Competitive interactions between supernumerary and normal sensory neurons in the cockroach are mediated through a change in quantal content and not quantal size

1995 ◽  
Vol 74 (4) ◽  
pp. 1573-1582 ◽  
Author(s):  
M. A. Sosa ◽  
J. M. Blagburn
Keyword(s):  
Sensory Neuron ◽  
Synapse Formation ◽  
Sensory System ◽  
Competitive Interactions ◽  
Quantal Content ◽  
Epsp Amplitude ◽  
Binomial Distributions ◽  
Quantal Size ◽  
Binomial Parameter ◽  
Common Target

1. The final steps in synapse formation and stabilization involve the adjustment of strength of connections through competitive interactions between neurons contacting a common target. The mechanisms underlying this competition-driven adjustment of synaptic strength are not well understood. We have studied one aspect of this phenomenon using the cercal sensory system of first instar cockroach nymphs. 2. Quantal analysis of excitatory postsynaptic potentials (EPSPs) recorded at the synapse between the lateral filiform hair sensory neuron (L) and giant interneuron 3 (GI3) was carried out to determine whether the reduction in EPSP amplitude observed in the presence of an additional sensory neuron ("space invader neuron" or SIN) was due to pre- or postsynaptic changes. 3. Mean quantal content, not quantal size, was reduced at the L-GI3 synapse in the presence of a SIN. Fitting binomial distributions to the EPSP amplitude histograms gave estimates of the number of releasable quanta or of synaptic sites (n) and the probability of release at these sites (p). The reduction in quantal content is associated with a decrease in the binomial parameter n and not p, suggesting that there is a decrease in the number of contacts, release sites, or quanta available for release, rather than a change in probability of release.

Two Neuropeptides Colocalized in a Command-Like Neuron Use Distinct Mechanisms to Enhance Its Fast Synaptic Connection

2003 ◽  
Vol 90 (3) ◽  
pp. 2074-2079 ◽  
Author(s):  
H.-Y. Koh ◽  
F. S. Vilim ◽  
J. Jing ◽  
K. R. Weiss
Keyword(s):  
High Frequency ◽  
Synaptic Connection ◽  
Quantal Content ◽  
Functional Consequence ◽  
Functional Implication ◽  
Quantal Size ◽  
Quantal Analysis ◽  
Cholinergic Interneuron ◽  
Single Synapse ◽  
Stimulation Of

In many neurons more than one peptide is colocalized with a classical neurotransmitter. The functional consequence of such an arrangement has been rarely investigated. Here, within the feeding circuit of Aplysia, we investigate at a single synapse the actions of two modulatory neuropeptides that are present in a cholinergic interneuron. In combination with previous work, our study shows that the command-like neuron for feeding, CBI-2, contains two neuropeptides, feeding circuit activating peptide (FCAP) and cerebral peptide 2 (CP2). Previous studies showed that high-frequency prestimulation or repeated stimulation of CBI-2 increases the size of CBI-2 to B61/62 excitatory postsynaptic potentials (EPSPs) and shortens the latency of firing of neuron B61/62 in response to CBI-2 stimulation. We find that both FCAP and CP2 mimic these two effects. The variance method of quantal analysis indicates that FCAP increases the calculated quantal size ( q) and CP2 increases the calculated quantal content ( m) of EPSPs. Since the PSP amplitude represents the product of q and m, the joint action of the two peptides is expected to be cooperative. This observation suggests a possible functional implication for multiple neuropeptides colocalized with a classical neurotransmitter in one neuron.

scholarly journals Function of Neuromuscular Synapses in the Zebrafish Choline-Acetyltransferase Mutant bajan

2008 ◽  
Vol 100 (4) ◽  
pp. 1995-2004 ◽  
Author(s):  
Meng Wang ◽  
Hua Wen ◽  
Paul Brehm
Keyword(s):  
Choline Acetyltransferase ◽  
Residual Activity ◽  
Direct Consequence ◽  
Synaptic Function ◽  
Congenital Myasthenic Syndrome ◽  
Quantal Content ◽  
Quantal Size ◽  
Gene Coding ◽  
Myasthenic Syndrome ◽  
The Impact

We have identified a zebrafish mutant line, bajan, in which compromised motility and fatigue result from a point mutation in the gene coding choline acetyltransferase (ChAT), the enzyme responsible for acetylcholine (ACh) synthesis. Although the mutation predicts loss of ChAT function, bajan inexplicably retains low levels of neuromuscular transmission. We exploited this residual activity and determined the consequences for synaptic function. The attenuated synaptic responses were a direct consequence of a decrease in both resting mean quantal size and quantal content. To replicate behavioral fatigue in swimming, motorneurons were stimulated at high frequencies. A prominent reduction in quantal content, reflecting vesicle depletion, was coincident with a small additional reduction in quantal size. In humans, defective ChAT leads to episodic apnea, a form of congenital myasthenic syndrome characterized by use-dependent fatigue. In contrast to bajan, however, afflicted individuals exhibit a normal resting quantal size and quantal content. The fatigue in humans results from a pronounced long-lasting drop in quantal size with little or no change in quantal content. These differences have important implications for interpreting fatigue as well as on understanding the impact of ACh availability on vesicle filling and recycling.

Regulation of Synaptic Depression Rates in the Cricket Cercal Sensory System

1998 ◽  
Vol 79 (3) ◽  
pp. 1277-1285 ◽  
Author(s):  
Andrew A. V. Hill ◽  
Ping Jin
Keyword(s):  
Sensory Neuron ◽  
Sensory Neurons ◽  
High Frequency ◽  
Sensory System ◽  
Synaptic Depression ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Short Term ◽  
Frequency Stimulation ◽  
Postsynaptic Target

Hill, Andrew A. V. and Ping Jin. Regulation of synaptic depression rates in the cricket cercal sensory system. J. Neurophysiol. 79: 1277–1285, 1998. To assess the roles of pre- and postsynaptic mechanisms in the regulation of depression, short-term synaptic depression was characterized at the synapses between sensory neurons and two interneurons in the cricket cercal sensory system. Changes in excitatory postsynaptic potential (EPSP) amplitude with repetitive stimulation at 5 and 20 Hz were quantified and fitted to the depletion model of transmitter release. The depression rates of different sensory neuron synapses on a single interneuron varied with the age of the sensory neurons such that old sensory neuron synapses depressed faster than young synapses. Although all synapses showed depression, short-term facilitation was selectively expressed only at sensory neuron synapses on one interneuron, the medial giant interneuron (MGI). These synapses showed concurrent facilitation and depression with high-frequency stimulation (100 Hz), whereas the synapses on another interneuron, 10-3, showed only depression at all stimulus frequencies. A previous study showed that the ability of a synapse to facilitate is correlated with the identity of the postsynaptic neuron. The present results indicate that depression and facilitation are regulated independently. Depression is regulated presynaptically in a manner related to sensory neuron age; whereas, facilitation is regulated by the postsynaptic target.

Facilitating effect of CCK on nicotinic neurotransmission in cat pancreatic ganglion

1996 ◽  
Vol 270 (3) ◽  
pp. G526-G534 ◽  
Author(s):  
R. C. Ma ◽  
J. H. Szurszewski
Keyword(s):  
Input Resistance ◽  
Postsynaptic Membrane ◽  
Excitatory Postsynaptic Potential ◽  
Nerve Terminals ◽  
Quantal Content ◽  
Quantal Size ◽  
Postsynaptic Potential ◽  
Ganglion Neurons ◽  
Ganglionic Transmission

Previous studies have demonstrated the presence of cholecystokinin (CCK)-like peptides in nerve terminals surrounding ganglion neurons of the cat pancreas. The present study was undertaken to determine the effect of cholecystokinin octapeptide (CCK-8) on ganglionic transmission. Recordings were made intracellularly in vitro from ganglion neurons in isolated pieces of the pancreas. Sulfated CCK-8 (S-CCK-8) and nonsulfated CCK-8 initiated or increased ongoing fast excitatory postsynaptic potential (fEPSP) activity, an effect antagonized by hexamethonium. Superfusion of S-CCK-8 in concentrations ranging from 10(-11) to 10(-8) M significantly augmented the amplitude of nerve-evoked subthreshold fEPSPs without a significant change in either membrane potential or membrane input resistance. S-CCK-8 (10(-8)M) also increased the quantal content and quantal size of nerve-evoked fEPSPs and increased the response to exogenously applied acetylcholine (ACh). Concentrations of S-CCK-8 higher than 10(-8)M caused depolarization and an increase in membrane input resistance, an effect unaltered by a low-Ca+, high-Mg2+ solution. It was concluded that S-CCK-8 potentiated nicotinic transmission by facilitating release of ACh from preganglionic nerve terminals and by increasing the postsynaptic membrane sensitivity to ACh.

scholarly journals Neurospecificity in the cricket cercal system

1984 ◽  
Vol 112 (1) ◽  
pp. 7-25
Author(s):  
R. K. Murphey ◽  
W. W. Walthall ◽  
G. A. Jacobs
Keyword(s):  
Nervous System ◽  
Receptive Fields ◽  
Sensory System ◽  
Dendritic Structure ◽  
Competitive Interactions ◽  
Joint Function ◽  
Detailed Understanding ◽  
First Order ◽  
Main Components ◽  
Cricket Cercal System

Studies of neurospecificity in the cricket cercal sensory system are reviewed and a decade of experimentation is examined in the light of recently obtained anatomical data. The nearly complete description of the anatomy indicates that the excitatory receptive fields of directionally-selective interneurones are a joint function of an orderly afferent projection and the dendritic structure of the first order interneurones. The detailed understanding of the anatomy is shown to be a powerful tool in the interpretation of previously published physiological experiments and the design of new ones. The mechanisms which shape the orderly afferent projection are then described and compared with the work on vertebrate sensory systems. It is concluded that both positional interactions of the type conceived by Sperry (1963) and competitive interactions of the type conceived by Hubel, Wiesel & LeVay (1977) are involved in producing the cercal afferent projection. Thus the two main components of the neurospecificity concept are shown to exist in the cricket nervous system. The limits of a purely anatomical approach to the study of neurospecificity are considered in light of the work on this cricket sensory system.

Exuberant growth and synapse formation of olfactory sensory neuron axonal arborizations

2011 ◽  
Vol 519 (18) ◽  
pp. 3713-3726 ◽  
Author(s):  
Florencia Marcucci ◽  
Elizabeth Maier-Balough ◽  
Dong-Jing Zou ◽  
Stuart Firestein
Keyword(s):  
Sensory Neuron ◽  
Synapse Formation ◽  
Olfactory Sensory Neuron

scholarly journals Proapoptotic RHG genes and mitochondria play a key non-apoptotic role in remodelling the Drosophila sensory system

2021 ◽  
Author(s):  
Amrita Mukherjee ◽  
Sinziana Pop ◽  
Shu Kondo ◽  
Darren W Williams
Keyword(s):  
Cell Death ◽  
Cell Fate ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Molecular Mechanisms ◽  
Sensory System ◽  
Caspase Activation ◽  
Effector Caspase ◽  
Effector Caspases

AbstractCaspases are best known for their role in programmed cell death but have also been found to be important in several non-apoptotic phenomena such as cell fate specification, cell migration and terminal differentiation. The dynamics of such sub-lethal caspase events and the molecular mechanisms regulating them are still largely unknown. As more tools for visualizing and manipulating caspase activation in vivo become available, greater insights into this biology are being made. Using a new and sensitive in vivo effector caspase probe, called SR4VH, we demonstrate that effector caspases are activated in pruning sensory neurons earlier than previously thought and that the level of caspase activation in these neurons is consistently lower than in neurons undergoing cell death. We reveal that Grim and Reaper, two of the four pro-apoptotic RHG proteins, are required for sensory neuron pruning and that disrupting the dynamics of the mitochondrial network prevents effector caspase activation in both pruning and dying sensory neurons. Overall, our findings demonstrate that a sublethal deployment of the ‘apoptotic machinery’ is critical for remodelling dendrites and also reveal a direct link between mitochondria and sensory neuron cell death in vivo.

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