The neurosteroid dehydroepiandrosterone sulfate (DHEAS) enhances hippocampal primed burst, but not long-term, potentiation

Diamond, David M.; Branch, Berrilyn J.; Fleshner, Monika

doi:10.1016/0304-3940(95)12233-8

Cited by 57 publications

(25 citation statements)

References 33 publications

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“…4 -6 Basic research has shown that both neurosteroids can interact with CNS neurotransmitter receptor systems to regulate fast neurotransmission and neuronal excitability. [7][8][9][10][11][12] Neurosteroids may also have a variety of neurotrophic factor-like roles in the CNS, including enhancement of neuron and glial cell survival 3,4 and neuroprotection against excitatory amino acid (EAA) toxicity. 13,14 Thus, DHEAS may be of use in treating ischemic stroke where there is enhanced EAA neurotransmission.…”

mentioning

confidence: 99%

Dehydroepiandrosterone Sulfate Is Neuroprotective in a Reversible Spinal Cord Ischemia Model

Lapchak

Chapman

Nunez

et al. 2000

Stroke

111

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Background and Purpose-Dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) may function as neurotrophic or neuroprotective factors to protect central nervous system (CNS) neurons against a variety of insults, including excitotoxicity. The present study evaluated the pharmacological effects of DHEAS in a reversible spinal cord ischemia model. Methods-DHEAS was administered (50 mg/kg IV) 5 or 30 minutes after the start of occlusion to groups of rabbits exposed to ischemia induced by temporary (15 to 60 minutes) occlusion of the infrarenal aorta. The group P 50 represents the duration of ischemia (in minutes) associated with 50% probability of resultant permanent paraplegia. Results-The P 50 of the vehicle-treated control group, when behavioral analysis was assessed 18 hours after aortal occlusion, was 28.8Ϯ2.0 minutes. Neuroprotection was demonstrated if a drug significantly prolonged the P 50 compared with the vehicle-treated control group. Treatment with DHEAS at 5 minutes significantly (PϽ0.05) prolonged the P 50 of the group to 36.8Ϯ3.9 minutes. In addition, the DHEAS effect appeared durable, because a significant difference between the control and DHEAS-treated groups was still measurable at the 4-day time point. At 4 days, the P 50 of the control group was 26.1Ϯ2.2 minutes, whereas the P 50 for the DHEAS-treated group was 38.6Ϯ5.9 minutes. DHEAS was not neuroprotective if administered 30 minutes after occlusion. In addition, the GABA A antagonist bicuculline abolished the neuroprotective effect of DHEAS. Conclusions-The present study suggests that neurosteroids may have substantial therapeutic benefit for the treatment of ischemic stroke.

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mentioning

confidence: 99%

Dehydroepiandrosterone Sulfate Is Neuroprotective in a Reversible Spinal Cord Ischemia Model

Lapchak

Chapman

Nunez

et al. 2000

Stroke

111

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“…Animal studies have shown that acute exposure to DHEAS may facilitate basal synaptic transmission in the CA1 region of the hippocampus through the noncompetitive potentiation of GABA A receptors [75][76][77]. In terms of learning and memory, studies have shown that acute administration of DHEAS facilitates primed-burst potentiation, but not the induction of long-term potentiation [78], whereas long-term potentiation is stimulated by the chronic administration of DHEAS [79].…”

Section: Dhea and Cognitionmentioning

confidence: 99%

“…Maintenance and endocrine control of pregnancy [51] Associated with human growth and organ maturation, particularly of the brain, during adrenarche [53][54][55] Promotes neurogenesis and neuronal survival in the CNS through the mediation of BDNF [86,87] Memory and learning: DHEAS may facilitate basal synaptic transmission in the CA1 region of the hippocampus [75][76][77] Acute DHEAS administration facilitates primed-burst potentiation [78] and chronic administration of DHEAS stimulates LTP [79] DHEA treatment significantly preserves working and reference memories and increases acetylcholine, norepinephrine, and dopamine concentrations in the rat brain [86] Neuroprotection:…”

Section: Effects/functionmentioning

confidence: 99%

Dehydroepiandrosterone (DHEA) and DHEA Sulfate: Roles in Brain Function and Disease

Quinn¹,

Robinson²,

Walker³

2018

Sex Hormones in Neurodegenerative Processes and Diseases

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Among the neuroactive steroids, dehydroepiandrosterone (3b-hydroxyandrost-5-ene-17-one, [DHEA]) and its sulfated metabolite DHEA sulfate (DHEAS) have been shown to be potent modulators of neural function, including neurogenesis, neuronal growth and differentiation, and neuroprotection. Highlighting the potential health significance of DHEA and DHEAS in humans, serum concentrations decrease steadily with age, with lowest concentrations present at the time many diseases of aging and neurodegeneration become apparent. This temporal association has led to the suggestion that pathology associated with cognitive decline, age-related neurological disorders such as Alzheimer's disease, dementia, amyotrophic lateral sclerosis (ALS), and adult onset schizophrenia may, in part at least, be attributed to decreased secretion of DHEA. Animal studies suggest neuroprotective functions for DHEA and DHEAS through reduction of glutamate-induced excitotoxicity. Reduced myelin loss and reactive gliosis after spinal cord injury by DHEA treatment also suggest a role for DHEA in the treatment of white matter pathologies such as multiple sclerosis. In this chapter, we discuss the physiological roles of DHEA and DHEAS in the central nervous system (CNS), their potential as neuroprotective hormones with reference to documented effects on excitotoxicity and oxidative stress, and their anti-glucocorticoid actions during chronic stress. The potential for metabolic derivatives of DHEA, such as estrogens and testosterone on brain function, and their contribution to neurodevelopment and neurodegenerative conditions are also discussed.

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“…Once water maze training had been completed, the rats continued to receive DHEAS in their drinking water until the day in which the electrophysiological recordings took place. On that day, the rats were anesthetized with urethane (1.5 g/kg, ip) and PB was recorded in the CA1 region of the hippocampus according to methods described previously (Bennett et al, 1991;Diamond et al, 1992Diamond et al, , 1996. The left-hand side of Figure 1 shows the magnitude of PB in the vehicle-and DHEAS-treated groups.…”

Section: Effects Of Chronic Oral Administration Of Dheas On Memory Anmentioning

confidence: 99%

Enhancement of Cognitive and Electrophysiological Measures of Hippocampal Functioning in Rats by a Low, but Not High, Dose of Dehydroepiandrosterone Sulfate (DHEAS)

The neurosteroid dehydroepiandrosterone sulfate (DHEAS) enhances hippocampal primed burst, but not long-term, potentiation

Cited by 57 publications

References 33 publications

Dehydroepiandrosterone Sulfate Is Neuroprotective in a Reversible Spinal Cord Ischemia Model

Dehydroepiandrosterone Sulfate Is Neuroprotective in a Reversible Spinal Cord Ischemia Model

Dehydroepiandrosterone (DHEA) and DHEA Sulfate: Roles in Brain Function and Disease

Enhancement of Cognitive and Electrophysiological Measures of Hippocampal Functioning in Rats by a Low, but Not High, Dose of Dehydroepiandrosterone Sulfate (DHEAS)

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