Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • The co localization of CRF and CCK has

    2019-07-05

    The co-localization of CRF and CCK has been investigated in extensive studies. Sutin and Jacobowitz (1988) examined the immunocytochemical localization of peptides and neurochemicals in the rat laterodorsal tegmental nucleus and found the existence of CRF, atrial natriuretic factor (ANF), neurotensin (NT), vasoactive intestinal polypeptide (VIP) and dynorphin B (Dyn B) cell bodies in addition to CCK, neuropeptide Y (NPY), serotonin (5HT), glutamic eicosapentaenoic acid of decarboxylase (GAD), and tyrosine hydroxylase (TH). Evidence from the neurons in the cat raphe nucleus also showed the immunoreaction for 5-HT, CRF, gamma-aminobutyric acid (GABA), CCK, NPY, thyrotropin-releasing hormone (TRH), and vasoactive intestinal polypeptide (VIP) (Batten, 1995). The coexistence of CCK and CRF peptides was even observed in the entire CNS in the marine worm Nereis by immunochemistrical and electron microscopical studies (Dhainaut-Courtois et al., 1985a, Dhainaut-Courtois et al., 1985b, Dhainaut-Courtois et al., 1986). The similar functions of CCK and CRF systems and their close localization raise a question: does the interaction between CCK and CRF systems exist and contribute to the modulation of anxiety-like behavior in animal models? Current knowledge in this field is quite limited. It was found that the chronic treatment of antalarmin, a CRF1 receptor antagonist, significantly increased CCK2 receptor-binding density and the expression of preproCCK mRNA (Lodge and Lawrence, 2003). Another direct example is the experiment from Biro et al. (1993), who indicated that the pretreatment with CRF antiserum and a CRF receptor antagonist, alpha-helical CRF (ahCRF) prevented the anxiogenic response to CCK8 in rats in a dose-dependent manner. Our preliminary data showed that the pre-treatment of CRF1 antagonist [Glu11,16]Astressin blocked the anxiogenic effect of CCK4 in mice (Wang et al., 2005). Recently, we demonstrated that chronic i.c.v. administration (5days) of CRF1 agonist cortagine resulted in the increased sensitivity of the central CCK system as indicated by the effectiveness of sub-threshold doses of CCK4 during elevated plus maze paradigm and fear conditioning (Sherrin et al., 2009). These data point to the possibility that some of the anxiogenic effects of the central CCK system take place via interacting with the CRF system. Thus, in the present study, we examined the immobilization-induced anxiety-like behavior in C57BL/6J mice tested by the elevated plus maze, screened the mRNA and protein expression of CCK and CRF systems in key brain regions and further explored the role of CRF1 and CCK2 receptors in the enhanced anxiety-like behavior. Although it has been demonstrated in rats that CRF and CRF1 receptor mRNAs were increased in several brain regions, e.g. hypothalamic paraventricular nucleus (PVN) and amygdala, after exposure to immobilization stress (Bonaz and Rivest, 1998, Imaki et al., 1996), the expression of CRF and CRF1 receptors in mice after immobilization has been poorly studied.
    Materials and methods
    Results
    Discussion Previous observations showed that the maximal responses of the stress effector systems are usually seen within the first 30min after the beginning of immobilization stress (Pacák and Palkovits, 2001). The magnitude of central stress responses usually gradually diminishes after the end of acute immobilization stress and returns to basal levels (Pacák and Palkovits, 2001). This is consistent with our observation that the increased anxiety induced by 30-min immobilization disappeared in stress30 mice, which were tested in EPM 30min after the cessation of immobilization stress. Todorovic et al. (2007) showed that mice subjected to 1-h immobilization exhibited the enhancement of anxiety-like behavior 15 and 30min after the end of immobilization and this enhancement disappeared 1h afterwards, which is in agreement with the observation from Radulovic et al. (1999). In their experiments, 1-h immobilization did not significantly alter the locomotor activity. In contrast to their findings, our results showed that 30-min immobilization reduced the total distance traveled in the stress group and meanwhile increased the anxiety-like behavior. This discrepancy might be related to the experimental design or time-dependent changes in immobilization stress-induced behavior. 30-min immobilization was chosen as the acute stressor in this experiment because preliminary work had indicated that a 30min of immobilization was sufficient to increase anxiety-like behavior in the behavioral tests (Henry et al., 2006). The correlation analysis among the percentage of time spent on open arms and the total distance traveled showed no significant correlation between the percentage of time spent on open arms and the total distance traveled. These data suggested that the effects of the immobilization stress on anxiety-related behavior were not confounded by alterations in locomotor activity, which is in agreement with the observation of Henry et al. (2006).