AI Article Synopsis
- The study explored how different neuropeptides and the bioactive amine 5-HT affect motoneurons (B15 and B16) and interneurons (B4, B5) that regulate feeding behavior in Aplysia californica.
- Unique patterns of synapse-induced neural bursting were triggered by egg-laying hormone (ELH), small cardioactive peptide b (SCPb), and 5-HT, while FMRFamide suppressed neuronal firing activity.
- The research indicates that these neuropeptides modulate neural circuits to create varied motoneuron activity patterns, with some neurons showing distinct intrinsic properties and differences in responsiveness to these substances.
Article Abstract
We examined the effects of 3 neuropeptides and the bioactive amine 5-HT on identified motoneurons (B15 and B16) and interneurons (B4, B5) involved in the control of feeding behavior in Aplysia californica. The application of egg-laying hormone (ELH), small cardioactive peptide b (SCPb), and 5-HT elicits distinct patterns of synaptically induced bursting in the neurons, while PheMetArgPheamide (FMRFamide) inhibits firing due to synaptic activity. Repetitive IPSPs recorded in B15 and B16 are induced by 5-HT and SCPb and inhibited by FMRFamide. The substances also may act directly: In solutions that block synaptic transmission SCPb excites B15, ELH excites B16, 5-HT excites B15, B16, and B4, and FMRFamide both inhibits B15 and B16 and excites B4. We suggest that the output of a buccal ganglion central pattern generator may be modulated to produce distinct patterns of motoneuron activity by these candidate transmitters. We also noted differences in the intrinsic properties of the 2 motoneurons. B15 contains SCPb immunoreactivity while B16 does not. This finding suggests that B15 may be the source for the SCPb immunoreactivity previously found at the ARC muscle and that SCPb may be acting in an autocrine mode. Also, B15 has a significantly lower resting potential than B16 and contains a large transient outward (Ia-like) current. The candidate transmitters act by exciting or inhibiting elements at every level within the hierarchically organized motor system that controls feeding. This expands the diversity of behavioral repertoires that may be elicited from a particular neural circuit.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6569063 | PMC |
| http://dx.doi.org/10.1523/JNEUROSCI.07-03-00671.1987 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Computational exploration of acefylline derivatives as MAO-B inhibitors for Parkinson's disease: insights from molecular docking, DFT, ADMET, and molecular dynamics approaches.
Front Chem
October 2024
Department of Chemistry, College of Science, Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Saudi Arabia.
Monoamine oxidase B (MAO-B) plays a pivotal role in the deamination process of monoamines, encompassing crucial neurotransmitters like dopamine and norepinephrine. The heightened interest in MAO-B inhibitors emerged after the revelation that this enzyme could potentially catalyze the formation of neurotoxic compounds from endogenous and exogenous sources. Computational screening methodologies serve as valuable tools in the quest for novel inhibitors, enhancing the efficiency of this pursuit.
View Article and Find Full Text PDFUSP50 suppresses alternative RecQ helicase use and deleterious DNA2 activity during replication.
Nat Commun
September 2024
Birmingham Centre for Genome Biology and Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, B15 2TT, UK.
Article Synopsis
- Mammalian DNA replication requires various helicases and nucleases for accurate genetic duplication, but the direction of these activities was previously unclear.
- The study identifies USP50 as a crucial chromatin-associated protein that aids in ongoing replication, fork restart, and telomere maintenance, while also preventing DNA breaks.
- USP50 works by ensuring the correct localization of other proteins like WRN and FEN1 during stalled replication, and its absence leads to increased activity of certain helicases and nucleases, causing replication issues and telomere instability.
Exploring the experiences and expectations of trainee representatives in medical specialties: A qualitative study in the West Midlands, UK.
Future Healthc J
March 2024
Institute of Applied Health Research, University of Birmingham, UK.
Introduction: Despite its importance, there is a paucity of evidence describing the role and responsibilities of trainee representatives.
Aim: This study explored key stakeholders' experiences and expectations of the trainee representative role.
Method: All eligible individuals in the West Midlands Deanery's School of Medicine were invited to participate in an interview exploring their experiences and expectations of the trainee representative role.
Genome-wide identification and expression analysis of NF-Y gene family in tobacco (Nicotiana tabacum L.).
Sci Rep
March 2024
College of Plant Protection and Agricultural Big-Data Research Center, Shandong Agricultural University, Tai'an, 271018, China.
Nuclear factor Y (NF-Y) gene family is an important transcription factor composed of three subfamilies of NF-YA, NF-YB and NF-YC, which is involved in plant growth, development and stress response. In this study, 63 tobacco NF-Y genes (NtNF-Ys) were identified in Nicotiana tabacum L., including 17 NtNF-YAs, 30 NtNF-YBs and 16 NtNF-YCs.
View Article and Find Full Text PDFMechanisms of synthetic lethality between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta targeting.
Nat Commun
November 2023
Birmingham Centre for Genome Biology and Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, UK.
A synthetic lethal relationship exists between disruption of polymerase theta (Polθ), and loss of either 53BP1 or homologous recombination (HR) proteins, including BRCA1; however, the mechanistic basis of these observations are unclear. Here we reveal two distinct mechanisms of Polθ synthetic lethality, identifying dual influences of 1) whether Polθ is lost or inhibited, and 2) the underlying susceptible genotype. Firstly, we find that the sensitivity of BRCA1/2- and 53BP1-deficient cells to Polθ loss, and 53BP1-deficient cells to Polθ inhibition (ART558) requires RAD52, and appropriate reduction of RAD52 can ameliorate these phenotypes.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!