Regulation of CCK mRNA expression in the rat brain by stress and treatment with sertraline, a selective serotonin re-uptake inhibitor

Giardino, Luciana; Bettelli, Carla; Pozza, Monica; Calzà, Laura

doi:10.1016/s0006-8993(99)01242-1

Cited by 18 publications

(8 citation statements)

References 17 publications

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“…42 Sertraline, an effective medication in the treatment of panic disorder, has been reported to influence the regional distribution of stress-induced CCK mRNA. 43 Our CCK results are similar to those of Kennedy et al As with the CCKBR results, differences between cases and controls may explain the discrepancy between our CCK results and those of Wang et al In their report, the frequency of the T allele varied with choice of control population, from 8.3% in 247 parents of children with cleft palate, to 28.3% among 99 newborns, to 13.9% in 79 ophthalmology patients. Less variability in the frequency of the T allele has been described using a British Caucasian population, 44 where no significant difference was seen between controls (9%), bipolar probands (11%), and schizophrenia probands (7%).…”

Section: Allelesupporting

confidence: 85%

No association or linkage between polymorphisms in the genes encoding cholecystokinin and the cholecystokinin B receptor and panic disorder

et al. 2000

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Growing animal data implicate cholecystokinin in the regulation of anxiety, while human clinical research confirms the role of cholecystokinin in the provocation of panic attacks. Antipanic medications suppress the ability of cholecystokinin to induce panic attacks, and may alter the expression of the cholecystokinin gene. Thus, there is increased interest in understanding the molecular genetic component of these observations. Recent association studies using persons with panic disorder described some association between polymorphisms in the genes encoding cholecystokinin and the cholecystokinin B-receptor and panic disorder. In this study, we used a family-based design, employing 596 individuals in 70 panic disorder pedigrees, as well as 77 haplotype relative risk 'triads'. Subjects were genotyped for two polymorphisms: the polymorphic microsatellite marker in the CCK-BR locus using PCR-based genotyping and at a single nucleotide polymorphism in the CCK promoter using a fluorescence polarization detection assay, and the data were analyzed for genetic association and linkage. Employing a variety of diagnostic and genetic models, linkage analysis produced no significant lod scores at either locus. Family-based tests of association, the haplotype-based haplotype relative risk statistic and the transmission disequilibrium test, were likewise nonsignificant. The results reported here provide little support for the role of these polymorphisms in panic disorder. Molecular Psychiatry (2001) 6, 59-65.

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Section: Allelesupporting

confidence: 85%

No association or linkage between polymorphisms in the genes encoding cholecystokinin and the cholecystokinin B receptor and panic disorder

et al. 2000

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“…Changes in the expression of CCK-related genes are however not restricted to the amygdala since a similar trend for CCK mRNA changes has been observed in the hippocampus after stress immobilization [113] as well as for CCK-2 receptor mRNA in the cerebral cortex and cerebellum of anxious rats as selected in the Elevated Plus-Maze [101].…”

Section: Molecular Biological Approachesmentioning

confidence: 59%

Wiring and Volume Transmission in Rat Amygdala. Implications for Fear and Anxiety

Mora

Jacobsen²,

Crespo-Ramírez

et al. 2008

Neurochem Res

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The amygdala plays a key role in anxiety. Information from the environment reaches the amygdaloid basolateral nucleus and after its processing is relayed to the amygdaloid central nucleus where a proper anxiogenic response is implemented. Experimental evidence indicates that in this information transfer a GABAergic interface controls the trafficking of impulses between the two nuclei. Recent work indicates that interneuronal communication can take place by classical synaptic transmission (wiring transmission) and by volume transmission in which the neurotransmitter diffuses and flows through the extracellular space from its site of release and binds to extrasynaptic receptors at various distances from the source. Based on evidence from our laboratory the concept is introduced that neurotransmitters in the amygdala can modulate anxiety involving changes in fear learning and memories by effects on receptor mosaics in the fear circuits through wiring and volume transmission modes of communication.

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“…Transcripts encoding three other peptides, NPY, ENK, and CCK, were all modulated in tandem at both time points in response to each stressor. These neuropeptides are all relatively abundant in CNS, are involved in major behavioral processes such as food intake and energy regulation, anxiety, and pain perception, and have been shown to be regulated by different stressors (Larsen and Mau, 1994;Giardino et al, 1999;Juaneda et al, 2001;Sweerts et al, 2001;Watts and Sanchez-Watts, 2002). Cellular NPY expression has not been localized to the PVH, and the response of this transcript is likely attributable to an adjoining population in the anterior hypothalamic area, which has been shown to exhibit responsiveness to a systemic cytokine challenge .…”

Section: Neuropeptidesmentioning

confidence: 99%

Categorically Distinct Acute Stressors Elicit Dissimilar Transcriptional Profiles in the Paraventricular Nucleus of the Hypothalamus

et al. 2003

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The paraventricular hypothalamic nucleus (PVH) is a key site for integrating neuroendocrine, autonomic, and behavioral adjustments to diverse homeostatic challenges, including "physiological" (e.g., infection or hemorrhage) and "emotional" [e.g., restraint (RST) or footshock] stresses. Both types of challenges ultimately converge to activate common response systems represented in PVH, including the hypothalamo-pituitary-adrenal axis and the sympathoadrenal system. Oligonucleotide microarrays (U74A; Affymetrix, Santa Clara, CA) were used to compare and contrast gene expression profiles in the PVH elicited at 1 and 3 hr after acute exposure to representative physiological [intraperitoneal injection of 10 microg lipopolysaccharide (LPS)] and emotional (30 min RST) stressors. In general, the two challenges recruited relatively few genes in common, with the degree of overlap varying across functional classes of genes. The greatest degree of commonality was seen among signaling molecules and neuropeptides, whereas transcription factors upregulated by RST and LPS were largely distinct. Unexpectedly, RST induced a number of immune-related molecules, which were not regulated by LPS. Hybridization histochemical analyses localized a subset of responsive transcripts to the PVH and/or immediately adjoining regions. Immunerelated molecules in particular distributed broadly to vascular and other barrier-associated cell types. These global transcriptional profiles inform the search for early (transcription factors) and late (target genes) mechanisms in the modulation of PVH, and generalized CNS, responses to categorically distinct stressors.

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Regulation of CCK mRNA expression in the rat brain by stress and treatment with sertraline, a selective serotonin re-uptake inhibitor

Cited by 18 publications

References 17 publications

No association or linkage between polymorphisms in the genes encoding cholecystokinin and the cholecystokinin B receptor and panic disorder

No association or linkage between polymorphisms in the genes encoding cholecystokinin and the cholecystokinin B receptor and panic disorder

Wiring and Volume Transmission in Rat Amygdala. Implications for Fear and Anxiety

Categorically Distinct Acute Stressors Elicit Dissimilar Transcriptional Profiles in the Paraventricular Nucleus of the Hypothalamus

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