Expression of c-&lt;i&gt;fos&lt;/i&gt; in the Brain after Activation of L-Type Calcium Channels

Jinnah, Hyder A.; Egami, Kiyoshi; Rao, Lekha M.; Shin, MeYeon; Kasim, Suhail; Hess, Ellen J.

doi:10.1159/000075666

Cited by 20 publications

(12 citation statements)

References 25 publications

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“…In the current study participation of central emetic neurons in FPL64176-induced vomiting is further indicated by upregulated c-Fos expression in brainstem emetic nuclei NTS, a key site for integration of diverse emetic signals (Ray et al, 2009a and 2009c), and DMNX, which receives axonal projections from NTS (Travagli and Anselmi, 2016). Thus, the blood-brain barrier permeable agent FPL64176 (Jinnah et al, 1999; 2000 and 2003) could excite emetic neurons directly in the NTS and DMNX. The absence of expected increase in Fos-immunoreactivity in the AP may be explained by findings that systemic administration of some emetics may not involve the AP (Miller and Leslie, 1994; Ray et al, 2009a).…”

Section: Discussionmentioning

confidence: 99%

Intracellular emetic signaling evoked by the L-type Ca2+ channel agonist FPL64176 in the least shrew (Cryptotis parva)

Zhong

Chebolu

Darmani

2018

European Journal of Pharmacology

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Ca2+ plays a major role in maintaining cellular homeostasis and regulates processes including apoptotic cell death and side-effects of cancer chemotherapy including vomiting. Currently we explored the emetic mechanisms of FPL64176, an L-type Ca2+ channel (LTCC) agonist with maximal emetogenic effect at its 10 mg/kg dose. FPL64176 evoked c-Fos immunoreactivity in shrew brainstem sections containing the vomit-associated nuclei, nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus. FPL64176 also increased phosphorylation of proteins ERK1/2, PKCα/βII and Akt in the brainstem. Moreover, their corresponding inhibitors (PD98059, GF 109203X and LY294002, respectively) reduced FPL64176-evoked vomiting. A 30 min subcutaneous (s.c.) pretreatment with the LTCC antagonist nifedipine (10 mg/kg) abolished FPL64176-elicited vomiting, c-Fos expression, and emetic effector phosphorylation. Ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs) mediate intracellular Ca2+ release from the sarcoplasmic/endoplasmic reticulum. The RyR antagonist dantrolene (i.p.), or a combination of low doses of nifedipine and dantrolene, but not the IP3R antagonist 2-APB, significantly attenuated FPL64176-induced vomiting. The serotonin type 3 receptor (5-HT3R) antagonist palonosetron (s.c.), the neurokinin 1 receptor (NK1R) antagonist netupitant (i.p.) or a combination of non-effective doses of netupitant and palonosetron showed antiemetic potential against FPL64176-evoked vomiting. Serotonin (5-HT) and substance P immunostaining revealed FPL64176-induced emesis was accompanied by an increase in 5-HT but not SP-immunoreactivity in the dorsomedial subdivision of the NTS. These findings demonstrate that Ca2+ mobilization through LTCCs and RyRs, and subsequent emetic effector phosphorylation and 5-HT release play important roles in FPL64176-induced emesis which can be prevented by 5-HT3R and NK1R antagonists.

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Section: Discussionmentioning

confidence: 99%

Intracellular emetic signaling evoked by the L-type Ca2+ channel agonist FPL64176 in the least shrew (Cryptotis parva)

Zhong

Chebolu

Darmani

2018

European Journal of Pharmacology

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“…The infl uence of 8 BayK 8644 on regional brain activity was recently delineated by mapping the induction of the immediate-early gene c-fos [Jinnah et al, 2004]. Despite the nearly ubiquitous expression of L-type calcium channels in the brain, these functional mapping studies revealed a heterogeneous effect on regional brain activity, with the most prominent changes in the striatum.…”

Section: Introductionmentioning

confidence: 99%

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

et al. 2006

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In rodents, activation of L-type calcium channels with ±BayK 8644 causes an unusual behavioral syndrome that includes dystonia and self-biting. Prior studies have linked both of these behaviors to dysfunction of dopaminergic transmission in the striatum. The current studies were designed to further elucidate the relationship between ±BayK 8644 and dopaminergic transmission in the expression of the behavioral syndrome. The drug does not appear to release presynaptic dopamine stores, since microdialysis of the striatum revealed dopamine release was unaltered by ±BayK 8644. In addition, the behaviors were preserved or even exaggerated in mice or rats with virtually complete dopamine depletion. On the other hand, pretreatment of mice with D₃ or D_1/5 dopamine receptor antagonists attenuated the behavioral effects of ±BayK 8644, while pretreatment with D₂ or D₄ antagonists had no effect. In D₃ receptor knockout mice, ±BayK 8644 elicited both dystonia and self-biting, but these behaviors were less severe than in matched controls. In D₁ receptor knockout mice, behavioral responses to ±BayK 8644 appeared exaggerated. These results argue that the behavioral effects of ±BayK 8644 are not mediated by a presynaptic influence. Instead, the behaviors appear to result from a postsynaptic activation of the drug, which does not require but can be modified by D₃ or D_1/5 receptors.

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“…The present result proposes that c-fos expression in the MGv is related to the corticothalamic inputs mediated by AMPA, NMDA, and mGluR receptors. c-fos expression has been proposed to link with calcium influx, which then triggers a cascade of Ca 2ϩ -sensitive gene expression (33)(34)(35). Extracellular Ca 2ϩ influx can occur through various channels, such as NMDA receptors and L-type voltage-operated Ca 2ϩ channels (36,37).…”

Section: Discussion C-fos Expression In the Auditory Pathwaymentioning

confidence: 99%

Corticothalamic synchronization leads to c-fos expression in the auditory thalamus

Guo

Sun

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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In this study, we investigated the relationship between c-fos expression in the auditory thalamus and corticofugal activation. The contribution of neurotransmitters and related receptors, the involvement of thalamic reticular nucleus (TRN), and the role of neuronal firing patterns in this process were also examined. The principal nuclei of the medial geniculate body (MGB) showed c-fos expression when the auditory cortex (AC) was activated by direct injection of bicuculline methobromide. However, no expression was detectable with acoustic stimuli alone. This indicated that c-fos expression in the principal nuclei of the MGB was triggered by the corticofugal projection. c-fos expression could be elicited in the MGB by direct injection of glutamate. Direct administration of acetylcholine, alternatively, had no effect. Bicuculline methobromide injection in the AC also triggered synchronized oscillatory activities sequentially in the AC and MGB. Cortically induced c-fos expression in the MGB was not mediated by a pathway involving the TRN because it remained intact after a TRN lesion with kainic acid. The present results also conclude that c-fos expression is not simply associated with firing rate, but also with neuronal firing pattern. Burst firings that are synchronized with the cortical oscillations are proposed to lead to c-fos expression in the principal nuclei of the MGB. activity marker ͉ cortical activation ͉ Fos ͉ glutamate receptor ͉ medial geniculate body T he thalamus relays sensory information to the cortex and, in return, receives massive feedback projections from the cortex (1-4). Corticothalamic projections are suggested to provide a gain-control mechanism on the transmission of sensory information (5-7) and to play an important role in the generation of neural oscillations (8-10). The thalamic reticular nucleus (TRN) is thought to be involved in the corticothalamic process and the genesis of the oscillations (1, 3). In the auditory system, highfrequency oscillation can be generated in the cortex, evoked by acoustic stimuli, and modulated by the thalamic stimulation (11). A slow oscillation of Ͻ1 Hz and a spindle-like oscillation of 5-10 Hz have also been described recently in the auditory thalamus (12).Neuronal expression of Fos protein after novel physiological input constitutes a useful marker for polysynaptic activation, allowing subpopulations of neurons in specific neuronal circuits to be identified (13,14). Fos-immunoreactivity has also been used to identify functionally activated neurons in the ascending auditory system (15-19). c-fos, however, did not express in the ventral and dorsal divisions of the MGB when the subject was exposed to acoustic stimulation in isolation (18,19).In an attempt to study the contribution of the corticofugal projection to thalamic neurons in the ascending auditory circuitry using c-fos as an activity marker, we found heavy Fos labeling in the MGB after the auditory cortex was activated by injecting bicuculline methobromide (BIM, a GABA A receptor antagonist). In t...

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Expression of c-<i>fos</i> in the Brain after Activation of L-Type Calcium Channels

Cited by 20 publications

References 25 publications

Intracellular emetic signaling evoked by the L-type Ca2+ channel agonist FPL64176 in the least shrew (Cryptotis parva)

Intracellular emetic signaling evoked by the L-type Ca2+ channel agonist FPL64176 in the least shrew (Cryptotis parva)

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

Corticothalamic synchronization leads to c-fos expression in the auditory thalamus

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