Modulation of Memory, Reinforcement and Anxiety Parameters by Intra-Amygdala Injection of Cholecystokinin-Fragments Boc-CCK-4 and CCK-8s

Huston, Joseph P.; Schildein, S.; Gerhardt, P.; Privou, Caroline; Fink, Heidrun; Hasenöhrl, Rüdiger U.

doi:10.1016/s0196-9781(97)00270-2

Cited by 36 publications

(17 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One way is with the discovery that only some CCK receptors mediate memory (CCK-A), while other receptors (such as CCK-B) interfere with memory (Hadjiivanova et al, 2003). In addition, the beneficial effects of CCK-8 on memory are dependent on an intact dopaminergic system (Huston et al, 1998;Winnicka and Wisniewski, 1999;Winnicka et al, 2001), which ID rats lack. Other effects of CCK-8 in the brain were also found to be dependent on an intact dopaminergic system (Penke et al, 1985;Ladurelle et al, 1995;Tieppo et al, 2001;Xie et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Guilmeau et al, 2002;Nishi et al, 2003). While the increased level of CCK-8 might explain the anorectic effect of ID, it somehow conflicts with the finding that increases of CCK-8 improve learning and memory (Voits et al, 2001;Hadjiivanova et al, 2003), yet ID rats suffer learning deficits Wasantwisut, 1997;Yehuda and Rabinovitz, 2001), although the learning effects seem to be mediated by the dopaminergic system (Huston et al, 1998;Winnicka and Wisniewski, 1999;Winnicka et al, 2001).…”

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

Yehuda¹,

Mostofsky²

2004

Nutritional Neuroscience

View full text Add to dashboard Cite

Iron deficiency (ID) is among the most common nutritional diseases, causing deleterious effects that include decreases in cognitive function and weight loss. The ID also induces a reduction in the number and affinity of dopaminergic D2 receptors. The new finding that ID induces an increase in the pancreas cells, leads to the hypothesis that cholecystokinin-8 (CCK-8) is involved in the ID effects. The level of CCK-8 was higher among ID rats, compared with normal rats. The ID rats in our study were anorectic and performed poorly in learning tests (Morris water maze and passive avoidance learning). Essential fatty acids (EFA) mediate dopamine activity and have been found to rehabilitate learning deficits. Treatment with a fatty acid compound blocked both the learning deficits and the anorexia, while a CCK-8 antagonist was successful only against the anorectic effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

Yehuda¹,

Mostofsky²

2004

Nutritional Neuroscience

View full text Add to dashboard Cite

show abstract

“…When injected into the amygdala, opioid antagonists enhance memory retention 38 , and the intra-amygdaloid administration of CCK agonists facilitates learning and memory 39,40 . Furthermore, CCK mRNA expression increases in the amygdala following repeated morphine administration, suggesting that the amygdala is a critical locus for a CCKmediated compensatory mechanism that contributes to opioid tolerance 41 .…”

Section: Discussionmentioning

confidence: 99%

A locus and mechanism of action for associative morphine tolerance

2000

View full text Add to dashboard Cite

Repeated administration of an opioid in the presence of specific environmental cues can induce tolerance specific to that setting (associative tolerance). Prolonged or repeated administration of an opioid without consistent contextual pairing yields non-associative tolerance. Here we demonstrate that cholecystokinin acting at the cholecystokinin-B receptor is required for associative but not non-associative morphine tolerance. Morphine given in the morphineassociated context increased Fos-like immunoreactivity in the lateral amygdala and hippocampal area CA1. Microinjection of the cholecystokinin B antagonist L-365,260 into the amygdala blocked associative tolerance. These results indicate that cholecystokinin acting in the amygdala is necessary for associative tolerance to morphine's analgesic effect.The role of cholecystokinin (CCK) as an anti-opioid peptide is firmly established. CCK suppresses the analgesic effect of morphine and other μ-opioid receptor agonists 1,2 . CCK antagonists potentiate the analgesic effects of exogenous and endogenous μ-opioid receptor agonists 3-8 and enhance the inhibitory effect of morphine on nociceptive dorsal horn neurons 9,10 . Additionally, CCK antagonists impede the acquisition of morphine tolerance yet have no effect on morphine dependence or withdrawal 3,[11][12][13][14][15][16] . Although CCK antagonists potentiate the effects of opioids, they do not alter nociceptive threshold levels when administered independently 8,16 . There are two distinct CCK receptors (CCK-A and CCK-B) in the CNS [17][18][19][20] .Learning can contribute to drug tolerance [21][22][23][24][25][26][27] . When morphine administration is paired with specific environmental cues, these cues can act as conditioned stimuli that elicit a conditioned response opposing the agonist effect of morphine (associative tolerance). Although associative analgesic tolerance following repeated opioid administration is well established, the underlying neurobiological mechanisms are unknown.

show abstract

“…As an example of this, it was shown that oxytocin, injected into the nucleus basalis of Meynert, plays an inhibitory role in spatial learning in the stressful Morris water maze task [203]. Next to vasopressin and oxytocin, cholecystokinin-8 also facilitates memory consolidation in the inhibitory avoidance paradigm [204] and the two-trial memory task [205] and reverses performance deficits of spatial learning in aged Fischer rats [206] and spatial recognition impairment induced by stress [207]. It protected against amnesia induced by electroconvulsive shock, scopolamine, NMDA antagonists or protein kinase inhibitors in the passive avoidance test [208][209][210][211].…”

Section: Mechanism(s) Of Action Of Angiotensin IV Through Interactionmentioning

confidence: 99%

Involvement of insulin-regulated aminopeptidase in the effects of the renin–angiotensin fragment angiotensin IV: a review

et al. 2007

View full text Add to dashboard Cite

For decades, angiotensin (Ang) II was considered as the end product and the only bioactive peptide of the renin-angiotensin system (RAS). However, later studies revealed biological activity for other Ang fragments. Amongst those, Ang IV has drawn a lot of attention since it exerts a wide range of central and peripheral effects including the ability to enhance learning and memory recall, anticonvulsant and anti-epileptogenic properties, protection against cerebral ischemia, activity at the vascular level and an involvement in atherogenesis. Some of these effects are AT(1) receptor dependent but others most likely result from the binding of Ang IV to insulin-regulated aminopeptidase (IRAP) although the exact mechanism(s) of action that mediate the Ang IV-induced effects following this binding are until now not fully known. Nevertheless, three hypotheses have been put forward: since Ang IV is an inhibitor of the catalytic activity of IRAP, its in vivo effects might result from a build-up of IRAP's neuropeptide substrates. Second, IRAP is co-localized with the glucose transporter GLUT4 in several tissue types and therefore, Ang IV might interact with the uptake of glucose. A final and more intriguing hypothesis ascribes a receptor function to IRAP and hence an agonist role to Ang IV. Taken together, it is clear that further work is required to clarify the mechanism of action of Ang IV. On the other hand, a wide range of studies have made it clear that IRAP might become an important target for drug development against different pathologies such as Alzheimer's disease, epilepsy and ischemia.

show abstract

Modulation of Memory, Reinforcement and Anxiety Parameters by Intra-Amygdala Injection of Cholecystokinin-Fragments Boc-CCK-4 and CCK-8s

Cited by 36 publications

References 73 publications

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

A locus and mechanism of action for associative morphine tolerance

Involvement of insulin-regulated aminopeptidase in the effects of the renin–angiotensin fragment angiotensin IV: a review

Contact Info

Product

Resources

About