Effect of dopaminergic and α-adrenergic modulation on corticotropin-releasing factor immunoreactivity in rat hypothalamus

1988 ◽  
Vol 66 (6) ◽  
pp. 754-761 ◽  
Author(s):  
Daniel A. Haas ◽  
Susan R. George
Keyword(s):  
Median Eminence ◽  
Potential Role ◽  
Corticotropin Releasing Factor ◽  
Male Rats ◽  
Dopamine Antagonist ◽  
Adrenergic Modulation ◽  
Selective Depletion ◽  
Dopaminergic Mechanisms ◽  
Monoamine Depletion ◽  
6 Hydroxydopamine

The potential role that dopaminergic mechanisms have in the regulation of corticotropin-releasing factor (CRF) in the hypothalamus was investigated. Adult male rats were administered bromocriptine, a potent dopamine agonist, for periods ranging up to 51 days. Overall, bromocriptine treatment resulted in a significant decline in CRF-like immunoreactivity (CRF-ir). The dopamine antagonist, haloperidol, was administered for similar periods and resulted in no overall significant effect, except for a transient decrease. Treatment with reserpine, known to deplete monoamines including dopamine, induced a significant decrease in CRF-ir 24 h post-treatment. The possibility that the original results were due to α-adrenergic inhibition by bromocriptine and haloperidol was studied next. α1-Stimulation by administration of methoxamine had no significant effect. α2-Stimulation by clonidine significantly reduced hypothalamic CRF-ir. Selective depletion of neurotransmitter from noradrenergic and adrenergic neurons by 6-hydroxydopamine also resulted in a significant reduction of hypothalamic CRF-ir, an effect localized entirely to the median eminence. These results show a reduction in CRF-ir subsequent to either bromocriptine administration, generalized monoamine depletion, α2-stimulation, or selective noradrenaline–adrenaline depletion. No direct dopaminergic effects could be confirmed. These data are consistent with a constant, near-maximal α1-adrenergic effect maintaining hypothalamic CRF concentrations, presumably by inhibition of CRF release from the median eminence.

Ultrastructural Localization of Acetylcholinesterase in the Arcuate Nucleus and Median Eminence of the Rat

1977 ◽  
Vol 35 ◽  
pp. 440-441
Author(s):  
K.A. Carson ◽  
C.B. Nemeroff ◽  
M.S. Rone ◽  
J.S. Kizer ◽  
J.S. Hanker
Keyword(s):  
Choline Acetyltransferase ◽  
Median Eminence ◽  
Arcuate Nucleus ◽  
Cholinergic Neurons ◽  
Ultrastructural Localization ◽  
Male Rats ◽  
Neonatal Rats ◽  
Good Marker ◽  
Chemical Studies ◽  
High Doses

Biochemical, physiological, pharmacological, and more recently enzyme histo- chemical data have indicated that cholinergic circuits exist in the hypothalamus. Ultrastructural correlates of these pathways such as acetylcholinesterase (AchE) positive neurons in the arcuate nucleus (ARC) and stained terminals in the median eminence (ME) have yet to be described. Initial studies in our laboratories utilizing chemical lesioning and microdissection techniques coupled with microchemical and light microscopic enzyme histo- chemical studies suggested the existence of cholinergic neurons in the ARC which project to the ME (1). Furthermore, in adult male rats with Halasz deafferentations (hypothalamic islands composed primarily of the isolated ARC and the ME) choline acetyltransferase (ChAc) activity, a good marker for cholinergic neurons, was not significantly reduced in the ME and was only somewhat reduced in the ARC (2). Treatment of neonatal rats with high doses of monosodium 1-glutamate (MSG) results in a lesion largely restricted to the neurons of the ARC.

109 Chemogenetic silencing of corticotropin releasing factor neurons in the paraventricular nucleus: the effect on post-stress sleep

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A45-A45
Author(s):  
Irma Gvilia ◽  
Sunil Kumar ◽  
Dennis McGinty ◽  
Ronald Szymusiak
Keyword(s):  
Paraventricular Nucleus ◽  
Nrem Sleep ◽  
Corticotropin Releasing Factor ◽  
Male Rats ◽  
Male Rat ◽  
Sleep Onset Latency ◽  
Post Surgery ◽  
Crf Neurons ◽  
Emg Electrodes ◽  
Post Stress

Abstract Introduction We have previously shown that pharmacological elevation of corticotropin releasing factor (CRF) signaling in the brain results in exacerbation of sleep disturbances evoked by the exposure of rats to an acute stressor, the dirty cage of a male rat. In the present study we (1) assessed wake-sleep behavior of mice after the exposure to the dirty cage stress paradigm, and (2) examined the effect of chemogenetic silencing of CRF neurons in the hypothalamic paraventricular nucleus (PVN) on sleep occurring following the exposure to this stressor. Methods First, a group of mice (n=12) was implanted with EEG/EMG electrodes. In two weeks, post-surgery, six mice were transferred to dirty cages of male rats and recorded for 24 hours. Control mice were transferred to clean cages. In the second study, a group of CRF-ires-cre mice (n=8) received bilateral injections of AAV-hSyn-DIO-hM4Di-mCherry targeting the PVN. The other group of CRF-ires-cre mice (n=8) was injected AAV-hSyn-DIO-mCherry (control vector). All mice were implanted with EEG/EMG electrodes. Dirty cage experiments were started following a 4-week postsurgical period to allow gene recombination and expression. Mice were subjected to intraperitoneal (IP) administration of clozapine-n-oxide (CNO; 3 mg/kg) at ZT1, placed into dirty cages, and recorded for post-stress sleep. Results: Results In mice expressing hM4Di inhibitory DREADDs (designer receptors activated by designer drugs) versus mice injected with control AAV, IP CNO (3 mg/kg) resulted in a significant decrease of post-stress sleep onset latency, decrease of time spent in wakefulness (first hour, 74±5.3 vs. 89±11.0, second hour, 37.2±10.3% vs. 81.3±9.3%; third hour, 40.1±3.3% vs. 47.1±14.3%; fourth hour, 44.4±6.0 vs. 55.5±9.9), and increase in non-rapid eye movement (NREM) sleep time (26.0±5.4% vs. 11.0±11.1%; 62.8%±9.8 vs. 18.7 ± 9.6%; 59.9±3.2% vs. 52.9±14.5%; 55.6±6.2 vs. 44.5±10.0). The hM4Di expressing mice exhibited longer episodes of NREM sleep, compared to mice injected with control AAV (first hour, 133.3±80.1sec vs. 21±1.7sec; second hour, 43256±83.4sec vs. 73.5±44.1sec; third hour, 459.2±139.8sec vs. 139±80.6sec; fourth hour, 233.1±82.6sec vs. 190±72.3sec). Conclusion Chemogenetic silencing of CRF neurons in the PVN attenuates acute stress-induced sleep disturbance in mice. Support (if any) Supported by Department of Veterans Affairs Merit Review Grant # BX00155605 and SRNSF (Georgia) grant FR-18-12533

scholarly journals Aqueous Extract of Semen Ziziphi Spinosae Exerts Anxiolytic Effects during Nicotine Withdrawal via Improvement of Amygdaloid CRF/CRF1R Signaling

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Changhong Gu ◽  
ZhengLin Zhao ◽  
Xiaodong Zhu ◽  
Tong Wu ◽  
Bong Hyo Lee ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Elevated Plus Maze ◽  
Plasma Corticosterone ◽  
Nicotine Withdrawal ◽  
Corticotropin Releasing Factor ◽  
Central Nucleus ◽  
Male Rats ◽  
General Anxiety ◽  
Plus Maze

Anxiety during nicotine withdrawal (NicW) is a key risk factor for smoking relapse. Semen Ziziphi Spinosae (SZS), which is a prototypical hypnotic-sedative herb in Oriental medicine, has been clinically used to treat insomnia and general anxiety disorders for thousands of years. Thus, the present study evaluated the effects of the aqueous extract of SZS (AESZS) on NicW-induced anxiety in male rats that received subcutaneous administrations of nicotine (Nic) (0.4 mg/kg, twice a day) for 7 d followed by 4 d of withdrawal. During NicW, the rats received four intragastric treatments of AESZS (60 mg/kg/d or 180 mg/kg/d). AESZS dose-dependently attenuated NicW-induced anxiety-like behaviors in the elevated plus maze (EPM) tests and 180 mg/kg/d AESZS inhibited NicW-induced increases in plasma corticosterone. Additionally, the protein and mRNA expressions of corticotropin-releasing factor (CRF) and CRF type 1 receptor (CRF1R) increased in the central nucleus of the amygdala (CeA) during NicW, but these changes were suppressed by 180 mg/kg/d AESZS. A post-AESZS infusion of CRF into the CeA abolished the attenuation of anxiety by AESZS and 180 mg/kg/d AESZS suppressed NicW-induced increases in norepinephrine and 3-methoxy-4-hydroxy-phenylglycol levels in the CeA. The present results suggest that AESZS ameliorated NicW-induced anxiety via improvements in CRF/CRF1R and noradrenergic signaling in the CeA.

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