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Journal of Smooth Muscle Research =... Jun 2005The micturition reflex is one of the autonomic reflexes, but the release of urine is regulated by voluntary neural mechanisms that involve centers in the brain and... (Review)
Review
The micturition reflex is one of the autonomic reflexes, but the release of urine is regulated by voluntary neural mechanisms that involve centers in the brain and spinal cord. The micturition reflex is a bladder-to-bladder contraction reflex for which the reflex center is located in the rostral pontine tegmentum (pontine micturition center: PMC). There are two afferent pathways from the bladder to the brain. One is the dorsal system and the other is the spinothalamic tract. Afferents to the PMC ascend in the spinotegmental tract, which run through the lateral funiculus of the spinal cord. The efferent pathway from the PMC also runs through the lateral funiculus of the spinal cord to inhibit the thoracolumbar sympathetic nucleus and the sacral pudendal nerve nucleus, while promoting the activity of the sacral parasymapathetic nucleus. Inhibition of the sympathetic nucleus and pudendal nerve nucleus induces relaxation of the bladder neck and the external urethral sphincter, respectively. There are two centers that inhibit micturition in the pons, which are the pontine urine storage center and the rostral pontine reticular formation. In the lumbosacral cord, excitatory glutamatergic and inhibitory glycinergic/GABAergic neurons influence both the afferent and efferent limbs of the micturition reflex. The activity of these neurons is affected by the pontine activity. There are various excitatory and inhibitory areas co-existing in the brain, but the brain has an overall inhibitory effect on micturition, and thus maintains continence. For micturition to occur, the cerebrum must abate its inhibitory influence on the PMC.
Topics: Animals; Central Nervous System; Humans; Urinary Bladder; Urination; Urine
PubMed: 16006745
DOI: 10.1540/jsmr.41.117 -
Veterinary Pathology Jan 2023This report describes 2 events of degenerative myelopathy in 4- to 27-day-old piglets, with mortality rates reaching 40%. Sows were fed rations containing low levels of...
This report describes 2 events of degenerative myelopathy in 4- to 27-day-old piglets, with mortality rates reaching 40%. Sows were fed rations containing low levels of pantothenic acid. Piglets presented with severe depression, weakness, ataxia, and paresis, which were more pronounced in the pelvic limbs. No significant gross lesions were observed. Histologically, there were degeneration and necrosis of neurons in the spinal cord, primarily in the thoracic nucleus in the thoracic and lumbar segments, and motor neurons in nucleus IX of the ventral horn in the cervical and lumbar intumescence. Minimal-to-moderate axonal and myelin degeneration was observed in the dorsal funiculus of the spinal cord and in the dorsal and ventral nerve roots. Immunohistochemistry demonstrated depletion of acetylcholine neurotransmitters in motor neurons and accumulation of neurofilaments in the perikaryon of neurons in the thoracic nucleus and motor neurons. Ultrastructurally, the thoracic nucleus neurons and motor neurons showed dissolution of Nissl granulation. The topographical distribution of the lesions indicates damage to the second-order neurons of the spinocerebellar tract, first-order axon cuneocerebellar tract, and dorsal column-medial lemniscus pathway as the cause of the conscious and unconscious proprioceptive deficit, and damage to the alpha motor neuron as the cause of the motor deficit. Clinical signs reversed and no new cases occurred after pantothenic acid levels were corrected in the ration, and piglets received parenteral administration of pantothenic acid. This study highlights the important and practical use of detailed neuropathological analysis to refine differential diagnosis.
Topics: Animals; Swine; Female; Pantothenic Acid; Spinal Cord; Neurons; Medulla Oblongata; Spinal Cord Diseases; Swine Diseases
PubMed: 36250539
DOI: 10.1177/03009858221128920 -
The Journal of Neuroscience : the... Aug 2023Axon fasciculation is thought to be a critical step in neural circuit formation and function. Recent studies have revealed various molecular mechanisms that underlie...
Axon fasciculation is thought to be a critical step in neural circuit formation and function. Recent studies have revealed various molecular mechanisms that underlie axon fasciculation; however, the impacts of axon fasciculation, and its corollary, defasciculation, on neural circuit wiring remain unclear. Corticospinal (CS) neurons in the sensorimotor cortex project axons to the spinal cord to control skilled movements. In rodents, the axons remain tightly fasciculated in the brain and traverse the dorsal funiculus of the spinal cord. Here we show that plexinA1 (PlexA1) and plexinA3 (PlexA3) receptors are expressed by CS neurons, whereas their ligands, semaphorin-5A (Sema5A) and semaphorin-5B (Sema5B) are expressed in the medulla at the decussation site of CS axons to inhibit premature defasciculation of these axons. In the absence of Sema5A/5B-PlexA1/A3 signaling, some CS axons are prematurely defasciculated in the medulla of the brainstem, and those defasciculated CS axons aberrantly transverse in the spinal gray matter instead of the spinal dorsal funiculus. In the absence of Sema5A/Sema5B-PlexA1/A3 signaling, CS axons, which would normally innervate the lumbar spinal cord, are unbundled in the spinal gray matter, and prematurely innervate the cervical gray matter with reduced innervation of the lumbar gray matter. In both and mutant mice (both sexes), stimulation of the hindlimb motor cortex aberrantly evokes robust forelimb muscle activation. Finally, and mutant mice show deficits in skilled movements. These results suggest that proper fasciculation of CS axons is required for appropriate neural circuit wiring and ultimately affect the ability to perform skilled movements. Axon fasciculation is believed to be essential for neural circuit formation and function. However, whether and how defects in axon fasciculation affect the formation and function of neural circuits remain unclear. Here we examine whether the transmembrane proteins semaphorin-5A (Sema5A) and semaphorin-5B (Sema5B), and their receptors, plexinA1 (PlexA1) and plexinA3 (PlexA3) play roles in the development of corticospinal circuits. We find that Sema5A/Sema5B and PlexA1/A3 are required for proper axon fasciculation of corticospinal neurons. Furthermore, and mutant mice show marked deficits in skilled motor behaviors. Therefore, these results strongly suggest that proper corticospinal axon fasciculation is required for the appropriate formation and functioning of corticospinal circuits in mice.
Topics: Female; Male; Mice; Animals; Semaphorins; Axon Fasciculation; Neurons; Axons; Spinal Cord
PubMed: 37344234
DOI: 10.1523/JNEUROSCI.0073-22.2023 -
Current Topics in Developmental Biology 2021Commissural axons have been a key model system for identifying axon guidance signals in vertebrates. This review summarizes the current thinking about the molecular and... (Review)
Review
Commissural axons have been a key model system for identifying axon guidance signals in vertebrates. This review summarizes the current thinking about the molecular and cellular mechanisms that establish a specific commissural neural circuit: the dI1 neurons in the developing spinal cord. We assess the contribution of long- and short-range signaling while sequentially following the developmental timeline from the birth of dI1 neurons, to the extension of commissural axons first circumferentially and then contralaterally into the ventral funiculus.
Topics: Animals; Axon Guidance; Axons; Neurons; Spinal Cord
PubMed: 33706918
DOI: 10.1016/bs.ctdb.2020.10.009 -
Journal of Neurology, Neurosurgery, and... Feb 1974In a patient with reflex myoclonus limited to the right side of the body, stimulation of the right median nerve in the index finger or wrist elicited a very large...
In a patient with reflex myoclonus limited to the right side of the body, stimulation of the right median nerve in the index finger or wrist elicited a very large somatosensory evoked response (SER) and a long loop C reflex which represents an electrically evoked myoclonic response. It is suggested that the pathway for the C reflex is through peripheral nerve, dorsal funiculus of spinal cord, contralateral VP nucleus of thalamus, sensorimotor cortex, corticospinal tract, and anterior horn cell. The large SER, C reflex, and myoclonic jerks are presumed to result from a release effect causing increased excitability at central synapses along this pathway. The patient presented has a large atrophic vascular lesion involving the left frontotemporoparietal region and involvement of pathways through the right superior cerebellar peduncle to account for the neural dysfunction.
Topics: Aged; Cerebrovascular Disorders; Diazepam; Electric Stimulation; Electroencephalography; Evoked Potentials; Female; Humans; Median Nerve; Muscle Contraction; Muscles; Myoclonus; Neural Pathways; Reflex; Secobarbital; Somatosensory Cortex; Spinal Cord; Thalamic Nuclei
PubMed: 4819909
DOI: 10.1136/jnnp.37.2.207 -
The Journal of Physiology Feb 2016Inflammatory kinins are released following spinal cord injury or neurotrauma. The effects of these kinins on ongoing locomotor activity of central pattern generator...
KEY POINTS
Inflammatory kinins are released following spinal cord injury or neurotrauma. The effects of these kinins on ongoing locomotor activity of central pattern generator networks are unknown. In the present study, kinins were shown to have short- and long-term effects on motor networks. The short-term effects included direct depolarization of interneurons and motoneurons in the ventral horn accompanied by modulation of transient receptor potential vanilloid 1-sensitive nociceptors in the dorsal horn. Over the long-term, we observed a bradykinin-mediated effect on promoting plasticity in the spinal cord. In a model of spinal cord injury, we observed an increase in microglia numbers in both the dorsal and ventral horn and, in a microglia cell culture model, we observed bradykinin-induced expression of glial-derived neurotrophic factor.
ABSTRACT
The expression and function of inflammatory mediators in the developing spinal cord remain poorly characterized. We discovered novel, short and long-term roles for the inflammatory nonapeptide bradykinin (BK) and its receptor bradykinin receptor B2 (B2R) in the neuromodulation of developing sensorimotor networks following a spinal cord injury (SCI), suggesting that BK participates in an excitotoxic cascade. Functional expression of B2R was confirmed by a transient disruptive action of BK on fictive locomotion generated by a combination of NMDA, 5-HT and dopamine. The role of BK in the dorsal horn nociceptive afferents was tested using spinal cord attached to one-hind-limb (HL) preparations. In the HL preparations, BK at a subthreshold concentration induced transient disruption of fictive locomotion only in the presence of: (1) noxious heat applied to the hind paw and (2) the heat sensing ion channel transient receptor potential vanilloid 1 (TRPV1), known to be restricted to nociceptors in the superficial dorsal horn. BK directly depolarized motoneurons and ascending interneurons in the ventrolateral funiculus. We found a key mechanism for BK in promoting long-term plasticity within the spinal cord. Using a model of neonatal SCI and a microglial cell culture model, we examined the role of BK in inducing activation of microglia and expression of glial-derived neurotrophic factor (GDNF). In the neonatal SCI model, we observed an increase in microglia numbers and increased GDNF expression restricted to microglia. In the microglia cell culture model, we observed a BK-induced increased expression of GDNF via B2R, suggesting a novel mechanism for BK spinal-mediated plasticity.
Topics: Animals; Anterior Horn Cells; Bradykinin; Cells, Cultured; Central Pattern Generators; Glial Cell Line-Derived Neurotrophic Factor; Interneurons; Locomotion; Mice; Microglia; Nerve Net; Neuronal Plasticity; Nociception; Posterior Horn Cells; Receptors, Bradykinin; Spinal Cord Injuries; TRPV Cation Channels
PubMed: 26634895
DOI: 10.1113/JP271152 -
Journal of Neurocytology Apr 1989Part of the dorsal funiculus of the adult male rat (Wistar) spinal cord was treated for 1 h at the thoracolumbar level by running hot water, at approximately 48-50...
Part of the dorsal funiculus of the adult male rat (Wistar) spinal cord was treated for 1 h at the thoracolumbar level by running hot water, at approximately 48-50 degrees C, through a polyethylene tube 2 mm in diameter in contact with the dura. Animals were fixed 1 day to 4 weeks later and the spinal cords were examined by light and electron microscopy. The affected area in the dorsal funiculus was approximately 1 mm long and less than 1 mm wide at the dorsal surface, and varied from 0.4 to 0.7 mm in depth. Within 3 days after treatment, almost all the myelin sheaths in the affected area were degraded, leaving the axons denuded, and at the same time astrocyte endfeet at the glial limiting membrane were swollen and partly destroyed. Almost all the denuded axons remained intact, exhibiting no noticeable morphological changes. There was evidence of a moderate vasogenic oedema, but minimal signs of haemorrhage in the lesion. Seven days after treatment, many immature Schwann cells but no oligodendrocytes were found between the denuded axons. By 2 weeks many of the denuded axons were remyelinated, and by 4 weeks almost all of those axons located near the pial and perivascular surfaces had been remyelinated by Schwann cells, while most of those located in the deep and marginal zones bordering the adjoining intact areas were remyelinated by oligodendrocytes. Longitudinal sections revealed that at nodes of Ranvier PNS-type myelin sheaths were apposed by either intact or newly formed CNS-type myelin sheaths. A typical glial limiting membrane was not reformed beneath the pial surface, but an inconspicuous one was found between the PNS- and CNS-type fibre areas.
Topics: Animals; Hyperthermia, Induced; Male; Microscopy, Electron; Myelin Sheath; Rats; Rats, Inbred Strains; Spinal Cord
PubMed: 2732760
DOI: 10.1007/BF01206664 -
The Journal of Comparative Neurology Nov 2009To characterize neuronal pathways that release opioid peptides in the rat dorsal horn, multiple-label immunohistochemistry, confocal microscopy, and computerized...
To characterize neuronal pathways that release opioid peptides in the rat dorsal horn, multiple-label immunohistochemistry, confocal microscopy, and computerized co-localization measures were used to characterize opioid-containing terminals and cells. An antibody that selectively recognized beta-endorphin labeled fibers and neurons in the ventral horn as well as fibers in the lateral funiculus and lamina X, but practically no fibers in the dorsal horn. An anti-enkephalin antibody, which recognized Leu-, Met-, and Phe-Arg-Met-enkephalin, labeled the dorsolateral funiculus and numerous puncta in laminae I-III and V of the dorsal horn. An antibody against Phe-Arg-Met-enkephalin, which did not recognize Leu- and Met-enkephalin, labeled the same puncta. Antibodies against dynorphin and prodynorphin labeled puncta and fibers in laminae I, II, and V, as well as some fibers in the rest of the dorsal horn. Dynorphin and prodynorphin immunoreactivities colocalized in some puncta and fibers, but the prodynorphin antibody additionally labeled cell bodies. There was no co-localization of dynorphin (or prodynorphin) with enkephalin (or Phe-Arg-Met-enkephalin). Enkephalin immunoreactivity did not colocalize with the C-fiber markers calcitonin gene-related peptide (CGRP), substance P, and isolectin B4. In contrast, there was some colocalization of dynorphin and prodynorphin with CGRP and substance P, but not with isolectin B4. Both enkephalin and dynorphin partly colocalized with vesicular glutamate transporter 2, a marker of glutamatergic terminals. The prodynorphin-positive neurons in the dorsal horn were distinct from neurons expressing mu-opioid receptors, neurokinin 1 receptors, and protein kinase C-gamma. These results show that enkephalins and dynorphins are present in different populations of dorsal horn neurons. In addition, dynorphin is present in some C-fibers.
Topics: Animals; Dynorphins; Enkephalins; Fluorescent Antibody Technique; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Nerve Fibers, Unmyelinated; Neural Pathways; Neurons; Neurons, Afferent; Posterior Horn Cells; Rats; Rats, Sprague-Dawley; Spinal Cord; beta-Endorphin
PubMed: 19711397
DOI: 10.1002/cne.22130 -
The Journal of Physiology Dec 19811. Extracellular and intracellular recordings were made from dorsal horn neurones sending their axons through the dorsal columns in cats anaesthetized with chloralose...
1. Extracellular and intracellular recordings were made from dorsal horn neurones sending their axons through the dorsal columns in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. 2. Seventeen neurones were injected with horseradish peroxidase through the intracellular micro-electrode, recovered from the histological material and shown to send their axons into the dorsal columns. 3. The cells had axonal conduction velocities of 30--47 ms-1; excitatory receptive fields that usually showed multireceptive characteristics, often including input from sensitive mechanoreceptors in glabrous skin; a third of the sample had a marked subliminal fringe to the excitatory field; inhibitory fields were usually situated proximal to the excitatory field and contiguous with it. 4. The cells were located in laminae III, IV and medial V. Dorsal cells had restricted dendritic trees that ascended in an essentially cylindrical volume of tissue through lamina II and often into I; cells intermediate in depth had more primary dendrites than the others, usually dorsally directed into lamina II, and a more extensive rostro-caudal development; deep, medial cells had dendritic trees that radiated extensively from the cell body but were restricted to the transverse plane. Two cells had axons that ascended the dorsolateral funiculus for a few mm before re-entering the dorsal horn, crossing it and reaching the dorsal columns. Collaterals were given off the axons in the grey matter, in the dorsolateral funiculus and the dorsal columns. 5. The form and function of the neurones are discussed.
Topics: Animals; Axons; Cats; Dendrites; Evoked Potentials; Horseradish Peroxidase; Neural Conduction; Neural Pathways; Neurons; Spinal Cord
PubMed: 7338813
DOI: 10.1113/jphysiol.1981.sp013970