Axonal projections within the brain-retrocerebral complex of the cricket, Teleogryllus commodus

1988 ◽  
Vol 252 (3) ◽  
pp. 501-514 ◽  
Author(s):  
Darrell Moore ◽  
Werner Loher
1987 ◽  
Vol 57 (4) ◽  
pp. 1101-1117 ◽  
Author(s):  
B. G. Lindsey ◽  
L. S. Segers ◽  
R. Shannon

Arrays of extracellular electrodes were used to monitor simultaneously several (2-8) respiratory neurons in the lateral medulla of anesthetized, paralyzed, bilaterally vagotomized, artificially ventilated cats. Efferent phrenic nerve activity was also recorded. The average discharge rate as a function of time in the respiratory cycle was determined for each neuron. Most cells were tested for spinal or vagal axonal projections using antidromic stimulation methods. Cross-correlational methods were used to analyze spike trains of 480 cell pairs. Each pair included at least one neuron most active during the expiratory phase. All simultaneously recorded neurons were located in the same side of the brain stem. Twenty-six percent (33/129) of the expiratory (E) neuron pairs exhibited short time scale correlations indicative of paucisynaptic interactions or shared inputs, whereas 8% (27/351) of the pairs consisting of an E neuron and an inspiratory (I) cell were similarly correlated. Evidence for several inhibitory actions of E neurons was found: 1) inhibition of I neurons by E neurons with both decrementing (DEC) and augmenting (AUG) firing patterns; 2) inhibition of E-DEC and E-AUG neurons by E-DEC cells; 3) inhibition of E-DEC and E-AUG neurons by E-AUG neurons; and 4) inhibition of E-DEC neurons by tonic I-E phase-spanning cells. Because several cells were recorded simultaneously, direct evidence for concurrent parallel and serial inhibitory processes was also obtained. The results suggest and support several hypotheses for mechanisms that may help to generate and control the pattern and coordination of respiratory motoneuron activities.


1996 ◽  
Vol 44 (6) ◽  
pp. 591-603 ◽  
Author(s):  
T Moos ◽  
P E Høyer

Despite the presence of a blood-brain barrier (BBB), plasma proteins have been detected intraneuronally in regions with axonal projections confined to the CNS. This finding raises the question of whether plasma proteins are taken up from the brain interstitium or whether the results are due to experimental artifact. We examined the effect of various protocols for tissue processing on the intraneuronal distribution of plasma proteins using immunohistochemistry. The detection level of plasma proteins decreased after prolonged fixation, irrespective of the fixative and embedding method employed. In cryostat sections, attempts to block nonspecific staining by serum protein caused considerable nonspecific staining in itself. When nonspecific staining was blocked with a serum-free buffer, specifically labeled neuronal perikarya were found in cryostat sections of brains fixed by perfusion with paraformaldehyde without postfixation. Albumin and IgG occurred predominantly in neurons having projections beyond the BBB but also sparsely in neurons having projections confined to the CNS. Transferrin was evenly distributed within neuronal somata, irrespective of the orientation of projections. The immunoreaction product of the three plasma proteins exhibited a specific intraneuronal localization in the differently projecting neurons. In circumventricular organs, plasma proteins were observed extracellularly and in projecting fibers. In conclusion, plasma proteins are present in neurons with projections confined to the CNS and are probably taken up from the brain interstitium.


1983 ◽  
Vol 61 (7) ◽  
pp. 579-593 ◽  
Author(s):  
W. D. Ruwe ◽  
W. L. Veale ◽  
K. E. Cooper

The neural elements of the rostral diencephalon in the mammal have been implicated in the regulation of body temperature. Moreover, it may be the neural elements within this region of the brain which activate the febrile mechanisms in response to pyrogen. Is it possible that the neuropeptides located within this area of the brain serve as neurochemical intermediaries involved in temperature regulation, fever, and (or) antipyresis? Central administration of several neuropeptides can elicit marked changes in the core temperature of an animal. Although most of these purative neuroregulators exert only a very minor influence on thermoregulation, a small number of the neuropeptides have been shown to have a profound effect on the system controlling this basic vegetative function. One of these peptides, arginine vasopressin (AVP) may play a role as an endogenous antipyretic. The neuroanatomical localization of this peptide, as well as its axonal projections, are consistent with such a role for this neurohypophyseal peptide in the mediation of antipyresis. In addition, current evidence suggests that AVP does function as a neurotransmitter. Examination of the febrile response to pyrogen in both the periparturient animal and the neonate indicates that an elevation in plasma levels of AVP is closely correlated with the diminution in the febrile response. Also, when AVP is perfused into punctate regions of the brain, a pyrogen-induced fever may be markedly suppressed. AVP appears to act primarily within the septal area, 2- to 3-mm rostral to the anterior commissure. During the development of fever, the release of AVP is altered within these same loci. As body temperature decreases during the febrile state, there is a concomitant increase in the amount of AVP released into the extracellular fluid of these septal sites. Very recent findings suggest that AVP may have additional central neurochemical functions. For example, this peptide may be involved in the etiology of some forms of convulsive disorders. The precise manner in which body temperature is regulated by the central nervous system normally and during fever is not well understood. In particular, the central mechanism of action of AVP in these processes remains to be determined. Currently, it is clear that the critical central mechanisms which are active in thermoregulation and fever are quite complex and will require many more years of investigation before the exact role of each can be enunciated.


2019 ◽  
Author(s):  
Soo-Eun Chang ◽  
Frank H H Guenther

Stuttering is a complex neurodevelopmental disorder that has to date eluded a clear explication of its pathophysiological bases. In this review, we utilize the Directions Into Velocities of Articulators (DIVA) neurocomputational modeling framework to mechanistically interpret relevant findings from the behavioral and neurological literatures on stuttering. Within this theoretical framework, we propose that the primary impairment underlying stuttering behavior is malfunction in the cortico-basal ganglia-thalamocortical (hereafter, cortico-BG) loop that is responsible for initiating speech motor programs. This theoretical perspective predicts three possible loci of impaired neural processing within the cortico-BG loop that could lead to stuttering behaviors: impairment within the basal ganglia proper, impairment of axonal projections between cerebral cortex, basal ganglia, and thalamus, and impairment in cortical processing. These theoretical perspectives are presented in detail, followed by a review of empirical data that make reference to these three possibilities. We also highlight any differences that are present in the literature based on examining adults versus children, which give important insights into potential core deficits associated with stuttering versus compensatory changes that occur in the brain as a result of having stuttered for many years in the case of adults who stutter. We conclude with outstanding questions in the field and promising areas for future studies that have the potential to further advance mechanistic understanding of neural deficits underlying persistent developmental stuttering.


2019 ◽  
Author(s):  
Soo-Eun Chang ◽  
Frank H H Guenther

Stuttering is a complex neurodevelopmental disorder that has to date eluded a clear explication of its pathophysiological bases. In this review, we utilize the Directions Into Velocities of Articulators (DIVA) neurocomputational modeling framework to mechanistically interpret relevant findings from the behavioral and neurological literatures on stuttering. Within this theoretical framework, we propose that the primary impairment underlying stuttering behavior is malfunction in the cortico-basal ganglia-thalamocortical (hereafter, cortico-BG) loop that is responsible for initiating speech motor programs. This theoretical perspective predicts three possible loci of impaired neural processing within the cortico-BG loop that could lead to stuttering behaviors: impairment within the basal ganglia proper, impairment of axonal projections between cerebral cortex, basal ganglia, and thalamus, and impairment in cortical processing. These theoretical perspectives are presented in detail, followed by a review of empirical data that make reference to these three possibilities. We also highlight any differences that are present in the literature based on examining adults versus children, which give important insights into potential core deficits associated with stuttering versus compensatory changes that occur in the brain as a result of having stuttered for many years in the case of adults who stutter. We conclude with outstanding questions in the field and promising areas for future studies that have the potential to further advance mechanistic understanding of neural deficits underlying persistent developmental stuttering.


Science ◽  
2017 ◽  
Vol 358 (6359) ◽  
pp. 64-69 ◽  
Author(s):  
Ed Lein ◽  
Lars E. Borm ◽  
Sten Linnarsson

The stereotyped spatial architecture of the brain is both beautiful and fundamentally related to its function, extending from gross morphology to individual neuron types, where soma position, dendritic architecture, and axonal projections determine their roles in functional circuitry. Our understanding of the cell types that make up the brain is rapidly accelerating, driven in particular by recent advances in single-cell transcriptomics. However, understanding brain function, development, and disease will require linking molecular cell types to morphological, physiological, and behavioral correlates. Emerging spatially resolved transcriptomic methods promise to fill this gap by localizing molecularly defined cell types in tissues, with simultaneous detection of morphology, activity, or connectivity. Here, we review the requirements for spatial transcriptomic methods toward these goals, consider the challenges ahead, and describe promising applications.


2021 ◽  
Author(s):  
Xiaowei Chen ◽  
Meng Wang ◽  
Ke Liu ◽  
Jialin Li ◽  
Junxia Pan ◽  
...  

Abstract Reconstructing axonal projections of single neurons at whole-brain level is a currently converging goal of the neuroscience community, which is fundamental to understanding the logic of information flow in the brain. Thousands of single neurons from different brain regions recently have been morphologically reconstructed, but the corresponding physiological functions of these reconstructed neurons are lacking. By combining two-photon Ca2+ imaging with targeted single-cell plasmid electroporation, we reconstructed the brain-wide morphologies of single neurons that were defined by a sound-evoked response map in the auditory cortex of awake mice. Long-range interhemispheric projections can be reliably labelled with co-injection of adeno-associated virus. This method avoids the randomness and ambiguity of conventional methods of neuronal morphological reconstruction, offering an avenue for developing a precise one-to-one map of neuronal projection and physiological function. Our method can be readily implemented in many laboratories that have been equipped with a standard two-photon microscope and electrophysiological devices.


2000 ◽  
Vol 80 (2) ◽  
pp. 615-647 ◽  
Author(s):  
Joel C. Glover

Astounding progress has been made during the past decade in understanding the general principles governing the development of the nervous system. An area of prime physiological interest that is being elucidated is how the neural circuitry that governs movement is established. The concerted application of molecular biological, anatomical, and electrophysiological techniques to this problem is yielding gratifying insight into how motoneuron, interneuron, and sensory neuron identities are determined, how these different neuron types establish specific axonal projections, and how they recognize and synapse upon each other in patterns that enable the nervous system to exercise precise control over skeletal musculature. This review is an attempt to convey to the physiologist some of the exciting discoveries that have been made, within a context that is intended to link molecular mechanism to behavioral realization. The focus is restricted to the development of monosynaptic connections onto skeletal motoneurons. Principal topics include the inductive mechanisms that pattern the placement and differentiation of motoneurons, Ia sensory afferents, and premotor interneurons; the molecular guidance mechanisms that pattern the projection of premotor axons in the brain stem and spinal cord; and the precision with which initial synaptic connections onto motoneurons are established, with emphasis on the relative roles played by cellular recognition versus electrical activity. It is hoped that this review will provide a guide to understanding both the existing literature and the advances that await this rapidly developing topic.


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