α2-Adrenergic Agonists Induce Basic Fibroblast Growth Factor Expression in PhotoreceptorsIn Vivoand Ameliorate Light Damage

Wen, Rong; Cheng, Tao; Li, Yiwen; Cao, Wenming; Steinberg, Roy H.

doi:10.1523/jneurosci.16-19-05986.1996

Cited by 126 publications

(98 citation statements)

References 35 publications

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“…While the distribution of b adrenoceptors within the choroidal blood vessels has not been described, it is known that these receptors are present on both smooth muscle cells (Bevan, 1983) and endothelial cells (Wang et al, 2000). b adrenergic receptors have been shown to modulate several angiogenic factors, although studies to date have only documented a role in increasing their release (Wen et al, 1996;Fredriksson et al, 2000;Jin et al, 2000). It is possible, however, that b adrenoceptors may also exert inhibitory e ects on the release of other angiogenic factors, and that this action could predominate in the choroid.…”

Section: Discussionmentioning

confidence: 99%

Role of adrenergic receptors in vascular remodelling of the rat choroid

Steinle

Smith²

2002

British J Pharmacology

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1 Choroidal blood vessels, located between the sclera and retina, constitute the principle source of blood¯ow to ocular structures. The choroid is innervated by vasoconstrictor sympathetic and vasodilator parasympathetic nerves. 2 We have shown previously that sympathetic denervation for 6 weeks leads to signi®cant increases in choroidal thickness, percentage of choroid occupied by vascular lumina, and numbers of choroidal venules, large arterioles and outer retinal capillaries. Sympathetic dea erentation produces similar increases, indicating that loss of sympathetic nerve activity is responsible for increased vascularity after sympathectomy. Thus, sympathetic neurotransmission normally may be important in suppressing vascular proliferation in the adult rodent eye. 3 The aim of the present study was to determine whether sympathetic nerves act by way of adrenergic receptors to maintain normal choroidal vascular integrity. 4 The a-adrenoceptor antagonist, phentolamine (1 mg kg 71 day 71 ), the b-receptor antagonist, propranolol (1 mg kg 71 day 71 ), or saline vehicle was infused for 3 weeks using subcutaneously implanted osmotic minipumps. 5 In phentolamine treated rats, no signi®cant changes were noted relative to saline infused controls. However, propranolol treatment resulted in increases in choroidal thickness, vascular luminal area, and numbers of large choroidal venules and both small and large arterioles, approximating the remodelling seen after chronic sympathectomy. 6 We conclude that sympathetic nerves play a role in maintaining normal choroidal vascular architecture through actions mediated primarily by b-adrenoceptors.

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Section: Discussionmentioning

confidence: 99%

Role of adrenergic receptors in vascular remodelling of the rat choroid

Steinle

Smith²

2002

British J Pharmacology

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“…Experimental models suggest that brimonidine confers neuroprotection in several types of ocular injury, including ischemia-induced injury, (Aktas et al, 2007;Danylkova et al, 2007) optic nerve compression or optic nerve crush injury (Levkovitch-Verbin et al, 2000),. photoreceptor degeneration, (Wen et al, 1996) and ocular hypertension and glaucoma (Hernandez et al, 2008;Wheeler et al, 2001 ). The mode of action of Brimonidine however remains unclear with various proposed mechanisms.…”

Section: Compounds With Multiple/novel Mechanisms Of Actionmentioning

confidence: 99%

Neuroprotective Agents in Glaucoma

Bagli¹,

Kitsos²

2011

The Mystery of Glaucoma

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“…After transient retinal ischemia, the α 2 -adrenergic agonist brimonidine also decreases the release of glutamate [502]. Up-regulation of growth factors, including BDNF [500], and basic fibroblast growth factor, FGF2 [501,503] may play a major role in the neuroprotective effect of the α 2 -adrenergic agonists. BDNF is a member of the NGF family, but FGF2 is neither a member of this family, nor of the EGF family.…”

Section: Glaucomamentioning

confidence: 99%

“…It has been shown immunocytochemically that the increase in ERK phosphorylation mainly occurs in Müller cells [504], an astrocyte-like cell type. The expression of basic fibroblast growth factor (FGF2) is increased in the inner segment region of the photoreceptors [503]. Like TGF-β1, FGF2 is not a direct product of transactivation, and it would be interesting to know if growth factor cascades similar to those occurring in astrocytes and tanycytes operate between Müller cells and photoreceptors.…”

Section: Glaucomamentioning

confidence: 99%

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

Hertz¹,

Chen²,

Gibbs³

et al. 2004

CDTCNSND

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Considerable attention has recently been paid to astrocyte functions, which are briefly summarized. A large amount of data is available about adrenoceptor expression and function in astrocytes, some of it dating back to the 1970's and some of it very recent. This material is reviewed in the present paper. The brain is innervated by noradrenergic fibers extending from locus coeruleus in the brain stem, which in turn is connected to a network of adrenergic and noradrenergic nuclei in the medulla and pons, contributing to the control of (nor)adrenergic, serotonergic, dopaminergic and cholinergic function, both in the central nervous system (CNS) and in the periphery. In the CNS astrocytes constitute a major target for noradrenergic innervation, which regulates morphological plasticity, energy metabolism, membrane transport, gap junction permeability and immunological responses in these cells. Noradrenergic effects on astrocytes are essential during consolidation of episodal, long-term memory, which is reinforced by β-adrenergic activation. Glycogenolysis and synthesis of glutamate and glutamine from glucose, both of which are metabolic processes restricted to astrocytes, occurs at several time-specific stages during the consolidation. Astrocytic abnormalities are almost certainly important in the pathogenesis of multiple sclerosis and in all probability contribute essentially to inflammation and malfunction in Alzheimer's disease and to mood disturbances in affective disorders. Noradrenergic function in astrocytes is severely disturbed by chronic exposure to cocaine, which also changes astrocyte morphology. Development of drugs modifying noradrenergic receptor activity and/or down-stream signaling is advocated for treatment of several neurological/psychiatric disorders and for neuroprotection. Astrocytic preparations are suggested for study of mechanism(s) of action of antidepressant drugs and pathophysiology of mood disorders.

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α₂-Adrenergic Agonists Induce Basic Fibroblast Growth Factor Expression in PhotoreceptorsIn Vivoand Ameliorate Light Damage

Cited by 126 publications

References 35 publications

Role of adrenergic receptors in vascular remodelling of the rat choroid

Role of adrenergic receptors in vascular remodelling of the rat choroid

Neuroprotective Agents in Glaucoma

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

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