Ciliary neurotrophic factor is expressed in the magnocellular neurosecretory system of the rat in vivo: Evidence for injury- and activity-induced upregulation

Watt, John A.; Bone, Sven; Pressler, Mandy; Cranston, Harwood J.; Paden, Charles M.

doi:10.1016/j.expneurol.2005.09.009

Cited by 24 publications

(35 citation statements)

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“…Moreover, CNTF is a potent promoter of hypothalamic magnocellular neuron survival in vitro (House, et al, 2009, Rusnak, et al, 2002, Rusnak, et al, 2003, Vutskits, et al, 1998, Vutskits, et al, 2003). In our studies we have demonstrated an increase in CNTF-immunoreactivity (Watt, et al, 2006) and CNTFRα mRNA expression (Watt, et al, 2009) within the non-injured contralateral SON, which contains the sprouting and metabolically active magnocellular neurons. Together, these observations suggest that CNTF contributes to the axonal sprouting response.…”

Section: Introductionmentioning

confidence: 55%

“…We demonstrated previously that unilateral lesion of the hypothalamo-neurohypophysial tract results in an increase in CNTF mRNA expression in the axotomized SON (Watt, et al, 2006). This occurs concomitant with an increase in CNTF-immunoreactivity (Watt, et al, 2006) and CNTFRα mRNA expression (Watt, et al, 2009) in the contralateral, sprouting SON.…”

Section: Resultsmentioning

confidence: 88%

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Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Askvig¹,

Leiphon²,

Watt³

2012

Experimental Neurology

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We demonstrated previously that the hypothalamic supraoptic nucleus (SON) undergoes a robust axonal sprouting response following unilateral transection of the hypothalamo-neurohypophysial tract. Concomitant with this response is an increase in ciliary neurotrophic factor (CNTF) and CNTF receptor alpha (CNTFRα) expression in the contralateral non-uninjured SON from which the axonal outgrowth occurs. While these findings suggest that CNTF may act as a growth factor in support of neuronal plasticity in the SON, it remained to be determined if the observed increase in neurotrophin expression was related to the sprouting response per se or more generally to the increased neurosecretory activity associated with the post-lesion response. Therefore we used immunocytochemistry and Western blot analysis to examine the expression of CNTF and the components of the CNTF receptor complex in sprouting versus osmotically-stimulated SON. Western blot analysis revealed a significant increase in CNTF, CNTFRα, and gp130, but not LIFRβ, protein levels in the sprouting SON at 10 days post lesion in the absence of neuronal loss. In contrast, osmotic stimulation of neurosecretory activity in the absence of injury resulted in a significant decrease in CNTF protein levels with no change in CNTFRα, gp130, or LIFRβ protein levels. Immunocytochemical analysis further demonstrated gp130 localization on magnocellular neurons and astrocytes while the LIFRβ receptor was found only on astrocytes in the SON. These results are consistent with the hypothesis that increased CNTF and CNTFR complex in the sprouting, metabolically active SON are related directly to the sprouting response and not the increase in neurosecretory activity.

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Section: Introductionmentioning

confidence: 55%

Section: Resultsmentioning

confidence: 88%

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Askvig¹,

Leiphon²,

Watt³

2012

Experimental Neurology

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“…2), was less intense than its constitutive expression in the hippocampus and basolateral amygdala. The ventral regions of the glia limitans (and meninges) expressed IL-1␤ with fibrous projections dorsally through the SON similar to distributions of GFAP and ciliary neurotrophic factor (116), consistent with expression in astrocytes (7). Similarly, immunoreactive IL-1R was present in the meninges (and ventral glia limitans; Fig.…”

Section: Patterns Of Immunoreactivity For Ox-42 Il-1␤ Il-1r and Comentioning

confidence: 76%

Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus

Summy-Long

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Summy-Long JY, Hu S. Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus. Am J Physiol Regul Integr Comp Physiol 297: R1532-R1545, 2009. First published September 16, 2009 doi:10.1152/ajpregu.00340.2009.-During the brain's innate immune response microglia, astroglia and ependymal cells resolve/repair damaged tissue and control infection. Released interleukin-1␤ (IL-1␤) reaching cerebroventricles stimulates circumventricular organs (CVOs; subfornical organ, SFO; organum vasculosum lamina terminalis, OVLT), the median preoptic nucleus (MePO), and magnocellular and parvocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei. Hypertonic saline (HS) also activates these osmosensory CVOs and neuroendocrine systems, but, in contrast to IL-1␤, inhibits the peripheral immune response. To examine whether the brain's innate immune response is attenuated by osmotic stimulation, sterile acidic perfusion fluid was microdialyzed (2 l/ min) in the SON area of conscious rats for 6 h with sterile HS (1.5 M NaCl) injected subcutaneously (15 ml/kg) at 5 h. ϩ ; amoeboid/hypertrophied; IL-1␤ ϩ ) in the adjacent SON and bilaterally in perivascular areas of the PVN, periventricular hypothalamus and ependyma, coincident with c-Fos expression in ependymal cells and COX-2 in the vasculature. These microglial responses were attenuated by HS, coincident with activating parvocellular and magnocellular neuroendocrine systems and elevating circulating IL-1␤, oxytocin, and vasopressin. Acidosis-induced cellular injury from microdialysis activated the brain's innate immune response by a mechanism inhibited by peripheral osmotic stimulation. hypertonic saline; interleukin-1␤; acidosis; magnocellular neurons; c-Fos MICRODIALYSIS OF BRAIN NUCLEAR sites is used widely to monitor endogenous neural activity (28) and, more selectively, the central release of oxytocin and vasopressin from dendrites and somas of magnocellular neurons in the supraoptic nucleus (SON) spatially separated from their axon terminals in the neural lobe (68,73). Using this method in conscious rats, we found previously that basal release of interleukin-1␤ (IL-1␤) into dialysates (121) of the SON area increased in response to osmotic stimulation (106). Originally, the present immunohistochemical study was designed to identify local cellular sources of the cytokine (IL-1␤ ϩ ) and its biologic targets expressing the IL-1 type 1 receptor (IL-1R; 101) and having cyclooxygenase (COX-2) (65) or c-Fos induced by the cytokine (32, 60, 62). Our attention, however, widened to include the brain's innate immune response when our microdialysis studies showed activation of microglia in the SON (106).Like other tissues, an innate immune system in the brain responds to injury, protecting against infection and repairing damage in an effort to restore function (74, 87). Largely excluded from circulating blood cells and the peripheral immune system, the brain relies on glia and epend...

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“…In physiological status terms, the levels of CNTF and its receptor are extremely low in brain parenchyma. However, significant elevation is noticeable in their expression in the presence of brain injury (18,19). Therefore, CNTF is considered to have important roles in coordinating the cellular response to insult in the CNS.…”

Section: Discussionmentioning

confidence: 99%

Ciliary neurotrophic factor-treated astrocyte-conditioned medium increases the intracellular free calcium concentration in rat cortical neurons

et al. 2016

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Abstract. Ciliary neurotrophic factor (CNTF) is involved in the activation of astrocytes. A previous study showed that CNTF-treated astrocyte-conditioned medium (CNTF-ACM) contributed to the increase of the calcium current and the elevation of corresponding ion channels in cortical neurons. On this basis, it is reasonable to assume that CNTF-ACM may increase the intracellular free calcium concentration ([Ca 2+ ] i ) in neurons. In the present study, the effects of CNTF-ACM on [Ca 2+ ] i in rat cortical neurons were determined, and on this basis, the aim was to investigate the potential active ingredients in ACM that are responsible for this biological process. As expected, the data indicated that CNTF-ACM resulted in a clear elevation of [Ca 2+ ] i in neurons. Additionally, the fibroblast growth factor-2 (FGF-2) contained in the CNTF-ACM was found to participate in the upregulation of [Ca 2+ ] i . Taken together, CNTF induces the production of active factors (at least including FGF-2) released from astrocytes, which finally potentiate the increase of [Ca 2+ ] i in cortical neurons. IntroductionCiliary neurotrophic factor (CNTF), a survival factor for chick ciliary neurons (1), is reported to facilitate the survival of several types of neurons such as sympathetic, sensory and motor neurons (2). In addition, it has important roles in triggering neurite outgrowth, preventing neuronal degeneration and attenuating motor deficits (3). Recent evidence suggests that CNTF is a potential activator of astrocytes, as it could induce astrocyte hypertrophy and glial fibrillary acidic protein (GFAP) overexpression (4,5), which is considered as a predominant feature for the activation of astrocytes.Astrocytes constitute the majority of the central nervous system (CNS), particularly in the brain. Bidirectional communication has been reported between astrocytes and neurons. On this basis, it is reasonable to speculate that astrocytes may respond to the neuronal activity and be involved in the regulation of neuron activity. Our previous study showed that CNTF-treated astrocyte-conditioned medium (CNTF-ACM) contributed to the elevation of the calcium current and the expression of ion channels in cortical neurons (6). Due to the increase of intracellular free calcium concentration ([Ca 2+ ] i ) preferentially induced by calcium influx mediated by calcium currents, we hypothesize that CNTF-ACM may affect the [Ca 2+ ] i in neurons. The present study aimed to evaluate the effects of CNTF-ACM on the [Ca 2+ ] i in cortical neurons in rats. Astrocytes can secrete several types of factors, such as nerve growth factor (NGF) (7,8) and fibroblast growth factor-2 (FGF-2). FGF-2 (9,10) and NGF (11,12) contribute to the expression of functional calcium channels. In addition, the concentrations of FGF-2 and NGF were determined in CNTF-ACM, as well as its roles in the regulation of [Ca 2+ ] i levels in neurons. Materials and methodsAstrocyte culture and collection of ACM. Pregnant Sprague-Dawley rats we...

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Ciliary neurotrophic factor is expressed in the magnocellular neurosecretory system of the rat in vivo: Evidence for injury- and activity-induced upregulation

Cited by 24 publications

References 50 publications

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus

Ciliary neurotrophic factor-treated astrocyte-conditioned medium increases the intracellular free calcium concentration in rat cortical neurons

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