5-HT2A receptor activation in the dorsolateral septum facilitates inhibitory avoidance in the elevated T-maze

2012 ◽  
Vol 226 (1) ◽  
pp. 50-55 ◽  
Author(s):  
D.C. de Paula ◽  
A.S. Torricelli ◽  
M.R. Lopreato ◽  
J.O.G. Nascimento ◽  
M.B. Viana
Keyword(s):  
Inhibitory Avoidance ◽  
Receptor Activation

scholarly journals Memory retrieval of inhibitory avoidance requires histamine H1 receptor activation in the hippocampus

2016 ◽  
Vol 113 (19) ◽  
pp. E2714-E2720 ◽  
Author(s):  
Roberta Fabbri ◽  
Cristiane Regina Guerino Furini ◽  
Maria Beatrice Passani ◽  
Gustavo Provensi ◽  
Elisabetta Baldi ◽  
...  
Keyword(s):  
Retention Test ◽  
Memory Retrieval ◽  
Inhibitory Avoidance ◽  
Emotional Memory ◽  
Receptor Activation ◽  
Control Group ◽  
Histaminergic System ◽  
Brain Histamine ◽  
Ventral Medial Prefrontal Cortex ◽  
Endogenous Histamine

Retrieval represents a dynamic process that may require neuromodulatory signaling. Here, we report that the integrity of the brain histaminergic system is necessary for retrieval of inhibitory avoidance (IA) memory, because rats depleted of histamine through lateral ventricle injections of α-fluoromethylhistidine (a-FMHis), a suicide inhibitor of histidine decarboxylase, displayed impaired IA memory when tested 2 d after training. a-FMHis was administered 24 h after training, when IA memory trace was already formed. Infusion of histamine in hippocampal CA1 of brain histamine-depleted rats (hence, amnesic) 10 min before the retention test restored IA memory but was ineffective when given in the basolateral amygdala (BLA) or the ventral medial prefrontal cortex (vmPFC). Intra-CA1 injections of selective H1 and H2 receptor agonists showed that histamine exerted its effect by activating the H1 receptor. Noteworthy, the H1 receptor antagonist pyrilamine disrupted IA memory retrieval in rats, thus strongly supporting an active involvement of endogenous histamine; 90 min after the retention test, c-Fos–positive neurons were significantly fewer in the CA1s of a-FMHis–treated rats that displayed amnesia compared with in the control group. We also found reduced levels of phosphorylated cAMP-responsive element binding protein (pCREB) in the CA1s of a-FMHis–treated animals compared with in controls. Increases in pCREB levels are associated with retrieval of associated memories. Targeting the histaminergic system may modify the retrieval of emotional memory; hence, histaminergic ligands might reduce dysfunctional aversive memories and improve the efficacy of exposure psychotherapies.

COVID-19 pathophysiology: interactions of gut microbiome, melatonin, vitamin D, stress, kynurenine and the alpha 7 nicotinic receptor: Treatment implications

2020 ◽  
Vol 3 (3) ◽  
pp. 322-345 ◽  
Author(s):  
George Anderson ◽  
Russel J Reiter
Keyword(s):  
Vitamin D ◽  
Coagulation Factors ◽  
Receptor Activation ◽  
Cytokine Induction ◽  
Aryl Hydrocarbon ◽  
Physiological Processes ◽  
Pulmonary Epithelial Cells ◽  
Vitamin D Levels ◽  
Complex Picture ◽  
Alpha 7

As data emerges on the pathophysiological underpinnings of severe acute respiratory syndrome coronavirus (SARS-CoV)-2, it is clear that there are considerable variations in its susceptibility and severity/fatality, which give indications as to its pathophysiology and treatment. SARS-CoV-2 modulatory factors include age, vitamin D levels, cigarette smoking, gender and ethnicity as well as premorbid medical conditions, including diabetes, cancer, obesity, cardiovascular disease, and immune-compromised conditions. A complex picture is emerging, with an array of systemic physiological processes interacting including circadian, immune, intestinal, CNS and coagulation factors. This article reviews data on SARS-CoV-2 pathoetiology and pathophysiology. It is proposed that a decrease in pineal and systemic melatonin is an important driver of SARS-CoV-2 susceptibility and severity, with the loss of pineal melatonin's induction of the alpha 7 nicotinic acetylcholine receptor (α7nAChR) in pulmonary epithelial cells and immune cells being a powerful regulator of susceptibility and severity, respectively. Stress, including discrimination stress, and decreased vitamin D also regulate SARS-CoV-2, including via gut dysbiosis and permeability, with a resultant decrease in the short-chain fatty acid, butyrate, and increase in circulating lipopolysaccharide. Stress and cytokine induction of the kynurenine pathways, leads to aryl hydrocarbon receptor activation, which primes platelets for heightened activity, coagulation and thrombin production, thereby driving elevations in thrombin that underpin many SARS-CoV-2 fatalities. On the basis of these pathophysiological changes, prophylactic and symptomatic treatments are proposed, including the use of melatonin and α7nAChR agonism. 

Effect of κ-opiate receptor activation on the levels of insulin, somatostatin and blood glucose in man

1989 ◽  
Vol 120 (3_Suppl) ◽  
pp. S230
Author(s):  
A. PFEIFFER ◽  
V. SCHUSDZIARRA ◽  
V. BRANTL
Keyword(s):  
Blood Glucose ◽  
Opiate Receptor ◽  
Receptor Activation

Coaction of Electrostatic and Hydrophobic Interactions: Dynamic Constraints on Disordered TrkA Juxtamembrane Domain

2019 ◽  
Author(s):  
Zichen Wang ◽  
Huaxun Fan ◽  
Xiao Hu ◽  
John Khamo ◽  
Jiajie Diao ◽  
...  
Keyword(s):  
Single Molecule ◽  
Protein Function ◽  
Hydrophobic Interactions ◽  
Transmembrane Helix ◽  
Point Mutations ◽  
Salt Bridge ◽  
Receptor Activation ◽  
Membrane Dynamics ◽  
Juxtamembrane Domain ◽  
Joint Work

<p>The receptor tyrosine kinase family transmits signals into cell via a single transmembrane helix and a flexible juxtamembrane domain (JMD). Membrane dynamics makes it challenging to study the structural mechanism of receptor activation experimentally. In this study, we employ all-atom molecular dynamics with Highly Mobile Membrane-Mimetic to capture membrane interactions with the JMD of tropomyosin receptor kinase A (TrkA). We find that PIP<sub>2 </sub>lipids engage in lasting binding to multiple basic residues and compete with salt bridge within the peptide. We discover three residues insertion into the membrane, and perturb it through computationally designed point mutations. Single-molecule experiments indicate the contribution from hydrophobic insertion is comparable to electrostatic binding, and in-cell experiments show that enhanced TrkA-JMD insertion promotes receptor ubiquitination. Our joint work points to a scenario where basic and hydrophobic residues on disordered domains interact with lipid headgroups and tails, respectively, to restrain flexibility and potentially modulate protein function.</p>

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