Presynaptic effects of glucocorticoids on dopaminergic and cholinergic synaptosomes. Implications for rapid endocrine-neural interactions in stress

Gilad, Gad M.; Rabey, J. M.; Gilad, Varda H.

doi:10.1016/0024-3205(87)90754-5

Cited by 109 publications

(44 citation statements)

References 47 publications

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“…DA uptake measured in septal or striatal synaptosomes was also increased after stress, but not after in z,it, o corticosterone injection (Gilad et al, 1987). However, in vitro incubation ofthe synaptosomal preparations with methylprednisolone rapidly reduced DA uptake, both in stimulated and unstimulated conditions (Gilad et al, 1987). Perhaps as a consequence of these changes in the availability of DA, long term changes in steroid content also affect DA receptor characteristics.…”

Section: Noradrenaline Dopamine and Acetylcholinementioning

confidence: 98%

“…Thus, in vitro microdialysis studies showed that stress and high corticosterone doses induce a transient increase of DA release in the nucleus accumbens and cortex, which peaks after 20 rain (Imperato et al, 1989). DA uptake measured in septal or striatal synaptosomes was also increased after stress, but not after in z,it, o corticosterone injection (Gilad et al, 1987). However, in vitro incubation ofthe synaptosomal preparations with methylprednisolone rapidly reduced DA uptake, both in stimulated and unstimulated conditions (Gilad et al, 1987).…”

Section: Noradrenaline Dopamine and Acetylcholinementioning

confidence: 98%

“…Brain regions containing ACh-producing cells are quite sparse in their GR content (Fuxe et al, 1985). However, chronic (2 was observed in rat hippocampus but not caudate, both in vivo (Imperato et al, 1989) and in vitro (Gilad et al, , 1987. The onset of the effects (within 10 min) is so fast as to be probably not mediated by genomic actions.…”

Section: Noradrenaline Dopamine and Acetylcholinementioning

confidence: 99%

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Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Joëls

Kloet

1994

Progress in Neurobiology

367

168

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Section: Noradrenaline Dopamine and Acetylcholinementioning

confidence: 98%

Section: Noradrenaline Dopamine and Acetylcholinementioning

confidence: 98%

Section: Noradrenaline Dopamine and Acetylcholinementioning

confidence: 99%

See 1 more Smart Citation

Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Joëls

Kloet

1994

Progress in Neurobiology

367

168

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“…Thus, we suggest that the ADX-induced decrease in dopaminergic transmission in the PFC is not caused by decreased DA synthesis in the area from which the neurons originate, and other mechanisms should be considered. For example, glucocorticoids may decrease DA catabolism by acting as reversible monoamine oxidase inhibitors (Veals et al, 1977) or they may decrease catecholamine reuptake by inhibiting its transporters (Gilad et al, 1987;Arnsten, 2000). Alternatively, dopaminergic neuronal degeneration may occur at the synaptic level because the DA release in response to KCl was greatly diminished in the ADX rats (Fig.…”

Section: Suppression Of Glucocorticoids Induces Working Memory Impairmentioning

confidence: 99%

Endogenous Glucocorticoids Are Essential for Maintaining Prefrontal Cortical Cognitive Function

Mizoguchi¹,

Ishige²,

Takeda³

et al. 2004

J. Neurosci.

170

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Glucocorticoid hormones are important in the maintenance of many brain functions. Although their receptors are distributed abundantly throughout the brain, including the prefrontal cortex (PFC), it is not clear how glucocorticoid functions, particularly with regard to cognitive processing in the PFC. There is evidence of PFC cognitive deficits such as working memory impairment in several stressrelated neuropsychiatric disorders, including depression, schizophrenia, and Parkinson's disease. Disruption of the hypothalamopituitary-adrenal (HPA) system, which is characterized by attenuated glucocorticoid negative feedback, is also observed. In rats, chronic stress induces working memory impairment as a result of decreased dopaminergic transmission in the PFC. These chronically stressed rats also show HPA disruption; this is caused in part by a reduced glucocorticoid response in the PFC. These findings implicate reduced glucocorticoid actions in working memory impairment. In the present study, we examined the effects of the suppression of endogenous glucocorticoids by adrenalectomy (ADX) on working memory in rats and explored the involvement of PFC dopaminergic activities in memory. The ADX impaired working memory, decreased dopamine release, and upregulated D 1 receptors in the PFC. These dysfunctions were prevented by corticosterone replacement that reproduced normal physiological plasma levels, indicating that suppression of glucocorticoids causes these dysfunctions. Moreover, the ADX-induced working memory impairment was ameliorated by intra-PFC infusions of a D 1 receptor agonist, SKF 81297. Thus, suppression of glucocorticoids impaired working memory through a D 1 receptormediated hypodopaminergic mechanism in the PFC. This finding indicates that endogenous glucocorticoids are essential for maintaining PFC cognitive function and suggests that HPA disruption contributes to PFC cognitive deficits.

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“…One possible mechanism may depend on the close link between activation of the hypothalamic-pituitary-adrenal axis by stress and stimulation of various neurotransmitter systems. [30][31][32] Previously it was shown that serum corticosteron levels are high in animals placed on small and large platform. 26) Therefore, increase in NA concentration and the decrease in MHPG/NA ratio in the striatum in the TC group might be a neurochemical correlate of the emotional arousal produced in our mice by the changes they experienced in environmental stimuli, irrespective of their aversive (REMSD) or nonaversive (TC) nature.…”

Section: Discussionmentioning

confidence: 99%

Effects of Atomoxetine on Levels of Monoamines and Related Substances in Discrete Brain Regions in Mice Intermittently Deprived of Rapid Eye Movement Sleep

Niijima

Saito

Murai

et al. 2010

Biological & Pharmaceutical Bulletin

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Sleep deprivation represents a common type of stress that can, when extreme, lead to psychological and physiological damage, and even death, in experimental animals. 1) After a period of intermittent rapid eye movement sleep deprivation (REMSD) (72-96 h), rats stay awake for approximately 30 min, and during this period display hyperactivity, irritability, aggressiveness, and hypersexuality. 2) Recently, we showed in mice that 5 days' intermittent REMSD (20 h/d) results in explosive jumping behavior. This behavior was antagonized dose-dependently and significantly by treatment with atomoxetine (0.41-0.55 mg/kg, subcutaneously (s.c.)), which is used clinically to treat the symptoms of attention deficit/hyperactivity disorder (ADHD), 3) raising the possibility such jumping behavior may serve as a useful animal model of ADHD. Moreover, there may be a positive association between this animal model and a hyperfunctional status of noradrenergic systems since the firing of noradrenergic neurons in locus ceruleus (LC) continuous during rapid eye movement (REM) sleep deprivation. [4][5][6] ADHD is a childhood psychiatric disorder characterized by the presence of symptoms in three domains: inattention, impulsivity, and motor overactivity. 7) It has been suggested that these symptoms may be due to a combination of alerting deficits and executive-control deficits involving the prefrontal cortex. 8,9) Although existing studies contain several inconsistencies, on balance the evidence supports dysfunctions of the fronto-striatal neuronal circuits regulated by dopaminergic and noradrenergic afferents, with resultant executive deficits in cognitive functioning. [7][8][9][10] The stimulants amphetamine and methylphenidate, which are indirect agonist that increase extracellular monoamine concentration by inhibiting reuptake and/or promoting release, are the primary treatment for ADHD. 11) The efficacy of stimulants suggests that dopaminergic and/or noradrenergic dysregulation contribute to the expression of ADHD, while diversity in psychostimulant response suggests that the ADHD is not attributable to any single pathophysiologic mechanism. In the absence of specific therapeutic targets, the treatment strategy progresses from stimulant to non-stimulant drugs. 12) Atomoxetine is a non-stimulant drug and a selective inhibitor of the presynaptic noradrenaline (NA)-reuptake transporter (NAT). Indeed, it has an approximately 300-fold selectivity for NAT over the dopamine (DA)-uptake transporter (DAT), a finding that has increased interest in the role of NAT and noradrenergic systems in ADHD. 13) In the frontal cortex, NAT density is higher than DAT density, [14][15][16] and NAT blockade by atomoxetine is thought to block sequestration of DA into NA neurons. 13) Moreover, NAT is poorly expressed in the striatum, in contrast to its robust expression within the frontal cortex. 13) The above findings suggest that the therapeutic effects of drugs that block NAT are mediated by increasing both NA and DA in noradrenergic terminal areas such as ...

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Presynaptic effects of glucocorticoids on dopaminergic and cholinergic synaptosomes. Implications for rapid endocrine-neural interactions in stress

Cited by 109 publications

References 47 publications

Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Mineralocorticoid and glucocorticoid receptors in the brain. Implications for ion permeability and transmitter systems

Endogenous Glucocorticoids Are Essential for Maintaining Prefrontal Cortical Cognitive Function

Effects of Atomoxetine on Levels of Monoamines and Related Substances in Discrete Brain Regions in Mice Intermittently Deprived of Rapid Eye Movement Sleep

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