CNS control of a critical period for peripheral induction of central neurons in the leech

Development ◽  
1992 ◽  
Vol 116 (2) ◽  
pp. 427-434 ◽  
Author(s):  
T. Becker ◽  
E.R. Macagno
Keyword(s):  
Central Nervous System ◽  
Male Genitalia ◽  
Critical Period ◽  
Central Neurons ◽  
Inductive Interaction ◽  
The Central Nervous System ◽  
Transplantation Experiments ◽  
Inductive Signal ◽  
Inductive Period ◽  
Cns Control

Most midbody ganglia in the central nervous system (CNS) of the leech Hirudo medicinalis contain about 400 neurons. However, those in the fifth and sixth midbody segments (ganglia M5 and M6) are specialized for reproductive functions, and each contain several hundred additional small neurons. These neurons arise late in embryogenesis as a result of an innervation-dependent inductive interaction between the male genitalia and M5 and M6 and are therefore known as peripherally induced central (PIC) neurons. The results of a series of ablation and transplantation experiments show that the PIC neurons are induced during a 1 to 2 day period about midway in embryogenesis (E15). The male genitalia are not necessary for induction before or after this period, and their presence for only one day may be sufficient for the induction to take place. Heterochronic transplantation of male genitalia shows that the critical period of interaction is independent of the age of the inducing tissues. Since the inductive signal is available from E10 to postembryonic stages, both the beginning and the end of the inductive period are determined by the CNS, not the periphery.

Target-induced neurogenesis in the leech CNS involves efferent projections to the target

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 359-369 ◽  
Author(s):  
T. Becker ◽  
A.J. Berliner ◽  
M.N. Nitabach ◽  
W.B. Gan ◽  
E.R. Macagno
Keyword(s):  
Sensory Neurons ◽  
Male Genitalia ◽  
Critical Period ◽  
Neuronal Cells ◽  
Sexual Organ ◽  
Central Neurons ◽  
Efferent Projections ◽  
Male Organ ◽  
Peripheral Sensory ◽  
Inductive Signal

During a critical period in leech embryogenesis, the sex nerves that connect the 5th and 6th midbody ganglia (MG5 and MG6) to the primordium of the male sexual organ carry a spatially localized signal that induces the birth of several hundred neurons specific to these ganglia. We examined particular cellular elements (afferents, efferents, non-neuronal components) within these nerves as potential conveyors of the inductive signal. We show that axons of peripheral sensory neurons in the male genitalia travel along the sex nerves and into MG5 and MG6, but reach the CNS after the critical period has elapsed and cannot, therefore, be involved in the induction. Of the six sex nerves, four contain non-neuronal cells that span the entire distance between the male genitalia and the sex ganglia. However, when male genitalia were transplanted to ectopic locations close to MG6, induction occurred frequently but only in MG6, mediated by ectopic nerves that do not contain these cells. Thus, non-neuronal cells specific to the normal sex nerves are not necessary for induction. In addition, dye injections into the target during the critical period failed to reveal migrating cells in the sex nerves that could convey the inductive signal to the CNS. Finally, we show that 11 pairs of central neurons in each ganglion project to the male organ early during the critical period. In the adult, at least 3 additional pairs of neurons in MG6 also innervate this target. We conclude that the only components of the sex nerves that connect the sex ganglia to the target during the critical period that could be associated with induced central mitogenesis are the axons of central neurons that innervate the male genitalia.

The development of central nervous system control of the gill withdrawal reflex evoked by siphon stimulation in Aplysia

1979 ◽  
Vol 57 (9) ◽  
pp. 987-997 ◽  
Author(s):  
Ken Lukowiak
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Abdominal Ganglion ◽  
System Control ◽  
Reflex Amplitude ◽  
Withdrawal Reflex ◽  
Reflex Latency ◽  
Neural Processes ◽  
The Central Nervous System ◽  
Cns Control

In older Aplysia, the central nervous system (CNS) (abdominal ganglion) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) which initially mediates the gill withdrawal reflex and its subsequent habituation evoked by tactile stimulation of the siphon. In young animals, both the suppressive and facilitatory CNS control were found to be absent. In older animals, removal of branchial nerve (Br) input to the gill resulted in a significantly reduced reflex latency and, with ctenidial (Ct) and siphon (Sn) nerves intact, a significantly increased reflex amplitude and an inability of the reflex to habituate with repeated siphon stimulation. In young animals, removal of Br had no effect on reflex latency and with Ct and Sn intact, the reflex amplitude latency was not increased and the reflex habituated. Older animals can easily discriminate between different intensity stimuli applied to the siphon as evidenced by differences in reflex amplitude, rates of habituation, and evoked neural activity. On the other hand, young animals cannot discriminate well between different stimulus intensities. The lack of CNS control in young animals was found to be due to incompletely developed neural processes within the abdominal ganglion and not the PNS. The lack of CNS control in young Aplysia results in gill reflex behaviours being less adaptive in light of changing stimulus conditions, but may be of positive survival value in that the young will not habituate as easily. The fact that CNS control is present in older animals strengthens the idea that in any analysis of the underlying neural mechanisms of habituation the entire integrated CNS–PNS must be taken into account.

scholarly journals Effects of Pregnancy Anesthesia on Fetal Nervous System

2021 ◽  
Vol 11 ◽  
Author(s):  
Xingyue Li ◽  
Xi Jiang ◽  
Ping Zhao
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
General Anesthesia ◽  
Critical Period ◽  
Medical Technology ◽  
Medical Field ◽  
The Public ◽  
Infancy And Childhood ◽  
The Central Nervous System ◽  
The Impact

The effects of general anesthesia on the developing brain remain a great concern in the medical field and even in the public, and most researches in this area focus on infancy and childhood. In recent years, with the continuous development of medical technology, the number of operations during pregnancy is increasing, however, studies on general anesthesia during pregnancy are relatively lacking. The mid-trimester of pregnancy is a critical period, and is regarded as a safe period for surgery, but it is a fragile period for the development of the central nervous system and is particularly sensitive to the impact of the environment. Our research group found that general anesthesia may have adverse effects on fetal neurodevelopment during the mid-trimester. Therefore, in this review, we summarize the characteristics of anesthesia during pregnancy, and the related research of the anesthesia’s impacts on the development of central nervous system were introduced.

Cortical Plasticity

2018 ◽  
Author(s):  
Sally A. Marik ◽  
Charles D. Gilbert
Keyword(s):  
Central Nervous System ◽  
Cortical Neurons ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Postnatal Life ◽  
Cortical Circuits ◽  
Cortical Areas ◽  
System P ◽  
Short Period ◽  
The Central Nervous System

The cerebral cortex is a learning engine. The ability to encode information about sensory experience or practiced movements is a universal property of all cortical areas. This capacity, known as cortical plasticity, is seen in experience dependent changes in the functional properties of cortical neurons and in the alteration of cortical circuits. Certain properties are mutable only during a short period in postnatal life, which is known as the critical period, while others retain the ability to change throughout life. The same changes associated with assimilating normal experiences can be implemented for functional recovery following lesions of the central nervous system.

Neurotrophin-Mediated Rapid Signaling in the Central Nervous System: Mechanisms and Functions

Physiology ◽  
2005 ◽  
Vol 20 (1) ◽  
pp. 70-78 ◽  
Author(s):  
Robert Blum ◽  
Arthur Konnerth
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Membrane Excitability ◽  
Cellular Functions ◽  
Trk Receptors ◽  
Ionotropic Receptors ◽  
Central Neurons ◽  
The Central Nervous System ◽  
Rapid Signaling ◽  
Activity Dependent

Neurotrophins regulate growth, survival, and differentiation of central neurons. In addition to the “classical” effects that are relatively slow neurotrophins also elicit rapid signaling that modulates a variety of cellular functions such as membrane excitability, synaptic transmission, and activity-dependent synaptic plasticity. These rapid actions are mediated mainly through the interaction of Trk receptors with ion channels and ionotropic receptors in the plasma membrane.

Induction of the epibranchial placodes

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 895-902 ◽  
Author(s):  
J. Begbie ◽  
J.F. Brunet ◽  
J.L. Rubenstein ◽  
A. Graham
Keyword(s):  
Neural Crest ◽  
Neuronal Cells ◽  
Signalling Molecule ◽  
Pharyngeal Endoderm ◽  
Inductive Interaction ◽  
Embryonic Origin ◽  
The Central Nervous System ◽  
Cranial Sensory Ganglia ◽  
Inductive Signal ◽  
Epibranchial Placodes

The cranial sensory ganglia, in contrast to those of the trunk, have a dual embryonic origin arising from both neurogenic placodes and neural crest. Neurogenic placodes are focal thickenings of ectoderm, found exclusively in the head of vertebrate embryos. These structures can be split into two groups based on the positions that they occupy within the embryo, dorsolateral and epibranchial. The dorsolateral placodes develop alongside the central nervous system, while the epibranchial placodes are located close to the top of the clefts between the branchial arches. Importantly, previous studies have shown that the neurogenic placodes form under the influence of the surrounding cranial tissues. In this paper, we have analysed the nature of the inductive signal underlying the formation of the epibranchial placodes. We find that epibranchial placodes do not require neural crest for their induction, but rather that it is the pharyngeal endoderm that is the source of the inductive signal. We also find that, while cranial ectoderm is competent to respond to this inductive signal, trunk ectoderm is not. We have further identified the signalling molecule Bmp7 as the mediator of this inductive interaction. This molecule is expressed in a manner consistent with it playing such a role and, when added to ectoderm explants, it will promote the formation of epibranchial neuronal cells. Moreover, the Bmp7 antagonist follstatin will block the ability of pharyngeal endoderm to induce placodal neuronal cells, demonstrating that Bmp7 is required for this inductive interaction. This work answers the long standing question regarding the induction of the epibranchial placodes, and represents the first elucidation of an inductive mechanism, and a molecular effector, underlying the formation of any primary sensory neurons in higher vertebrates.

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