scholarly journals The brain matters: effects of descending signals on motor control

2012 ◽  
Vol 107 (10) ◽  
pp. 2730-2741 ◽  
Author(s):  
Olivia J. Mullins ◽  
W. Otto Friesen
Keyword(s):  
Nerve Cord ◽  
Motor Output ◽  
Swimming Activity ◽  
Neuronal Circuit ◽  
Numerous Species ◽  
Physiological Conditions ◽  
Synaptic Interactions ◽  
Hirudo Verbana ◽  
Episode Duration ◽  
The Brain

The ability of nerve cords and spinal cords to exhibit fictive rhythmic locomotion in the absence of the brain is well-documented in numerous species. Although the brain is important for modulating the fictive motor output, it is broadly assumed that the functional properties of neuronal circuits identified in simplified preparations are conserved with the brain attached. We tested this assumption by examining the properties of a novel interneuron recently identified in the leech ( Hirudo verbana) nerve cord. This neuron, cell E21, initiates and drives stereotyped fictive swimming activity in preparations of the isolated leech nerve cord deprived of the head brain. We report that, contrary to expectation, the motor output generated when cell E21 is stimulated in preparations with the brain attached is highly variable. Swim frequency and episode duration are increased in some of these preparations and decreased in others. Cell E21 controls swimming, in part, via excitatory synaptic interactions with cells 204, previously identified gating neurons that reliably initiate and strongly enhance leech swimming activity when the brain is absent. We found that in preparations with the brain present, the magnitude of the synaptic interaction from cell E21 to cell 204 is reduced by 50% and that cell 204-evoked responses also were highly variable. Intriguingly, most of this variability disappeared in semi-intact preparations. We conclude that neuronal circuit properties identified in reduced preparations might be fundamentally altered from those that occur in more physiological conditions.

scholarly journals Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury

2021 ◽  
Vol 7 (10) ◽  
pp. eabe0207
Author(s):  
Charles-Francois V. Latchoumane ◽  
Martha I. Betancur ◽  
Gregory A. Simchick ◽  
Min Kyoung Sun ◽  
Rameen Forghani ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Large Scale ◽  
Growth Factor Signaling ◽  
Neuronal Circuit ◽  
Reach To Grasp ◽  
Function Recovery ◽  
Cellular Repair ◽  
The Brain

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brain’s poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery chronically after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely after sTBI significantly enhanced cellular repair and gross motor function recovery when compared to controls 20 weeks after sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations demonstrated the significant recovery of “reach-to-grasp” function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely after sTBI can support complex cellular, vascular, and neuronal circuit repair chronically after sTBI.

The Larval Eclosion Hormone Neurones in Manduca Sexta: Identification of the Brain-Proctodeal Neurosecretory System

1989 ◽  
Vol 147 (1) ◽  
pp. 457-470 ◽  
Author(s):  
JAMES W. TRUMAN ◽  
PHILIP F. COPENHAVER
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Nerve Cord ◽  
Release Site ◽  
Neurosecretory System ◽  
Nerve Activity ◽  
Eclosion Hormone ◽  
The Central Nervous System ◽  
The Brain

Larval and pupal ecdyses of the moth Manduca sexta are triggered by eclosion hormone (EH) released from the ventral nervous system. The major store of EH activity in the latter resides in the proctodeal nerves that extend along the larval hindgut. At pupal ecdysis, the proctodeal nerves show a 90% depletion of stored activity, suggesting that they are the major release site for the circulating EH that causes ecdysis. Surgical experiments involving the transection of the nerve cord or removal of parts of the brain showed that the proctodeal nerve activity originates from the brain. Retrograde and anterograde cobalt fills and immunocytochemistry using antibodies against EH revealed two pairs of neurons that reside in the ventromedial region of the brain and whose axons travel ipsilaterally along the length of the central nervous system (CNS) and project into the proctodeal nerve, where they show varicose release sites. These neurons constitute a novel neuroendocrine pathway in insects which appears to be dedicated solely to the release of EH.

scholarly journals Ventilation and neurochemical changes during µ-opioid receptor activation or blockade of excitatory receptors in the hypoglossal motor nucleus of goats

2017 ◽  
Vol 123 (6) ◽  
pp. 1532-1544 ◽  
Author(s):  
Thomas M. Langer ◽  
Suzanne E. Neumueller ◽  
Emma Crumley ◽  
Nicholas J. Burgraff ◽  
Sawan Talwar ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Pulmonary Ventilation ◽  
Respiratory Control ◽  
Nrem Sleep ◽  
Receptor Activation ◽  
Motor Nucleus ◽  
Physiological Conditions ◽  
Neurochemical Changes ◽  
Underlying Mechanisms ◽  
The Brain

Neuromodulator interdependence posits that changes in one or more neuromodulators are compensated by changes in other modulators to maintain stability in the respiratory control network. Herein, we studied compensatory neuromodulation in the hypoglossal motor nucleus (HMN) after chronic implantation of microtubules unilaterally ( n = 5) or bilaterally ( n = 5) into the HMN. After recovery, receptor agonists or antagonists in mock cerebrospinal fluid (mCSF) were dialyzed during the awake and non-rapid eye movement (NREM) sleep states. During day studies, dialysis of the µ-opioid inhibitory receptor agonist [d-Ala2, N-MePhe4, Gly-ol]enkephalin (DAMGO; 100 µM) decreased pulmonary ventilation (V̇i), breathing frequency ( f), and genioglossus (GG) muscle activity but did not alter neuromodulators measured in the effluent mCSF. However, neither unilateral dialysis of a broad spectrum muscarinic receptor antagonist (atropine; 50 mM) nor unilateral or bilateral dialysis of a mixture of excitatory receptor antagonists altered V̇i or GG activity, but all of these did increase HMN serotonin (5-HT) levels. Finally, during night studies, DAMGO and excitatory receptor antagonist decreased ventilatory variables during NREM sleep but not during wakefulness. These findings contrast with previous dialysis studies in the ventral respiratory column (VRC) where unilateral DAMGO or atropine dialysis had no effects on breathing and bilateral DAMGO or unilateral atropine increased V̇i and f and decreased GABA or increased 5-HT, respectively. Thus we conclude that the mechanisms of compensatory neuromodulation are less robust in the HMN than in the VRC under physiological conditions in adult goats, possibly because of site differences in the underlying mechanisms governing neuromodulator release and consequently neuronal activity, and/or responsiveness of receptors to compensatory neuromodulators. NEW & NOTEWORTHY Activation of inhibitory µ-opioid receptors in the hypoglossal motor nucleus decreased ventilation under physiological conditions and did not affect neurochemicals in effluent dialyzed mock cerebral spinal fluid. These findings contrast with studies in the ventral respiratory column where unilateral [d-Ala2, N-MePhe4, Gly-ol]enkephalin (DAMGO) had no effects on ventilation and bilateral DAMGO or unilateral atropine increased ventilation and decreased GABA or increased serotonin, respectively. Our data support the hypothesis that mechanisms that govern local compensatory neuromodulation within the brain stem are site specific under physiological conditions.

Neurochemical effects of choline supplementation

1986 ◽  
Vol 64 (3) ◽  
pp. 329-333 ◽  
Author(s):  
Lynn Wecker
Keyword(s):  
Brain Tissue ◽  
Neuronal Activity ◽  
Cholinergic Neurons ◽  
Lipid Phosphorus ◽  
Drug Induced ◽  
Pharmacological Agents ◽  
Physiological Conditions ◽  
Free Choline ◽  
Drug Challenge ◽  
The Brain

Whether or not the brain can use supplemental choline to enhance the synthesis of acetylcholine (ACh) is an important consideration for assessing the merits of using choline or phosphatidylcholine (lecithin) for the treatment of neuropsychiatric disorders postulated to involve hypocholinergic activity. While it is well documented that administered choline is incorporated into ACh, the ability of supplemental choline to increase the synthesis and release of ACh has been questionable. Studies in my laboratory have demonstrated that acute or chronic choline supplementation does not, by itself, enhance the levels of ACh in brain under normal biochemical and physiological conditions. However, supplemental choline prevents the depletion of ACh in brain induced by numerous pharmacological agents that increase the firing of cholinergic neurons. Since the levels of free choline in brains from supplemented rats were not different from controls prior to drug challenge, evidence suggested that the observed effects of choline were mediated by alterations in the mobilization of choline from choline-containing compounds. Studies investigating the release of choline from brain indicated that more choline was released per unit time in tissues from choline-supplemented rats than from controls. In addition, brain tissue from choline-supplemented rats had increased concentrations of total lipid phosphorus as compared with controls. Hence, although choline supplementation does not alter the levels of ACh in brain under normal conditions, it does appear to support ACh synthesis during drug-induced increases in neuronal activity, an effect most likely mediated by alterations in the metabolism of choline-containing phospholipids.

scholarly journals The functional organization of descending sensory-motor pathways in Drosophila

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Shigehiro Namiki ◽  
Michael H Dickinson ◽  
Allan M Wong ◽  
Wyatt Korff ◽  
Gwyneth M Card
Keyword(s):  
Nerve Cord ◽  
Functional Organization ◽  
Cell Types ◽  
The Body ◽  
Layered System ◽  
Descending Pathways ◽  
Motor Pathways ◽  
Transgenic Lines ◽  
Functional Map ◽  
The Brain

In most animals, the brain controls the body via a set of descending neurons (DNs) that traverse the neck. DN activity activates, maintains or modulates locomotion and other behaviors. Individual DNs have been well-studied in species from insects to primates, but little is known about overall connectivity patterns across the DN population. We systematically investigated DN anatomy in Drosophila melanogaster and created over 100 transgenic lines targeting individual cell types. We identified roughly half of all Drosophila DNs and comprehensively map connectivity between sensory and motor neuropils in the brain and nerve cord, respectively. We find the nerve cord is a layered system of neuropils reflecting the fly’s capability for two largely independent means of locomotion -- walking and flight -- using distinct sets of appendages. Our results reveal the basic functional map of descending pathways in flies and provide tools for systematic interrogation of neural circuits.

scholarly journals Blindsight and Unconscious Vision: What They Teach Us about the Human Visual System

2016 ◽  
Vol 23 (5) ◽  
pp. 529-541 ◽  
Author(s):  
Sara Ajina ◽  
Holly Bridge
Keyword(s):  
Visual Cortex ◽  
Visual System ◽  
Primary Visual Cortex ◽  
Neural Activity ◽  
Human Visual System ◽  
Visual Information ◽  
Visual Loss ◽  
Physiological Conditions ◽  
The World ◽  
The Brain

Damage to the primary visual cortex removes the major input from the eyes to the brain, causing significant visual loss as patients are unable to perceive the side of the world contralateral to the damage. Some patients, however, retain the ability to detect visual information within this blind region; this is known as blindsight. By studying the visual pathways that underlie this residual vision in patients, we can uncover additional aspects of the human visual system that likely contribute to normal visual function but cannot be revealed under physiological conditions. In this review, we discuss the residual abilities and neural activity that have been described in blindsight and the implications of these findings for understanding the intact system.

scholarly journals Identification and Expression Analysis of Tryptophan Hydroxylase in the Brain and Ventral Nerve Cord of RagwormNeanthes japonica(Polychaeta, Annelida)

2016 ◽  
Vol 300 (2) ◽  
pp. 415-424
Author(s):  
Shun Wang ◽  
Zhe Dong ◽  
Shen Li ◽  
Haotian Yin ◽  
Zhifu Zhao ◽  
...  
Keyword(s):  
Expression Analysis ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Tryptophan Hydroxylase ◽  
The Brain

scholarly journals The Contribution ofα-Synuclein Spreading to Parkinson’s Disease Synaptopathy

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Francesca Longhena ◽  
Gaia Faustini ◽  
Cristina Missale ◽  
Marina Pizzi ◽  
PierFranco Spano ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorders ◽  
Physiological Conditions ◽  
Age Related ◽  
Endogenous Protein ◽  
Synaptic Failure ◽  
Nigrostriatal Neurons ◽  
Somatic Nervous System ◽  
The Brain

Synaptopathies are diseases with synapse defects as shared pathogenic features, encompassing neurodegenerative disorders such as Parkinson’s disease (PD). In sporadic PD, the most common age-related neurodegenerative movement disorder, nigrostriatal dopaminergic deficits are responsible for the onset of motor symptoms that have been related toα-synuclein deposition at synaptic sites. Indeed,α-synuclein accumulation can impair synaptic dopamine release and induces the death of nigrostriatal neurons. While in physiological conditions the protein can interact with and modulate synaptic vesicle proteins and membranes, numerous experimental evidences have confirmed that its pathological aggregation can compromise correct neuronal functioning. In addition, recent findings indicate thatα-synuclein pathology spreads into the brain and can affect the peripheral autonomic and somatic nervous system. Indeed, monomeric, oligomeric, and fibrillaryα-synuclein can move from cell to cell and can trigger the aggregation of the endogenous protein in recipient neurons. This novel “prion-like” behavior could further contribute to synaptic failure in PD and other synucleinopathies. This review describes the major findings supporting the occurrence ofα-synuclein pathology propagation in PD and discusses how this phenomenon could induce or contribute to synaptic injury and degeneration.

First detection of serotonin in the nervous system of the marine calanoid copepod Centropages typicus

2005 ◽  
Vol 85 (1) ◽  
pp. 71-72 ◽  
Author(s):  
D. Benzid ◽  
C. Morris ◽  
R.-M. Barthélémy
Keyword(s):  
Nervous System ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Calanoid Copepod ◽  
Marine Species ◽  
Biological Processes ◽  
Calanoid Copepods ◽  
The Brain ◽  
Serotoninergic Nervous System ◽  
Centropages Typicus

This investigation constitutes the first study of the serotoninergic nervous system in calanoid copepods (crustaceans). Serotonin (5-HT), a neurotransmitter which plays a part in many biological processes, has been detected by immunofluorescence in the brain, the circumoesophageal collar and the ventral nerve cord of the marine species Centropages typicus.

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