Release of cholecystokinin from rat cerebral cortex in vivo: role of GABA and glutamate receptor systems

Yaksh, Tony L.; Furui, Tomoo; Kanawati, Isa S.; Go, Vay Liang W.

doi:10.1016/0006-8993(87)90784-0

Cited by 61 publications

(7 citation statements)

References 27 publications

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“…It is interesting to note that TTX (1 p M ) , which completely inhibited veratridine-stimulated somatostatin release in our model, was unable to modify excitatory amino acid agonist responses, although it has been found to block glutamate-induced release of acetylcholine in striatal slices (Scatton and Lehmann, 1982) and of cholecystokinin in rat cerebral cortex in vivo (Yaksh et al, 1987). Furthermore, TTX did not modify K+ depolarization, which is probably due to the opening of various types of voltage-sensitive Ca2+ channels (Miller, 1987).…”

Section: Discussionmentioning

confidence: 67%

Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures

Tapia‐Arancibia

Astier

1989

Journal of Neurochemistry

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L-Glutamate, N-methyl-D-aspartic acid (NMDA), quisqualate, and kainate were found to increase endogenous somatostatin release from primary cultures of rat cortical neurons in a dose-dependent manner. The rank order of potency calculated from the dose-response curves was quisqualate greater than glutamate = NMDA greater than kainate, with EC50 values of 0.4, 20, and 40 microM, respectively. Alanine, glutamine, and glycine did not modify the release of somatostatin. The stimulation of somatostatin release elicited by L-glutamate was Ca2+ dependent, was decreased by Mg2+, and was blocked by DL-amino-5-phosphonovaleric acid (APV) and thienylphencyclidine (TCP), two specific antagonists of NMDA receptors. The NMDA stimulatory effect was strongly inhibited by APV in a competitive manner (IC50 = 50 microM) and by TCP in a noncompetitive manner (IC50 = 90 nM). The release of somatostatin induced by the excitatory amino acid agonists was not blocked by tetrodotoxin (1 microM), a result suggesting that tetrodotoxin-sensitive, sodium-dependent action potentials are not involved in the effect. Somatostatin release in response to NMDA was potentiated by glycine, but the inhibitory strychnine-sensitive glycine receptor did not appear to be involved. Our data suggest that glutamate exerts its stimulatory action on somatostatin release essentially through an NMDA receptor subtype.

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Section: Discussionmentioning

confidence: 67%

Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures

Tapia‐Arancibia

Astier

1989

Journal of Neurochemistry

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“…Moreover, Rattray et al (1993) showed that GABA seems to affect the expression of the CCK-gene in that CCK mRNA is increased both after a single benzodiazepine injection and after benzodiazepine withdrawal (Rattray et al, 1993). Furthermore, it has been shown in rat studies that GABA and benzodiazepines attenuated CCK release, whereas GABA A -receptor antagonists such as bicuculline led to an increase in CCK release (Yaksh et al, 1987). Finally, discontinuation of chronic treatment with benzodiazepines was followed by an increase in CCK receptor density in the frontal cortex and the hippocampus (Harro et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Effects of Alprazolam on Cholecystokinin-Tetrapeptide-Induced Panic and Hypothalamic–Pituitary–Adrenal-Axis Activity: A Placebo-Controlled Study

Zwanzger

Eser

Aicher

et al. 2002

Neuropsychopharmacol

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Cholecystokinin-tetrapeptide (CCK-4) induces panic attacks both in patients with panic disorder (PD) and healthy volunteers. It has been shown that panic elicited by CCK-4 is improved after treatment with antidepressants. Moreover, a reduction of CCK-4-induced panic has also been demonstrated after treatment with lorazepam in single subjects and after selective GABAergic treatment with vigabatrin. Although benzodiazepines are widely used as anxiolytics, no controlled study on the effects of benzodiazepines on CCK-4-induced panic symptoms is available so far. Therefore, we investigated the effects of alprazolam and placebo on CCK-4-induced panic symptoms in a double-blind, placebo-controlled study. A total of 30 healthy subjects were challenged with 50 mg CCK-4. Out of these 30 subjects, 26 showed a marked panic response to CCK-4. Subjects were rechallenged after a 7-day interval and treated with 1 mg alprazolam or placebo 1 h prior to the second CCK-4 challenge. Panic was assessed using the acute panic inventory (API) and a DSM-IV-derived panic symptom scale (PSS). Moreover, the number of reported symptoms and self-rated anxiety and arousal were recorded. We found a significant reduction of the API and PSS scores and of the number of reported symptoms compared to placebo. Moreover, compared to placebo the CCK-4-induced ACTH and cortisol release were significantly attenuated during the CCK-4 challenge after alprazolam treatment. However, also placebo treatment reduced CCK-4-induced anxiety and HPA-axis activation to a certain extent. In conclusion, our data show that alprazolam reduces CCK-4-induced panic, which supports the hypothesis of a possible interaction between the GABA and the CCK system.

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“…[128][129][130] No influence has been shown for CCK-4 induced panic on plasma GABA levels. [131] Furthermore, it has been shown that CCK release is attenuated after GABA and benzodiazepine administration [132] and that CCK receptor density is increased after cessation of chronic benzodiazepine treatment. [133] Also, flumazenil significantly antagonized the anxiolytic-like effect of the CCK-A receptor antagonist devazepide in rats.…”

Section: Cck and The γ -Amino-butyric-acid (Gaba) Systemmentioning

confidence: 99%

Neuronal Network of Panic Disorder: The Role of the Neuropeptide Cholecystokinin

2012

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Panic disorder (PD) is characterized by panic attacks, anticipatory anxiety and avoidance behavior. Its pathogenesis is complex and includes both neurobiological and psychological factors. With regard to neurobiological underpinnings, anxiety in humans seems to be mediated through a neuronal network, which involves several distinct brain regions, neuronal circuits and projections as well as neurotransmitters. A large body of evidence suggests that the neuropeptide cholecystokinin (CCK) might be an important modulator of this neuronal network. Key regions of the fear network, such as amygdala, hypothalamus, peraqueductal grey, or cortical regions seem to be connected by CCKergic pathways. CCK interacts with several anxiety-relevant neurotransmitters such as the serotonergic, GABA-ergic and noradrenergic system as well as with endocannabinoids, NPY and NPS. In humans, administration of CCK-4 reliably provokes panic attacks, which can be blocked by antipanic medication. Also, there is some support for a role of the CCK system in the genetic pathomechanism of PD with particularly strong evidence for the CCK gene itself and the CCK-2R (CCKBR) gene. Thus, it is hypothesized that genetic variants in the CCK system might contribute to the biological basis for the postulated CCK dysfunction in the fear network underlying PD. Taken together, a large body of evidence suggests a possible role for the neuropeptide CCK in PD with regard to neuroanatomical circuits, neurotransmitters and genetic factors. This review article proposes an extended hypothetical model for human PD, which integrates preclinical and clinical findings on CCK in addition to existing theories of the pathogenesis of PD.

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Release of cholecystokinin from rat cerebral cortex in vivo: role of GABA and glutamate receptor systems

Cited by 61 publications

References 27 publications

Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures

Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures

Effects of Alprazolam on Cholecystokinin-Tetrapeptide-Induced Panic and Hypothalamic–Pituitary–Adrenal-Axis Activity: A Placebo-Controlled Study

Neuronal Network of Panic Disorder: The Role of the Neuropeptide Cholecystokinin

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