Biological actions of cholecystokinin

Crawley, Jacqueline N.; Corwin, Rebecca L.

doi:10.1016/0196-9781(94)90104-x

Cited by 648 publications

(464 citation statements)

References 419 publications

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“…rTMS could furthermore modulate mesolimbic DA concentrations through stimulation of glutamatergic projections from the prefrontal cortex to the NAS (You et al, 1998), which are able to increase DA release by a local effect of glutamate on adjacent dopaminergic nerve terminals from the VTA (Cheramy et al, 1998;Taber and Fibiger, 1995). Additional rTMS-induced neurobiological changes, such as an increase in gene expression of the neuropeptide cholecystokinin (CCK), may contribute to the effects reported, since CCK, acting as a neuromodulator, increases the firing rate of dopaminergic neurons (Crawley and Corwin, 1994;Müller et al, 2000).…”

Section: Mesolimbic Dopaminergic System As a Therapeutic Target For Rmentioning

confidence: 99%

Repetitive Transcranial Magnetic Stimulation Increases the Release of Dopamine in the Nucleus Accumbens Shell of Morphine-Sensitized Rats During Abstinence

Erhardt

Sillaber

Welt

et al. 2004

Neuropsychopharmacol

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Recent studies in rodents have shown that withdrawal from chronic drug abuse is associated with a significant decrease in dopamine (DA) release in mesolimbic structures, especially in the shell region of the nucleus accumbens. Since the DA system is known to play an important role in reward processes, a withdrawal-associated impairment in mesolimbic DA-mediated transmission could possibly implicate reward deficit and thus enhance vulnerability to drug craving and relapse. We have previously demonstrated that acute repetitive transcranial magnetic stimulation (rTMS) has a modulatory effect on DA release in several areas of the rat brain, including dorsal striatum, hippocampus, and nucleus accumbens shell. In the present study, we investigated the possible use of rTMS as a tool in reestablishing the dysregulated DA secretion observed during withdrawal in morphine-sensitized male Sprague-Dawley rats. Using intracerebral microdialysis, we monitored the effects of acute rTMS (20 Hz) on the intra-accumbal release-patterns of DA in freely moving animals that were subjected to a morphine sensitization scheme for a period of 8 days. We provide first evidence that acute rTMS (20 Hz) is able to increase DA concentration in the shell region of the nucleus accumbens in both control animals and morphinesensitized rats during abstinence. The DA release in morphine-sensitized rats was significantly higher than in controls. rTMS, therefore, might gain a potential therapeutic role in the treatment of dysphoric and anhedonic states during drug withdrawal in humans.

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Section: Mesolimbic Dopaminergic System As a Therapeutic Target For Rmentioning

confidence: 99%

Repetitive Transcranial Magnetic Stimulation Increases the Release of Dopamine in the Nucleus Accumbens Shell of Morphine-Sensitized Rats During Abstinence

Erhardt

Sillaber

Welt

et al. 2004

Neuropsychopharmacol

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“…CCK, acting as a neuromodulator, increases the firing rate of dopaminergic ventral tegmental and substantia nigra neurons, and the ability of CCK to directly affect local dopamine release has been examined in numerous experiments (for review see Crawley and Corwin 1994;Moran and Schwartz 1994).…”

Section: Rtms Differentially Affects the Expression Of The Modulatorymentioning

confidence: 99%

“…CCK is the most abundant neuropeptide in the mammalian brain, and its anatomical distribution, with high levels of expression in the cerebral cortex, the amygdala, the hippocampus and the septum strongly suggests that it is one of the modulators of emotionality (for review see Moran and Schwartz 1994). CCK is colocalized with dopamine in a large proportion of the neurons in the mesolimbic system (for review see Crawley and Corwin 1994). These CCK-containing dopaminergic pathways have been implicated in the pathophysiology of human affective disorders and Parkinson's disease, and in both of these disease states rTMS has been suggested to exert beneficial effects (Pascual-Leone and Catala 1995;Pascual-Leone et al 1994;Siebner et al 1999).…”

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confidence: 99%

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Müller

Toschi

Kresse

et al. 2000

Neuropsychopharmacology

255

107

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Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a therapeutic tool in various neurological and psychiatric disorders, and we recently found that it has a neuroprotective effect both in vitro andTranscranial magnetic stimulation (TMS), a technique in which a time-varying strong electric current is applied through a coil held in direct contact with the subject's head, was originally developed for diagnostic use in neurology (for review see Rossini and Rossi 1998). A possible effect of TMS on mood was first reported in 1987 (Bickford et al. 1987) and, although discussed controversially, to date several lines of evidence resulting from both preclinical (Fleischmann et al. 1995;Zyss et al. 1997) and clinical (e.g., Pascual-Leone et al. 1996) studies support the notion that repetitive TMS (rTMS) may have antidepressant properties: rTMS induces transient enhancement of mood in healthy subjects, and daily application alleviates symptoms in patients suffering from treatment-resistant major depression (for review see George et al. 1999).Although rTMS is currently being evaluated as a possible alternative or add-on therapy in the treatment of refractory depression, knowledge concerning its effects at the molecular and cellular level is still very limited. Recently, Ji et al. (1998) reported a specific activation of brain regions in terms of immediate early gene expression in rats in response to rTMS. In addition, we provided a first evidence for a neuroprotective effect of long-term rTMS in vivo and in vitro (Post et al. 1999). The in vitro studies showed that magnetic stimulation analogous to TMS increased the overall viability of mouse monoclonal hippocampal HT22 cells and had a neuroprotective effect against oxidative stressors such as amyloid beta (A ␤ ) and glutamate. Moreover, the treatment increased the release of the potentially neuroprotective secreted amyloid precursor protein (sAPP) into the supernatant of HT22 cells and into cerebrospinal fluid from rats. Accordingly, HT22 cells preincubated with cerebrospinal fluid from long-term rTMStreated rats were found to be protected against A ␤ (Post et al. 1999). However, the neurochemical mechanisms underlying these neuroprotective properties as well as the putative therapeutic effects of rTMS in neurological and psychiatric disorders still remain to be elucidated.Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is abundantly expressed in the adult brain. The neurotrophic and also neuroprotective effects of BDNF have been characterized extensively both in vitro and in vivo. In addition, upregulation of BDNF has been implicated in neuronal responses to various kinds of injuries, such as epileptic seizures, cerebral ischemia, and hypoglycemia (for review see Connor and Dragunow 1998). Recent work raised the possibility that one of the many long-term effects of antidepressant treatment may be regulation of neurotrophins: antidepressant drug treatment and electroconvulsive seizures (ECS) were shown to marke...

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“…Furthermore, we recently reported that rTMS induced an increase in the expression of neuropeptide CCK mRNA after chronic treatment in rats (Müller et al 2000). CCK, acting as a neuromodulator, increases the firing rate of dopaminergic ventral tegmental and substantia nigra neurons, and the ability of CCK to directly affect local dopamine release has been demonstrated in numerous experiments (for review, see Crawley and Corwin 1994). Therefore, the increase in CCK expression reported could possibly contribute to the behavioral effects of rTMS measured in the forced swim test.…”

Section: Behavioral Effects Of Rtms: Changes In Stress Coping Strategiesmentioning

confidence: 99%

Neuroendocrine and Behavioral Effects of Repetitive Transcranial Magnetic Stimulation in a Psychopathological Animal Model Are Suggestive of Antidepressant-like Effects

Keck

Welt

Post

et al. 2001

Neuropsychopharmacology

129

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Biological actions of cholecystokinin

Cited by 648 publications

References 419 publications

Repetitive Transcranial Magnetic Stimulation Increases the Release of Dopamine in the Nucleus Accumbens Shell of Morphine-Sensitized Rats During Abstinence

Repetitive Transcranial Magnetic Stimulation Increases the Release of Dopamine in the Nucleus Accumbens Shell of Morphine-Sensitized Rats During Abstinence

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Neuroendocrine and Behavioral Effects of Repetitive Transcranial Magnetic Stimulation in a Psychopathological Animal Model Are Suggestive of Antidepressant-like Effects

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