Erratum to “Alterations of steroid receptor coactivator-1 (SRC-1) immunoreactivities in specific brain regions of young and middle-aged female Sprague–Dawley rats” [Brain Res. 1381 (2011) 88–97]

2011 ◽  
Vol 1389 ◽  
pp. 200-201
Author(s):  
Dongmei Zhang ◽  
Qiang Guo ◽  
Chen Bian ◽  
Jiqiang Zhang ◽  
Sen Lin ◽  
...  
Biologia ◽  
2011 ◽  
Vol 66 (6) ◽  
Author(s):  
Xuechai Chen ◽  
Abida Arshad ◽  
Hong Qing ◽  
Rui Wang ◽  
Jianqing Lu ◽  
...  

AbstractSalsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; Sal) is structurally similar to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is supposed to have a role in the development of Parkinson-like syndrome in both human and non-human subjects. In the human brain, the amount of (R)-enantiomer of Sal is much higher than (S)-enantiomer, suggesting that a putative enzyme may participate in the synthesis of (R)-salsolinol, called (R)-salsolinol synthase. In this study, the (R)-salsolinol synthase activity in the condensation of dopamine and acetaldehyde was investigated in the crude extracts from the brains of Sprague Dawley rats. Identification of the enzymatic reaction products and enzyme activity detection were achieved by HPLC-electrochemical detection. The discovery of this enzyme activity in rat’s brain indicates the natural existence of (R)-salsolinol synthase in the brains of humans and rats, and it is distributed in most brain regions of rat with higher activity in soluble proteins extracted from striatum and substantia nigra.


PLoS ONE ◽  
2019 ◽  
Vol 14 (5) ◽  
pp. e0217553 ◽  
Author(s):  
Nikita Girish Deshpande ◽  
Juhi Saxena ◽  
Tristan G. Pesaresi ◽  
Casey Dylan Carrell ◽  
Grayson Breneman Ashby ◽  
...  

2003 ◽  
Vol 284 (4) ◽  
pp. R916-R927 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Shun-Guang Wei ◽  
Joseph Francis ◽  
Robert B. Felder

In pathophysiological conditions, increased blood-borne TNF-α induces a broad range of biological effects, including activation of the hypothalamic-pituitary-adrenal axis and sympathetic drive. In urethane-anesthetized adult Sprague-Dawley rats, we examined the mechanisms by which blood-borne TNF-α activates neurons in paraventricular nucleus (PVN) of hypothalamus and rostral ventrolateral medulla (RVLM), two critical brain regions regulating sympathetic drive in normal and pathophysiological conditions. TNF-α (0.5 μg/kg), administered intravenously or into ipsilateral carotid artery (ICA), activated PVN and RLVM neurons and increased sympathetic nerve activity, arterial pressure, and heart rate. Responses to intravenous TNF-α were not affected by vagotomy but were reduced by mid-collicular decerebration. Responses to ICA TNF-α were substantially reduced by injection of the cyclooxygenase inhibitor ketorolac (150 μg) into lateral ventricle. Injection of PGE2 (50 ng) into lateral ventricle or directly into PVN increased PVN or RVLM activity, respectively, and sympathetic drive, with shorter onset latency than blood-borne TNF-α. These findings suggest that blood-borne cytokines stimulate cardiovascular and renal sympathetic responses via a prostaglandin-dependent mechanism operating at the hypothalamic level.


1985 ◽  
Vol 249 (2) ◽  
pp. R214-R218 ◽  
Author(s):  
A. V. Ferguson ◽  
C. W. Bourque ◽  
L. P. Renaud

Extracellular single unit recordings obtained in pentobarbital-anesthetized male Sprague Dawley rats were utilized to examine the electrophysiology of connections of medial septum-diagonal band of Broca (MS-DBB) neurons with the subfornical organ (SFO), hippocampal commissure (HC), and supraoptic nucleus (SON). Of the 119/216 cells tested that demonstrated antidromic activation from SON, many (60%) were orthodromically excited by SFO stimulation, whereas most (68%) were unresponsive to stimulation in the adjacent HC. Separate populations of MS-DBB neurons that displayed antidromic activation from the SFO (11/140 cells tested) or HC (24/78 tested) were orthodromically excited by SON stimulation. Three cells were activated antidromically from both the SFO and SON. These observations reveal some possible interconnections between these three brain regions and point to the existence of an indirect pathway whereby the SFO can influence SON neurons through an influence on MS-DBB neurons.


2011 ◽  
Vol 26 (S2) ◽  
pp. 1231-1231
Author(s):  
E.F. Buonaguro ◽  
F. Marmo ◽  
L. Avvisati ◽  
G. Latte ◽  
R. Rossi ◽  
...  

Enkephalin is an opioidergic neuromodulator that has been implicated in long-term behavioural sensitization after administration of drugs of abuse. Enkephalin is also a molecular marker of GABAergic neurons in the striato-pallidal pathway that is involved in sensory-motor gating and has been considered dysfunctional in the pathophysiology of psychosis.In this study we investigated in male Sprague Dawley rats putative changes in Enkephalin transcripts by in situ hybridization after acute or subchronic administration of ketamine in either high or low subanaesthetic doses (50 mg/kg and 12 mg/kg respectively). Ketamine is a non-competitive NMDA-R antagonist that perturbs glutamate neurotransmission and provides a preclinical model of psychosis-like behaviour in rats.In the acute paradigm the expression of Enkephalin was reduced in the motor, premotor, somatosensory cortices as well as in anterior cingulate. In the subchronic paradigm Enkephalin expression was reduced in the premotor cortex, in the ventromedial caudate-putamen and in the shell of nucleus accumbens. Comparative analysis showed that the relative decrement in gene expression was not significantly different between the acute and subchronic paradigm for each region of interest.Changes in distribution of Enkephalin expression and correlation analysis of functionally related brain regions suggest that Enkephalin transcripts reduction may be implicated in the motivational aspects of drug addiction and may help explaining some aspects of the pathophysiology in ketamine-induced psychosis.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sandra Högler ◽  
Ursula Teubenbacher ◽  
Wolfgang Weihs ◽  
Fritz Sterz ◽  
Ingrid A M Magnet ◽  
...  

Background: Evolution of histological lesions in selectively vulnerable brain regions in animal models of cardiac arrest (CA)give evidence of potential therapeutic windows. Delayed cell death is of special interest in this regard. Methods: In male Sprague-Dawley rats (350g) ventricular fibrillation (VF) CA was induced for 6 min followed by chest compressions, ventilation and drugs for 2 min. To achieve return of spontaneous circulation animals were defibrillated every 2 min. Animals were sacrificed after one week (n=5) or two weeks (n=7) of survival and compared to four sham animals. Brains were fixed in formalin, embedded in paraffin wax and cut into 3 μm thick coronary sections for histological examination. Viable neurons with nucleolus were counted in Hematoxylin-Eosin (HE)-stained sections in a 250 μm sector of the medial CA1 region. FluoroJade B staining was applied to count dying neurons in the same sector. Results: In HE-staining sham animals had 31±4 viable neurons. In one week survivors 11±9 viable neurons (p=0.003) and in two week survivors 7±7 viable neurons (p=0.001 vs sham, p=0.49 vs one week survivors) were counted. Furthermore, a lot of degenerated hypereosinophilic neurons were present in HE-staining in both CA-groups. FluoroJade B-staining was negative in sham animals. In one week survivors 29±8 dying neurons (p=0.006) and in two week survivors 33±13 dying neurons (p= 0.016 vs sham, p=0.343 vs one week survivors) were detectable. Conclusions: Consistent damage in the medial CA1 region was present after 6 min VFCA in both survival time groups. Lesions seemed to be constant, with no significant differences between time points. Contrary to expectations, FluoroJade B-staining was still positive after two weeks of survival, suggesting that delayed cell death might go on for a longer time period than assumed so far.


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