Rats living in small cages respond to restraint stress with adrenocortical corticosterone release but not with hippocampal acetylcholine release

Repeated restraint stress (RRS; 3 h of restraint on 3 consecutive days) in rodents produces temporary hypophagia, but a long-term downregulation of body weight. The mild stress (MS) of an intraperitoneal injection of saline and housing in a novel room for 2 h also inhibits food intake and weight gain, but the effects are smaller than for RRS. Previous exposure to RRS exaggerates hypophagia, glucocorticoid release, and anxiety-type behavior caused by MS. Here we tested the involvement of brain stem corticotrophin-releasing factor receptors (CRFR) in mediating energetic and glucocorticoid responses to RRS or MS and in promoting stress hyperresponsiveness in RRS rats. Administration of 1.3 nmol αhCRF(9-41), a nonspecific CRFR antagonist, exaggerated hypophagia and weight loss in both RRS and MS rats, whereas 0.26 nmol had no effect in RRS or MS rats. In contrast, 2 nmol of the nonspecific antagonist astressin had no effect on weight loss or hypersensitivity to subsequent MS in RRS rats, but blocked weight loss and inhibition of food intake caused by MS alone. MS rats infused with 3 nmol antisauvagine-30, a CRFR2 antagonist, did not lose weight in the 48 h after MS, but 0.3 nmol did not prevent weight loss in MS rats. These data suggest that inhibition of food intake and weight loss induced by RRS or by MS involve different pathways, with hindbrain CRFR mediating the effect of MS on body weight and food intake. Hindbrain CRFR do not appear to influence stress-induced corticosterone release in RRS rats.

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Urocortin 3 in the posterodorsal medial amygdala mediates stress-induced suppression of LH pulsatility in female mice

Endocrinology ◽

10.1210/endocr/bqab206 ◽

2021 ◽

Author(s):

Deyana Ivanova ◽

Xiao-Feng Li ◽

Caitlin McIntyre ◽

Yali Liu ◽

Lingsi Kong ◽

...

Keyword(s):

Psychosocial Stress ◽

Restraint Stress ◽

Pulse Generator ◽

Suppressive Effect ◽

Medial Amygdala ◽

Corticosterone Secretion ◽

Reproductive Axis ◽

Lh Pulsatility ◽

Factor Type ◽

Corticosterone Release

Abstract Psychosocial stress disrupts reproduction and interferes with pulsatile LH secretion. The posterodorsal medial amygdala (MePD) is an upstream modulator of the reproductive axis and stress. Corticotropin-releasing factor type-2 receptors (CRFR2) are activated in the presence of psychosocial stress together with increased expression of the CRFR2 ligand Urocortin3 (Ucn3) in the MePD of rodents. We investigate whether Ucn3 signalling in the MePD is involved in mediating the suppressive effect of psychosocial stress on LH pulsatility. Firstly, we administered Ucn3 into the MePD and monitored the effect on LH pulses in ovariectomised mice. Next, we delivered Astressin2B, a selective CRFR2 antagonist, intra-MePD in the presence of predator odor, 2,4,5-Trimethylthiazole (TMT) and examined the effect on LH pulses. Subsequently, we virally infected Ucn3-cre-tdTomato mice with inhibitory DREADDs targeting MePD Ucn3 neurons while exposing mice to TMT or restraint stress and examined the effect on LH pulsatility as well as corticosterone release. Administration of Ucn3 into the MePD dose-dependently inhibited LH pulses and administration of Astressin2B blocked the suppressive effect of TMT on LH pulsatility. Additionally, DREADDs inhibition of MePD Ucn3 neurons blocked TMT and restraint stress-induced inhibition of LH pulses and corticosterone release. These results demonstrate for the first time that Ucn3 neurons in the MePD mediate psychosocial stress-induced suppression of the GnRH pulse generator and corticosterone secretion. Ucn3 signalling in the MePD plays a role in modulating the hypothalamic-pituitary-ganadal and hypothalamic-pituitary-adrenal axes, and this brain locus may represent a nodal centre in the interaction between the reproductive and stress axes.

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Effects of ethanol on locomotor depression and corticosterone release induced by restraint-stress: Support for a stress-ethanol interaction

Pharmacology Biochemistry and Behavior ◽

10.1016/0091-3057(90)90403-5 ◽

1990 ◽

Vol 36 (2) ◽

pp. 273-278 ◽

Cited By ~ 17

Author(s):

L-E. Trudeau ◽

C.M.G. Aragon ◽

Z. Amit

Keyword(s):

Restraint Stress ◽

Corticosterone Release ◽

Ethanol Interaction

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Severe Drooling and Treatment With Botulinum Toxin

Perspectives on Swallowing and Swallowing Disorders (Dysphagia) ◽

10.1044/sasd21.1.15 ◽

2012 ◽

Vol 21 (1) ◽

pp. 15-21

Author(s):

Merete Bakke ◽

Allan Bardow ◽

Eigild Møller

Keyword(s):

Botulinum Toxin ◽

Side Effects ◽

Health Risk ◽

Flow Rate ◽

Clinical Evidence ◽

Acetylcholine Release ◽

Psychosocial Problems ◽

Rate Reduction ◽

Local Inhibition ◽

Surgical Treatments

Severe drooling is associated with discomfort and psychosocial problems and may constitute a health risk. A variety of different surgical and non-surgical treatments have been used to diminish drooling, some of them with little or uncertain effect and others more effective but irreversible or with side effects. Based on clinical evidence, injection with botulinum toxin (BTX) into the parotid and submandibular glands is a useful treatment option, because it is local, reversible, and with few side effects, although it has to be repeated. The mechanism of BTX is a local inhibition of acetylcholine release, which diminishes receptor-coupled secretion and results in a flow rate reduction of 25–50% for 2–7 months.

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