ABSTRACT
The dorsal raphe nucleus (DRN)-serotonin (5-HT) system plays a key role in stress-related psychiatric disorders such as anxiety and depression. The habenular nucleus (Hb) is closely connected with the DRN both morphologically and functionally. Here, we used two types of depressive animal models by exposing rats to chronic mild stress (CMS) and by chronically administering the tricyclic antidepressant clomipramine (CLI) in the rat during the neonatal state of life to produce adult depressed rats. We investigated the effects of lateral habenular nucleus (LHb) lesions on the behavioral response and on the level of 5-HT in DRN in the depressed rats. Forced-swimming test (FST) showed that the immobility time decreased, and the climbing time increased after lesioning LHb of depressed rats. Microdialysis results indicated that the 5-HT level in DRN in depressed rats was lower than that of the control group. Lesion of the LHb was followed by an increased 5-HT turnover in the DRN. Our results suggested that the lesion of the LHb could improve the behavioral response of the depressed rats and the 5-HT level of the DRN increased by LHb lesions could be involved in the effects.
Subject(s)
Depressive Disorder/physiopathology , Habenula/physiology , Raphe Nuclei/metabolism , Serotonin/metabolism , Stress, Psychological/metabolism , Animals , Antidepressive Agents , Chronic Disease , Clomipramine , Depressive Disorder/chemically induced , Depressive Disorder/etiology , Disease Models, Animal , Habenula/physiopathology , Immobility Response, Tonic/physiology , Male , Neural Pathways/physiology , Rats , Rats, Wistar , Stress, Psychological/complicationsSubject(s)
Blood Pressure/drug effects , Epimedium , Flavonoids/pharmacology , Animals , Arteries/drug effects , Arteries/physiology , Rats , Rats, Inbred SHR , Rats, WistarABSTRACT
AIM: The effect and possible mechanism of Melatonin (MEL) on firing rate of pain neurons in lateral habenular nucleus of rats were investigated in the experiment. METHODS: Single extracellular firing were recorded to study the firing rate changes of pain neurons and sensitivity changes to pain stimulation induced by MEL in LHb of rats. Reverse effect of naloxone on the analgesia induced by melatonin was also observed. RESULTS: Melatonin showed the effects on the firing of pain neurons in the LHb and decreased the sensitivity of pain neurons to pain stimulation, which could be reversed by naloxone. CONCLUSION: Melatonin can change the responses of pain neurons to pain stimulation via opioid receptor in the LHb, which might be one of analgesic mechanisms by MEL.
Subject(s)
Habenula/drug effects , Melatonin/pharmacology , Neurons/drug effects , Analgesics/pharmacology , Animals , Habenula/physiology , Male , Neuralgia/physiopathology , Neurons/physiology , Rats , Rats, WistarABSTRACT
This study was conducted to determine the effect of pregnanolone (PGN) on blood pressure of a rat model of stress-induced hypertension (SIH). This model was established by applying electric shock to animal feet together with noise. PGN was administered intraperitoneally at 0.24 mg/kg.d(-1) and blood pressure, angiotensin II (Ang II) levels, and the expression of Fos-like protein immunoreactive (FLI) neurons in brain areas were determined. Rats were randomly divided into five groups: (1) control, (2) stressed for 1 h, (3) stressed for 1 h after PGN pretreatment, (4) stressed for a 2 h session, twice a day, for 15 d, and (5) stressed for a 2 h session after PGN pretreatment, twice a day, for 15 d. The results showed that increased systolic pressure of tail artery caused by a 15-d stress treatment was significantly reduced by PGN pretreatment (P<0.001). Ang II levels, measured by radioactive immunoreactivity, were significantly elevated (P<0.001) after the rats were stressed for 1 h or 15 d, the Ang II level was significantly reduced by PGN treatment in both 1 h and 15 d stress groups (P<0.05). Only a small number of FLI neurons were found in the brain areas of the control group, 15 d stress group, and 15 d stress with PGN group. In the 1 h stress group, more FLI neurons were found in the lateral habenular nucleus, the medial habenular nucleus, the paraventricular nucleus, the central nucleus of amgydaloid and the lateral hypothalamus compared with the control group. PGN pretreatment significantly prevented the increase in the number of FLI neurons. These results indicate that PGN pretreatment prevents elevation of tail artery systolic pressure in SIH rats and that this effect of PGN may be mediated through reducing Ang II level and inhibiting the activity of cardiovascular center involved in stress.
