ACTH and Attention in Humans:A Review

Born, Jan; Fehm, H. L.; Voigt, Kai‐Ingo

doi:10.1159/000118261

Cited by 44 publications

(18 citation statements)

References 39 publications

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“…Holland and Gallagher have found that the CEA is involved in increasing attention to significant events, but not in tuning out redundant cues [10]. Thus, the idea that the central amygdala is the site of action of ORG 2766 seems in agreement with an effect of the peptide on non-selective attention, which has been suggested after some lesion studies in rats and after studies on human subjects [3].…”

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confidence: 79%

“…Fragments and analogs of the adrenocorticotrophic hormone (ACTH) can influence behavior of rats and humans [3,5] and enhance functional recovery after damage to the central and peripheral nervous system [14,18]. Chronic administration of the ACTH(4-9) analog ORG 2766 affects the behavior of brain lesioned and aged rats.…”

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confidence: 99%

“…Chronic administration of the ACTH(4-9) analog ORG 2766 affects the behavior of brain lesioned and aged rats. The peptides efficacy has been supposed to depend on an acceleration of spontaneous recovery through a neurotrophic influence involving some paradigms on functional recovery after peripheral or central nerve damage [7,18], while in studies on the acute effect of ORG 2766 on behavior [5], in various clinical studies [3] and in some brain damage studies [14,23,24] the peptides efficacy was interpreted as an enhancement of (non-selective) attention. Recently a relation between these neurotrophic and attentional effects was suggested [17], when a hypothesis was put forward that both peptide effects were caused by a modulation of NMDA-receptor activity.…”

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Chronic and intra-amygdala administrations of the ACTH(4–9) analog ORG 2766 modulate behavioral changes after manipulation of NMDA-receptor activity

Rijzingen¹,

Gispen²,

Dam³

et al. 1996

Brain Research

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Microinjection of N-methyl-D-aspartic acid (NMDA, 300 ng/3/xl) into the left lateral ventricle causes a substantial increase in locomotor activity which can be significantly reduced by a chronic pretreatment with the ACTH(4-9) analogue ORG 2766 (1 /,g/0.5 ml saline, subcutaneous (s.c.) every day for 7 days, last injection 24 h before the NMDA-injection). A single dose of ORG 2766 (1 ng/1/xl) injected into the left central amygdaloid nucleus 30 min before the NMDA-injection was equally effective in reducing the increase in locomotion. Furthermore it counteracted the predominance of contralateral turning induced by the NMDA-injection. The data give support for the idea that ORG 2766 excerts its effects on behavior and neural recovery by modulating NMDA receptor activity in the brain.Keywords." ORG 2766; Locomotion; Amygdala; Behavior; Hyperactivity Fragments and analogs of the adrenocorticotrophic hormone (ACTH) can influence behavior of rats and humans [3,5] and enhance functional recovery after damage to the central and peripheral nervous system [14,18]. Chronic administration of the ACTH(4-9) analog ORG 2766 affects the behavior of brain lesioned and aged rats. The peptides efficacy has been supposed to depend on an acceleration of spontaneous recovery through a neurotrophic influence involving some paradigms on functional recovery after peripheral or central nerve damage [7,18], while in studies on the acute effect of ORG 2766 on behavior [5], in various clinical studies [3] and in some brain damage studies [14,23,24] the peptides efficacy was interpreted as an enhancement of (non-selective) attention. Recently a relation between these neurotrophic and attentional effects was suggested [17], when a hypothesis was put forward that both peptide effects were caused by a modulation of NMDA-receptor activity.Acute subcutaneous administration of ORG 2766 counteracted the impairment in In studies on isolation-induced disturbances in social behavior, it appeared that the amygdala may be the site of action of the peptide: administration of ORG 2766 into the amygdala was seen to have an effect comparable to subcutaneous administration [9,22]. The aim of the present study was threefold: 1. In the previous study it was assumed that chronic treatment with ORG 2766 had a similar effect to acute treatment, and subsequently ORG 2766 was administered acutely. To verify this assumption we investigated whether chronic pre-treatment could also suppress the NMDA-induced locomotor behavior. 2. The possibility that the amygdala is involved in the peptide effects was assessed by examining the effect off ORG 2766 administration into the central nucleus of the amygdala on the NMDA-induced increase in locomotor activity.

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confidence: 79%

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confidence: 99%

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confidence: 99%

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Chronic and intra-amygdala administrations of the ACTH(4–9) analog ORG 2766 modulate behavioral changes after manipulation of NMDA-receptor activity

Rijzingen¹,

Gispen²,

Dam³

et al. 1996

Brain Research

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“…The pharmacological characteristics of the acute effects of ACTH 4–10 on ERP signs of attention in humans have been well documented in foregoing studies [3, 4, 12]. Effects on the ‘processing negativity’ (PN) of the ERP which is a classical marker of focussed attention were found to increase in strength linearly with logarithmically increasing doses of ACTH 4–10 (0.1–10 mg i.v.)…”

Section: Introductionmentioning

confidence: 99%

“…Together with other natural peptides such as α-melanocytestimulating hormone (α-MSH, corresponding to acetylated ACTH 1–13 amide) and synthetic deviations this group is called melanocortins which are known to be most potent regulators of neurobehavioral functions in animals and man [1, 2]. In humans, ACTH and its behaviorally active fragment ACTH 4–10 as well as ORG 2766 (an analog of ACTH 4–9) have been consistently found to weaken event-related brain potential (ERP) signs of selective attention [3, 4]. Substances in those experiments were administered systemically, i.e.…”

Section: Introductionmentioning

confidence: 99%

Brain Potentials and Attention after Acute and Subchronic Intranasal Administration of ACTH 4–10 and Desacetyl-α-MSH in Humans

et al. 1999

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Neuropeptides related to adrenocorticotropin (ACTH) are potent regulators of neurobehavioral functions. In humans, ACTH and its behaviorally active fragment ACTH 4–10 have been consistently found to diminish event-related brain potential (ERP) signs of focussing attention. This study aimed at (1) evaluating effects of ACTH 4–10 on ERP indicators of attention in healthy controls after intranasal administration of the peptide. This route of administration has been proposed to provide a more direct access to the brain than the intravenous administration of the peptide, (2) comparing acute effects and effects of a subchronic treatment with ACTH 4–10, and (3) comparing effects of ACTH 4–10 with those of desacetyl-α-MSH (corresponding to ACTH 1–13 amide) which like ACTH 4–10 binds to subgroups of the melanocortin receptor family. Double-blind placebo-controlled experiments were completed in 54 healthy young subjects. ERPs were recorded while the subject performed an auditory selective attention task. Moreover, a modified Stroop interference test including motivational (food, sex) and nonmotivational words was performed. Acute intranasal administration of ACTH 4–10 (1 mg) reduced the processing negativity (PN) of the ERP over frontal and central cortical areas (p < 0.05) indicating diminished focussing of attention. Moreover, on this condition subjects were more prone to interference on the Stroop task especially with motivational words (p < 0.05). Subchronic administration of ACTH 4–10 (1 mg/day over 6 weeks) did not affect PN and Stroop performance. Acute intranasal administration of desacetyl-α-MSH at equimolar doses (1.68 mg) also remained ineffective. However, some measures of Stroop performance appeared to improve after subchronic desacetyl-α-MSH treatment. Results confirm an acute decrease in focussing of attention after ACTH 4–10. These effects of intranasal administration are likely to reflect a direct action of the peptide on respective brain functions. Moreover, they were specific to ACTH 4–10 and were not obtained after equimolar doses of desacetyl-α-MSH, thus excluding a mediation via the known melanocortin receptors.

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