scholarly journals Reelin restricts dendritic growth of interneurons in the neocortex

Development ◽  
2021 ◽  
Vol 148 (17) ◽  
Author(s):  
Mohammad I. K. Hamad ◽  
Petya Petrova ◽  
Solieman Daoud ◽  
Obada Rabaya ◽  
Abdalrahim Jbara ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Ampa Receptors ◽  
Neuronal Migration ◽  
Neurotransmitter Release ◽  
Dendritic Growth ◽  
Embryonic Brain ◽  
Retzius Cells ◽  
Ca2 Channels ◽  
Interneuron Development

ABSTRACT Reelin is a large secreted glycoprotein that regulates neuronal migration, lamination and establishment of dendritic architecture in the embryonic brain. Reelin expression switches postnatally from Cajal-Retzius cells to interneurons. However, reelin function in interneuron development is still poorly understood. Here, we have investigated the role of reelin in interneuron development in the postnatal neocortex. To preclude early cortical migration defects caused by reelin deficiency, we employed a conditional reelin knockout (RelncKO) mouse to induce postnatal reelin deficiency. Induced reelin deficiency caused dendritic hypertrophy in distal dendritic segments of neuropeptide Y-positive (NPY+) and calretinin-positive (Calr+) interneurons, and in proximal dendritic segments of parvalbumin-positive (Parv+) interneurons. Chronic recombinant Reelin treatment rescued dendritic hypertrophy in Relncko interneurons. Moreover, we provide evidence that RelncKO interneuron hypertrophy is due to presynaptic GABABR dysfunction. Thus, GABABRs in RelncKO interneurons were unable to block N-type (Cav2.2) Ca2+ channels that control neurotransmitter release. Consequently, the excessive Ca2+ influx through AMPA receptors, but not NMDA receptors, caused interneuron dendritic hypertrophy. These findings suggest that reelin acts as a ‘stop-growth-signal’ for postnatal interneuron maturation.

Physiological role of neuropeptide Y in the regulation of the ascending phase of the peristaltic reflex

2003 ◽  
Vol 285 (6) ◽  
pp. G1139-G1146 ◽  
Author(s):  
John R. Grider ◽  
Lea E. Langdon
Keyword(s):  
Neuropeptide Y ◽  
Neurotransmitter Release ◽  
Receptor Agonist ◽  
Mechanical Response ◽  
Physiological Role ◽  
Rat Colon ◽  
Inhibitory Influence ◽  
Muscle Stretch ◽  
Peristaltic Reflex

The physiological role of neuropeptide Y (NPY) and of specific NPY receptors in regulating the intestinal peristaltic reflex was examined in three-compartment flat-sheet preparations of rat colon. Graded muscle stretch or mucosal stimulation applied to the central compartment inhibited NPY release in the orad compartment where ascending contraction was measured. NPY and the Y1-receptor agonist [Leu31, Pro34]NPY inhibited, whereas the selective Y1-receptor antagonist BIBP 3226 augmented ascending contraction and substance P (SP) release in the orad compartment induced by muscle stretch or mucosal stimulation. Neither agonist nor antagonist had any effect on descending relaxation or VIP release in the caudad compartment. The Y2-receptor agonist NPY13-36 and antagonist BIIE 0246 had no effect on peptide release or mechanical response. The results indicate that suppression of a tonic inhibitory influence of NPY neurons on excitatory neurotransmitter release contributes substantially to the orad contractile phase of the peristaltic reflex. The effect of NPY on neurotransmitter release is mediated by Y1 receptors.

scholarly journals The Role of Mutations on HLA Genes in Lambert-Eaton Myasthenic Syndrome

2021 ◽  
Vol 10 (1) ◽  
pp. 01-06
Author(s):  
Shahin Asadi ◽  
Mahsa Hemati ◽  
Naser Shagerdi Esmaeli
Keyword(s):  
Neurotransmitter Release ◽  
Neuromuscular Transmission ◽  
Proximal Muscle Weakness ◽  
Proximal Muscle ◽  
Autonomic Changes ◽  
Release Of Acetylcholine ◽  
Myasthenic Syndrome ◽  
Ca2 Channels ◽  
Tendon Reflexes

Lambert-Eaton myasthenic syndrome (LEMS) is a rare presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine (ACh) is impaired, causing a unique set of clinical characteristics, which include proximal muscle weakness, depressed tendon reflexes, posttetanic potentiation, and autonomic changes. [1] The initial presentation can be similar to that of myasthenia gravis (MG), but the progressions of the 2 diseases have some important differences. LEMS disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca2+ channels involved with neurotransmitter release.

scholarly journals Effects of Nifedipine on Renal and Cardiovascular Responses to Neuropeptide Y in Anesthetized Rats

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4460
Author(s):  
Angela Bischoff ◽  
Martina Stickan-Verfürth ◽  
Martin C. Michel
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular Responses ◽  
Receptor Subtypes ◽  
Y1 Receptor ◽  
Mediated Effects ◽  
Anesthetized Rats ◽  
Pre Treatment ◽  
Multiple Receptor ◽  
Ca2 Channels

Neuropeptide Y (NPY) acts via multiple receptor subtypes termed Y1, Y2 and Y5. While Y1 receptor-mediated effects, e.g., in the vasculature, are often sensitive to inhibitors of L-type Ca2+ channels such as nifedipine, little is known about the role of such channels in Y5-mediated effects such as diuresis and natriuresis. Therefore, we explored whether nifedipine affects NPY-induced diuresis and natriuresis. After pre-treatment with nifedipine or vehicle, anesthetized rats received infusions or bolus injections of NPY. Infusion NPY (1 µg/kg/min) increased diuresis and natriuresis, and this was attenuated by intraperitoneal injection of nifedipine (3 µg/kg). Concomitant decreases in heart rate and reductions of renal blood flow were not attenuated by nifedipine. Bolus injections of NPY (0.3, 1, 3, 10 and 30 μg/kg) dose-dependently increased mean arterial pressure and renovascular vascular resistance; only the higher dose of nifedipine (100 μg/kg/min i.v.) moderately inhibited these effects. We conclude that Y5-mediated diuresis and natriuresis are more sensitive to inhibition by nifedipine than Y1-mediated renovascular effects. Whether this reflects a general sensitivity of Y5 receptor-mediated responses or is specific for diuresis and natriuresis remains to be investigated.

The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis

2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropeptide Y ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
Vital Role ◽  
Gut Peptides ◽  
Nonalcoholic Fatty Liver ◽  
The Central Nervous System

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.

Role of Ca2+ channels on the hypothermic response produced by activation of κ-opioid receptors

2002 ◽  
Vol 72 (1-2) ◽  
pp. 93-99 ◽  
Author(s):  
Srinivas Gullapalli ◽  
Kumar V.S. Nemmani ◽  
Poduri Ramarao
Keyword(s):  
Opioid Receptors ◽  
Hypothermic Response ◽  
Ca2 Channels
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