Rise of Intrasynaptosomal Ca2+ Level and Activation of Nitric Oxide Synthase in Adult Rat Cerebral Cortex Pretreated with 3-5-3′-L-Triiodothyronine

Chakrabarti, N.B.; Ray, Arun Kumar

doi:10.1016/s0893-133x(99)00073-1

Cited by 24 publications

(22 citation statements)

References 33 publications

(34 reference statements)

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“…An increasing amount of evidence has indicated that Ca 2+ serves as the first messenger for the rapid non-genomic effect of T 3 in vivo in several tissues of the rat [25]. T 3 has been demonstrated to cause a rapid influx of Ca 2+ and raise the intrasynaptosomal [Ca 2+ ] i in adult rats during depolarized condition [11, 26]. In this study, a fall in [Ca 2+ ] i has been noted on the days of onset and termination of the central homeostasis for thyroid hormone (Days 2 and 20).…”

Section: Discussionmentioning

confidence: 99%

“…The [Ca 2+ ] i was measured using the fluorescent indicator, Fura-2, according to the method of Grynkiewicz et al [10] with slight modifications [11]. Briefly, synaptosomes (1 mg protein/ml) suspended in BSS-NaCl (containing 20 m M Tris-HCl, 136 m M NaCl, 5.6 m M KCl, 1.3 m M MgCl 2 and 11 m M D -glucose at pH 7.4) were loaded with 10 µ M Fura-2/AM in DMSO and incubated at 37°C in the dark for 30 min.…”

Section: Methodsmentioning

confidence: 99%

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Thyroid Hormone Homeostasis in Brain: Possible Involvement of Adrenergic Phenomenon in Adult Rat

et al. 2008

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Background: Imbalance in thyroid hormone concentrations has been linked with profound neurobehavioral alterations in the adult. Peripheral hypothyroidism is associated with a phenomenon of central thyroid hormone homeostasis in adult rat. This central homeostasis mechanism could be maintained by adrenergic interplay due to close physiological association between sympathetic nervous system activity and thyroid hormones. The central homeostasis is characterized by increased cerebrocortical synaptosomal T₃ content, deiodinase type II (DII) activity, and cAMP content. Methods: We injected specific α- and β-adrenergic receptor (AR) agonists and antagonists along with an anti-thyroid drug to find out any AR-mediated action on central homeostasis. Results: The α₂-AR agonist did not alter the onset of central homeostasis, but prolonged its duration. Similar prolongation was observed with α₂-AR antagonist and β-AR agonist, but these compounds amplified the normal anti-thyroid drug-induced rise in cerebrocortical T₃ content on the day of onset of central homeostasis. Injections of the β-AR antagonist did not cause any perturbations. All these observations have been supported by parallel changes in cerebrocortical DII activity, cAMP and [Ca²⁺]_i content. Conclusion: There emerges a close correlation between cerebral T₃ content, DII activity, cAMP and [Ca²⁺]_i content that are regulated by the AR system. Thus, thyroid hormone homeostasis in the adult mammalian brain is maintained primarily by the β-adrenergic pathway along with an unexpected pharmacological involvement of the α-ARs.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Thyroid Hormone Homeostasis in Brain: Possible Involvement of Adrenergic Phenomenon in Adult Rat

et al. 2008

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“…There are other factors that could contribute to increased NOS activity, including a direct nongenomic effect of T 3 (Chakrabarti and Ray, 2000) or the increased release of vasoactive molecules such as Ang II (Hennington et al, 1998) or endothelin (Hirata et al, 1995), which are increased in hyperthyroid rats, and are known to stimulate NO production (Marchant et al, 1993;Singh et al, 1994).…”

Section: N O N G E N O M I C E F F E C T S O F T 3 T 4 a N D T 1 A Mmentioning

confidence: 99%

Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

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Ferrão

et al. 2010

Journal Cellular Physiology

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Thyroid hormones play a wide range of important physiological activities in almost all organism. As changes in these hormones levels-observed in hypothyroidism and hyperthyroidism-promote serious derangements of the cardiovascular system, it is important to know their mechanisms of action. Although the classic genomic actions which are dependent on interaction with nuclear receptors to modulate cardiac myocytes genes expression, there is growing evidence about T(3) and T(4)-triggered nongenomic pathways, resulted from their binding to plasma membrane, cytoplasm, or mitocondrial receptors that leads to a rapidly regulation of cardiac functions. Interestingly both actions converge to amplify thyroid hormone effects on cardiovascular system. T(3) and T(4) nongenomic actions modify inotropic and chronotropic effects, cardiac action potential duration, cardiac growth, and myocyte shape by protein translation through protein kinases-dependent signaling cascades, which include PKA, PKC, PI3K, and MAPK, and changes on ion channels and pumps activity. In respect to the decreased systemic vascular resistance seen in hyperthyroidism, T(3) appears to activate NOS or ATP-sensitive K(+) channels. In addition, a novel biologically active T(4)-derived metabolite has been described, 3-iodothyronamine, T(1)AM, which also acts through membrane receptors to mediate nongenomic cardiac effects. This metabolite influences the physiological manifestations of thyroid hormone actions by inducing opposite effects from those stimulated by T(3) and T(4), such as negative inotropic and chronotropic effects. Therefore, beyond genomic and nongenomic effects of thyroid hormones, it is crucial for there to be an equilibrium between T(3) or T(4) and T(1)AM levels for maintaining cardiac homeostasis.

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“…Another pathway through which TH regulates NO and subsequently cerebellar development can be plasma membrane calcium influx increased directly by TH [25]. Calcium can trigger nNOS activity and also induces nNOS gene transcription [49].…”

Section: Discussionmentioning

confidence: 99%

“…Up to now, only a small number of studies have dealt with the possible interaction of TH and NO in the CNS, showing downregulation of nNOS expression in the embryonic cerebral cortex [22], but upregulation of nNOS expression in the postnatal cerebral cortex [23], in the adult hypothalamus [24], and enhanced nNOS activity in adult cortical synaptosomes [25] followed by the elevation of T 3 level. On the other hand, in recent non-neural studies, more attention was paid to hyperthyroidism-induced NOS-dependent vasodilatation [for review, see [26]].…”

Section: Introductionmentioning

confidence: 99%

Thyroid Hormone Level Positively Regulates NOS and cGMP in the Developing Rat Cerebellum

2009

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Thyroid hormones and nitric oxide/cyclic guanosine monophosphate (NO/cGMP) signaling play a significant role in the structural development of the cerebellum, respectively. In the present study, the possible contribution of neuronal NO synthase (NOS) and cGMP in the thyroid hormone-induced structural changes was investigated in the cerebella of postnatal rats at different hormone levels. Animals were treated from postnatal day 4 until days 7, 14, and 21, by i.p. injection of 1 μg thyroxine (T₄)/10 g body weight/4 days, or p.o. with 100 μg 6-n-propyl-2-thyouracil (PTU)/10 g body weight/day. Control groups consisted of i.p. and p.o. vehicle controls and PTU/T₄-treated animals. Measurement of serum fT₄, TSH as well as total T₃ and T₄ concentration of the cerebellar tissue indicated the changed thyroid status. nNOS extensively expressed in growing parallel fibers revealed by quantitative Western blot and layer analysis of immunohistochemically labeled coronal sections. Simultaneously, the cGMP concentration increased and the distribution of cGMP-immunoreactive (cGMP-IR) material in Purkinje cell perikarya and in the molecular layer expanded during cerebellar development. T₄ increased nNOS and cGMP level, and accelerated the development of nNOS-IR parallel fibers and cGMP-IR molecular layer. In contrast, PTU retarded the development by decreasing nNOS and cGMP concentration and slowing down layer formation. A single dose of T₄ could rescue the PTU-induced changes. Results suggest that the contribution of nNOS- NO/cGMP signaling in thyroid hormone regulated structural maturation of the cerebellum. The possible involvement of neurotrophins, calcium, and apoptotic events in this process was discussed.

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Rise of Intrasynaptosomal Ca2+ Level and Activation of Nitric Oxide Synthase in Adult Rat Cerebral Cortex Pretreated with 3-5-3′-L-Triiodothyronine

Abstract: Accumulation of free, ionized calcium (Ca 2 ϩ ) and stimulation of nitric oxide synthase (NOS) activity in depolarization-induced synaptosomes prepared from adult rat cerebral cortex have been demonstrated after addition of various doses

Cited by 24 publications

References 33 publications

Thyroid Hormone Homeostasis in Brain: Possible Involvement of Adrenergic Phenomenon in Adult Rat

Thyroid Hormone Homeostasis in Brain: Possible Involvement of Adrenergic Phenomenon in Adult Rat

Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

Thyroid Hormone Level Positively Regulates NOS and cGMP in the Developing Rat Cerebellum

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