA, sulfated CCK-octapeptide was found to attenuate the potassium-evoked release of [3H]DA from the NAc in a concentration-dependent fashion from 2 X 10(-9) to 2 X 10(-6) M. The unsulfated form of the octapeptide had no effect on evoked release. Potassium 111-120 cholecystokinin Rattus norvegicus 68-71 6896838-6 1982 In rats, the addition of potassium (40 mM in excess) resulted in a 138% and 46% increase in the levels of CCK and VIP, respectively above resting levels (3.7 +/- 1.2 fmol/ml/10 min and 1.7 +/- 0.5 fmol/ml/10 min, respectively). Potassium 25-34 cholecystokinin Rattus norvegicus 106-109 16192299-9 2006 However, further isolation of background currents by recording in solutions that contained only sodium or only potassium revealed that both leptin and CCK were capable of increasing a sodium-dependent conductance or inhibiting a potassium-dependent conductance. Potassium 111-120 cholecystokinin Rattus norvegicus 151-154 17569742-9 2007 In voltage clamp, the CCK-8s-induced inward current reversed at -106 +/- 3 mV and the input resistance increased by 150 +/- 15%, suggesting an effect mediated by the closure of a potassium conductance. Potassium 179-188 cholecystokinin Rattus norvegicus 22-25 16192299-9 2006 However, further isolation of background currents by recording in solutions that contained only sodium or only potassium revealed that both leptin and CCK were capable of increasing a sodium-dependent conductance or inhibiting a potassium-dependent conductance. Potassium 229-238 cholecystokinin Rattus norvegicus 151-154 15353211-7 2004 In animals with carrageenan-induced arthritis, both basal and potassium-evoked release of CCK-LI were significantly increased compared to controls. Potassium 62-71 cholecystokinin Rattus norvegicus 90-93 15353211-8 2004 HPLC analysis of dialysates from the ACC during potassium stimulation showed that the main part of the immunoreactive material was sulphated CCK-8. Potassium 48-57 cholecystokinin Rattus norvegicus 141-144 14623130-1 2003 The recent discovery that subsets of rat taste receptor cells (TRCs) express the peptide cholecystokinin (CCK) and that subsets of TRCs respond to CCK with altered potassium currents or elevated intracellular calcium via CCK-A receptor has lead to the hypothesis that CCK may play a novel signaling role within the taste bud, perhaps modifying tastant responses by co-transmission with a classic transmitter. Potassium 164-173 cholecystokinin Rattus norvegicus 147-150 14623130-1 2003 The recent discovery that subsets of rat taste receptor cells (TRCs) express the peptide cholecystokinin (CCK) and that subsets of TRCs respond to CCK with altered potassium currents or elevated intracellular calcium via CCK-A receptor has lead to the hypothesis that CCK may play a novel signaling role within the taste bud, perhaps modifying tastant responses by co-transmission with a classic transmitter. Potassium 164-173 cholecystokinin Rattus norvegicus 147-150 12427859-7 2002 An outward potassium current, recorded with the patch-clamp technique, was inhibited by exogenous application of sulfated cholecystokinin octapeptide in a reversible and concentration-dependent manner. Potassium 11-20 cholecystokinin Rattus norvegicus 122-137 12427859-9 2002 An inwardly rectifying potassium current, typically invariant to stimulation, was also inhibited by cholecystokinin. Potassium 23-32 cholecystokinin Rattus norvegicus 100-115 9593865-2 1998 In the present in vivo microdialysis study, the effect of unilateral sciatic nerve section on basal and potassium-induced release of CCK-like (CCK-LI) immunoreactivity in the rat dorsal horn was investigated. Potassium 104-113 cholecystokinin Rattus norvegicus 133-136 11239718-0 2001 Activation of CB1 cannabinoid receptors in rat hippocampal slices inhibits potassium-evoked cholecystokinin release, a possible mechanism contributing to the spatial memory defects produced by cannabinoids. Potassium 75-84 cholecystokinin Rattus norvegicus 92-107 11239718-4 2001 The CB1 agonist R(+)WIN 55,212-2 (WIN+), at 1 and 10 micromol, strongly inhibited potassium-evoked CCK release from rat hippocampal slices, while the inactive isomer S(-)WIN,55,212-3 (WIN-) had no effect. Potassium 82-91 cholecystokinin Rattus norvegicus 99-102 11059899-2 2000 In the present microdialysis study, performed in the awake rat, we demonstrate a bilateral 4- to 6-fold increase of the potassium-induced release of CCK-like immunoreactivity (CCK-LI) in the ACC 2-3 weeks after a unilateral transection of the sciatic nerve (axotomy), an animal model of phantom limb or deafferentiation pain. Potassium 120-129 cholecystokinin Rattus norvegicus 149-152 11059899-2 2000 In the present microdialysis study, performed in the awake rat, we demonstrate a bilateral 4- to 6-fold increase of the potassium-induced release of CCK-like immunoreactivity (CCK-LI) in the ACC 2-3 weeks after a unilateral transection of the sciatic nerve (axotomy), an animal model of phantom limb or deafferentiation pain. Potassium 120-129 cholecystokinin Rattus norvegicus 176-179 9593865-2 1998 In the present in vivo microdialysis study, the effect of unilateral sciatic nerve section on basal and potassium-induced release of CCK-like (CCK-LI) immunoreactivity in the rat dorsal horn was investigated. Potassium 104-113 cholecystokinin Rattus norvegicus 143-146 9593865-3 1998 We also compared the effects of the CCK-B receptor antagonist CI988 on basal and potassium-stimulated CCK-LI release in intact animals and in chronically axotomized rats. Potassium 81-90 cholecystokinin Rattus norvegicus 102-105 8958576-3 1996 The possibility that elevation of cAMP also alters potassium-evoked release of CCK from rat brain slices incubated in vitro was also investigated. Potassium 51-60 cholecystokinin Rattus norvegicus 79-82 8517868-5 1993 Potassium-induced release of cholecystokinin from minislices of dorsal and ventral regions of the bed nucleus of stria terminalis was measured successfully using the above procedure to concentrate the peptide. Potassium 0-9 cholecystokinin Rattus norvegicus 29-44