Angiotensin II Receptor Development in the Bed Nucleus of the Stria terminalis and Other Perihypothalamic Brain Regions of the Female and Male Rat

1992 ◽  
Vol 56 (2) ◽  
pp. 169-177 ◽  
Author(s):  
Kevin L. Grove ◽  
Vickie I. Cook ◽  
Robert C. Speth
Keyword(s):  
Angiotensin Ii ◽  
Brain Regions ◽  
Male Rat ◽  
Stria Terminalis ◽  
Angiotensin Ii Receptor ◽  
Bed Nucleus

scholarly journals Deletion of proton-sensing receptor GPR4 associates with lower blood pressure and lower binding of angiotensin II receptor in SFO

2016 ◽  
Vol 311 (6) ◽  
pp. F1260-F1266 ◽  
Author(s):  
Xuming Sun ◽  
Ellen Tommasi ◽  
Doris Molina ◽  
Renu Sah ◽  
K. Bridget Brosnihan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Fractional Excretion ◽  
Urine Osmolality ◽  
Brain Regions ◽  
Lower Blood Pressure ◽  
Angiotensin Ii Receptor ◽  
Lower Blood ◽  
Fractional Excretion Of Sodium ◽  
The Impact

Diets rich in grains and meat and low in fruits and vegetables (acid-producing diets) associate with incident hypertension, whereas vegetarian diets associate with lower blood pressure (BP). However, the pathways that sense and mediate the effects of acid-producing diets on BP are unknown. Here, we examined the impact of the deletion of an acid sensor GPR4 on BP. GPR4 is a proton-sensing G protein-coupled receptor and an acid sensor in brain, kidney, and blood vessels. We found that GPR4 mRNA was higher in subfornical organ (SFO) than other brain regions. GPR4 protein was abundant in SFO and present in capillaries throughout the brain. Since SFO partakes in BP regulation through the renin-angiotensin system (RAS), we measured BP in GPR4−/− and GPR4+/+ mice and found that GPR4 deletion associated with lower systolic BP: 87 ± 1 mmHg in GPR4−/− ( n = 35) vs. 99 ± 2 mmHg ( n = 29) in GPR4+/+; P < 0.0001, irrespective of age and sex. Angiotensin II receptors detected by 125I-Sarthran binding were lower in GPR4−/− than GPR4+/+ mice in SFO and in paraventricular nucleus of hypothalamus. Circulating angiotensin peptides were comparable in GPR4−/− and GPR4+/+ mice, as were water intake and excretion, serum and urine osmolality, and fractional excretion of sodium, potassium, or chloride. A mild metabolic acidosis present in GPR4−/− mice did not associate with elevated BP, implying that deficiency of GPR4 may preclude the effect of chronic acidosis on BP. Collectively, these results posit the acid sensor GPR4 as a novel component of central BP control through interactions with the RAS.

scholarly journals Microarray analysis reveals distinctive signaling between the bed nucleus of the stria terminalis, nucleus accumbens, and dorsal striatum

2008 ◽  
Vol 32 (3) ◽  
pp. 283-298 ◽  
Author(s):  
Christopher M. Olsen ◽  
Yong Huang ◽  
Shirlean Goodwin ◽  
Daniel C. Ciobanu ◽  
Lu Lu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Nucleus Accumbens ◽  
Signaling Pathways ◽  
Microarray Analysis ◽  
Dorsal Striatum ◽  
Brain Regions ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Insight Into

To identify distinct transcriptional patterns between the major subcortical dopamine targets commonly studied in addiction we studied differences in gene expression between the bed nucleus of the stria terminalis (BNST), nucleus accumbens (NAc), and dorsal striatum (dStr) using microarray analysis. We first tested for differences in expression of genes encoding transcripts for common neurotransmitter systems as well as calcium binding proteins routinely used in neuroanatomical delineation of brain regions. This a priori method revealed differential expression of corticotropin releasing hormone ( Crh), the GABA transporter ( Slc6a1), and prodynorphin ( Pdyn) mRNAs as well as several others. Using a gene ontology tool, functional scoring analysis, and Ingenuity Pathway Analysis, we further identified several physiological pathways that were distinct among these brain regions. These two different analyses both identified calcium signaling, G-coupled protein receptor signaling, and adenylate cyclase-related signaling as significantly different among the BNST, NAc, and dStr. These types of signaling pathways play important roles in, amongst other things, synaptic plasticity. Investigation of differential gene expression revealed several instances that may provide insight into reported differences in synaptic plasticity between these brain regions. The results support other studies suggesting that crucial pathways involved in neurotransmission are distinct among the BNST, NAc, and dStr and provide insight into the potential use of pharmacological agents that may target region-specific signaling pathways. Furthermore, these studies provide a framework for future mouse-mouse comparisons of transcriptional profiles after behavioral/pharmacological manipulation.

scholarly journals Orexin A role in mechanisms of reinforcement in the bed nucleus of stria terminalis

2015 ◽  
Vol 13 (2) ◽  
pp. 20-26
Author(s):  
Andrei Andreevich Lebedev ◽  
Eugeny Grigorievich Shumilov ◽  
Eugeny Rudolfovich Bychkov ◽  
Vitaly Ivanovich Morozov ◽  
Petr Dmitriyevich Shabanov
Keyword(s):  
Lateral Hypothalamus ◽  
Behavioral Sensitization ◽  
Brain Regions ◽  
Brain Stimulation Reward ◽  
Stria Terminalis ◽  
Self Administration ◽  
Orexin A ◽  
Drug Reinforcement ◽  
Bed Nucleus ◽  
Self Stimulation

The orexin family of hypothalamic neuropeptides has been implicated in reinforcement mechanisms relevant to both food and drug reward. Previous behavioral studies with antagonists at the orexin A-selective receptor OX(1), have demonstrated its involvement in behavioral sensitization, conditioned place-preference, self-administration and reinstatement of drugs abuse. There are dense concentrations of hypocretin receptors, in brain regions implicated in drug reinforcement processes, such as the nucleus accumbens, ventral tegmental area and bed nucleus of the stria terminalis Adult male Wistar rats were implanted the stimulating electrodes to the lateral hypothalamus. Simultaneously, the microcanules were implanted into the BNST to inject the OX(1) receptor antagonist. Rats were trained to perform intracranial self-stimulation. The effects of the OX(1)-selective antagonist SB-408124 on brain stimulation-reward (BSR) were measured. SB-408124 injected into the BNST (1µg/1 µl in volume for each injection.) alone had no effect on self-stimulation of lateral hypothalamus. Amphetamine (1 mg/kg i.p.) potentiated BSR, measured as lowering of BSR threshold and enhancing of BSR frequency. Amphetamine-induced stimulatory effects on intracranial self-stimulation was blocked by injections of SB-408124 into BNST. These data demonstrate that OX(1) play an important role in regulating the reinforcing and reward-enhancing properties of amphetamine and suggest that orexin transmission is likely essential for establishing and maintaining the amphetamine habit in human addicts. However, the observations that OX1 antagonism reduce brain reward and block stress- and cue-induced reinstatement of drug-seeking suggests that this class of compounds may be useful additions to stress-reduction and other behavioral therapies in the treatment of substance abuse disorders.

Angiotensin II Receptors in the Ventral Portion of the Bed Nucleus of the Stria terminalis

1991 ◽  
Vol 53 (4) ◽  
pp. 339-343 ◽  
Author(s):  
Kevin L. Grove ◽  
Vickie I. Cook ◽  
Robert C. Speth
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Ii Receptors ◽  
Stria Terminalis ◽  
Bed Nucleus

scholarly journals Mass spectrometry imaging identifies abnormally elevated brain l-DOPA levels and extrastriatal monoaminergic dysregulation in l-DOPA–induced dyskinesia

2021 ◽  
Vol 7 (2) ◽  
pp. eabe5948
Author(s):  
Elva Fridjonsdottir ◽  
Reza Shariatgorji ◽  
Anna Nilsson ◽  
Theodosia Vallianatou ◽  
Luke R. Odell ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Side Effects ◽  
Mass Spectrometry Imaging ◽  
Brain Regions ◽  
Stria Terminalis ◽  
Brain Areas ◽  
Bed Nucleus ◽  
Neuronal Signaling ◽  
Cortical Areas ◽  
The Brain

l-DOPA treatment for Parkinson’s disease frequently leads to dyskinesias, the pathophysiology of which is poorly understood. We used MALDI-MSI to map the distribution of l-DOPA and monoaminergic pathways in brains of dyskinetic and nondyskinetic primates. We report elevated levels of l-DOPA, and its metabolite 3-O-methyldopa, in all measured brain regions of dyskinetic animals and increases in dopamine and metabolites in all regions analyzed except the striatum. In dyskinesia, dopamine levels correlated well with l-DOPA levels in extrastriatal regions, such as hippocampus, amygdala, bed nucleus of the stria terminalis, and cortical areas, but not in the striatum. Our results demonstrate that l-DOPA–induced dyskinesia is linked to a dysregulation of l-DOPA metabolism throughout the brain. The inability of extrastriatal brain areas to regulate the formation of dopamine during l-DOPA treatment introduces the potential of dopamine or even l-DOPA itself to modulate neuronal signaling widely across the brain, resulting in unwanted side effects.

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