scholarly journals Drosophila larval to pupal switch under nutrient stress requires IP3R/Ca2+ signalling in glutamatergic interneurons

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Siddharth Jayakumar ◽  
Shlesha Richhariya ◽  
O Venkateswara Reddy ◽  
Michael J Texada ◽  
Gaiti Hasan
Keyword(s):  
Calcium Imaging ◽  
Cholinergic Neurons ◽  
Neurosecretory Cells ◽  
Nutrient Stress ◽  
Ventral Ganglion ◽  
Glutamatergic Neurons ◽  
Ring Gland ◽  
Drosophila Larvae ◽  
Circuit Components ◽  
And Function

Neuronal circuits are known to integrate nutritional information, but the identity of the circuit components is not completely understood. Amino acids are a class of nutrients that are vital for the growth and function of an organism. Here, we report a neuronal circuit that allows Drosophila larvae to overcome amino acid deprivation and pupariate. We find that nutrient stress is sensed by the class IV multidendritic cholinergic neurons. Through live calcium imaging experiments, we show that these cholinergic stimuli are conveyed to glutamatergic neurons in the ventral ganglion through mAChR. We further show that IP3R-dependent calcium transients in the glutamatergic neurons convey this signal to downstream medial neurosecretory cells (mNSCs). The circuit ultimately converges at the ring gland and regulates expression of ecdysteroid biosynthetic genes. Activity in this circuit is thus likely to be an adaptation that provides a layer of regulation to help surpass nutritional stress during development.

scholarly journals Spontaneous activations follow a common developmental course across primary sensory areas in mouse neocortex

2016 ◽  
Vol 116 (2) ◽  
pp. 431-437 ◽  
Author(s):  
Charles G. Frye ◽  
Jason N. MacLean
Keyword(s):  
Calcium Imaging ◽  
Sensory Input ◽  
Primary Auditory Cortex ◽  
Developmental Trajectory ◽  
Two Photon ◽  
Developmental Progression ◽  
Sensory Modalities ◽  
Spatially Distributed ◽  
And Function ◽  
Insight Into

Spontaneous propagation of spiking within the local neocortical circuits of mature primary sensory areas is highly nonrandom, engaging specific sets of interconnected and functionally related neurons. These spontaneous activations promise insight into neocortical structure and function, but their properties in the first 2 wk of perinatal development are incompletely characterized. Previously, we have found that there is a minimal numerical sample, on the order of 400 cells, necessary to fully capture mature neocortical circuit dynamics. Therefore we maximized our numerical sample by using two-photon calcium imaging to observe spontaneous activity in populations of up to 1,062 neurons spanning multiple columns and layers in 52 acute coronal slices of mouse neocortex at each day from postnatal day (PND) 3 to PND 15. Slices contained either primary auditory cortex (A1) or somatosensory barrel field (S1BF), which allowed us to compare sensory modalities with markedly different developmental timelines. Between PND 3 and PND 8, populations in both areas exhibited activations of anatomically compact subgroups on the order of dozens of cells. Between PND 9 and PND 13, the spatiotemporal structure of the activity diversified to include spatially distributed activations encompassing hundreds of cells. Sparse activations covering the entire field of view dominated in slices taken on or after PND 14. These and other findings demonstrate that the developmental progression of spontaneous activations from active local modules in the first postnatal week to sparse, intermingled groups of neurons at the beginning of the third postnatal week generalizes across primary sensory areas, consistent with an intrinsic developmental trajectory independent of sensory input.

Glutamate elicits release of BDNF from basal forebrain astrocytes in a process dependent on metabotropic receptors and the PLC pathway

2008 ◽  
Vol 4 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Ying Y. Jean ◽  
Lauren D. Lercher ◽  
Cheryl F. Dreyfus
Keyword(s):  
Basal Forebrain ◽  
Metabotropic Glutamate Receptors ◽  
Cholinergic Neurons ◽  
Metabotropic Receptors ◽  
Western Blots ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Initial Work ◽  
Neuronal Signal ◽  
And Function

A key neurotrophin responsible for the survival and function of basal forebrain (BF) cholinergic neurons is brain-derived neurotrophic factor (BDNF). A number of studies now indicate that a source of this factor may be BF astrocytes. This study was designed to define the role of BF-astrocyte-derived BDNF on cholinergic neurons. Moreover, it investigated regulatory events that modulate BDNF content and release. In initial work BDNF derived from BF-astrocyte-conditioned medium (ACM) was found to increase both numbers of BF acetylcholinesterase (AChE+) cholinergic neurons and the cholinergic synthetic enzyme choline acetyltransferase (ChAT). Western blots, immunocytochemistry and pharmacological inhibition studies revealed that glutamate, through group I metabotropic glutamate receptors (mGluR), increases the intracellular levels of BDNF in BF astrocytes in culture, as well as its release. Furthermore, the release of BDNF is mediated by the actions of PLC, IP3 and internal stores of Ca2+. These results suggest that BF astrocytes serve as local sources of BDNF for cholinergic neurons, and that they may be regulated as such by the neuronal signal, glutamate, through the mediation of group I metabotropic receptors and the PLC pathway.

scholarly journals Cholinergic Degeneration and Alterations in the TrkA and p75NTR Balance as a Result of Pro-NGF Injection into Aged Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Ashley M. Fortress ◽  
Mona Buhusi ◽  
Kris L. Helke ◽  
Ann-Charlotte E. Granholm
Keyword(s):  
Basal Forebrain ◽  
Cholinergic Neurons ◽  
Memory Impairments ◽  
Age Related ◽  
High Affinity Receptor ◽  
Affinity Receptor ◽  
Cholinergic Degeneration ◽  
And Function ◽  
Do So

Learning and memory impairments occurring with Alzheimer's disease (AD) are associated with degeneration of the basal forebrain cholinergic neurons (BFCNs). BFCNs extend their axons to the hippocampus where they bind nerve growth factor (NGF) which is retrogradely transported to the cell body. While NGF is necessary for BFCN survival and function via binding to the high-affinity receptor TrkA, its uncleaved precursor, pro-NGF has been proposed to induce neurodegeneration via binding to the p75NTR and its coreceptor sortilin. Basal forebrain TrkA and NGF are downregulated with aging while pro-NGF is increased. Given these data, the focus of this paper was to determine a mechanism for how pro-NGF accumulation may induce BFCN degeneration. Twenty-four hours after a single injection of pro-NGF into hippocampus, we found increased hippocampal p75NTR levels, decreased hippocampal TrkA levels, and cholinergic degeneration. The data suggest that the increase in p75NTR with AD may be mediated by elevated pro-NGF levels as a result of decreased cleavage, and that pro-NGF may be partially responsible for age-related degenerative changes observed in the basal forebrain. This paper is the firstin vivoevidence that pro-NGF can affect BFCNs and may do so by regulating expression of p75NTR neurotrophin receptors.

scholarly journals Neuronal control of suppression, initiation and completion of egg deposition in Drosophila melanogaster

2021 ◽  
Author(s):  
Cristina Oliveira-Ferreira ◽  
Miguel Gaspar ◽  
Maria Luisa Vasconcelos
Keyword(s):  
Cholinergic Neurons ◽  
Egg Laying ◽  
Glutamatergic Neurons ◽  
Neuronal Populations ◽  
Motor Circuits ◽  
Neuronal Control ◽  
Egg Deposition ◽  
Complex Motor ◽  
A Site

Egg-laying in Drosophila is the product of post-mating physiological and behavioural changes that culminate in a stereotyped sequence of actions. While egg-laying behaviour has been mostly used as a system to understand the neuronal basis of decision making in the context of site selection, it harbours a great potential as a paradigm to uncover how, once a site is selected, the appropriate motor circuits are organized and activated to deposit an egg. To study this programme, we first describe the different stages of the egg-laying programme and the specific actions associated with each stage. Using a combination of neuronal activation and silencing experiments we characterize the role of three distinct neuronal populations in the abdominal ganglion with different contributions to the egg deposition motor elements. Specifically, we identify a subset of glutamatergic neurons and a subset of cholinergic neurons that promote the initiation and completion of egg expulsion respectively, while a subset of GABAergic neurons suppresses egg-laying. This study provides insight into the organization of neuronal circuits underlying complex motor behaviour.

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