scholarly journals Sexual Experience Induces the Expression of Gastrin-Releasing Peptide and Oxytocin Receptors in the Spinal Ejaculation Generator in Rats

2021 ◽  
Vol 22 (19) ◽  
pp. 10362
Author(s):  
Takumi Oti ◽  
Ryota Ueda ◽  
Ryoko Kumagai ◽  
Junta Nagafuchi ◽  
Takashi Ito ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Sexual Activity ◽  
Neural Circuits ◽  
Sexual Experience ◽  
Lumbar Spinal Cord ◽  
Gastrin Releasing Peptide ◽  
Oxytocin Receptors ◽  
Male Sexual Function ◽  
Lumbar Spinal ◽  
The Brain

Male sexual function in mammals is controlled by the brain neural circuits and the spinal cord centers located in the lamina X of the lumbar spinal cord (L3–L4). Recently, we reported that hypothalamic oxytocin neurons project to the lumbar spinal cord to activate the neurons located in the dorsal lamina X of the lumbar spinal cord (dXL) via oxytocin receptors, thereby facilitating male sexual activity. Sexual experiences can influence male sexual activity in rats. However, how this experience affects the brain–spinal cord neural circuits underlying male sexual activity remains unknown. Focusing on dXL neurons that are innervated by hypothalamic oxytocinergic neurons controlling male sexual function, we examined whether sexual experience affects such neural circuits. We found that >50% of dXL neurons were activated in the first ejaculation group and ~30% in the control and intromission groups in sexually naïve males. In contrast, in sexually experienced males, ~50% of dXL neurons were activated in both the intromission and ejaculation groups, compared to ~30% in the control group. Furthermore, sexual experience induced expressions of gastrin-releasing peptide and oxytocin receptors in the lumbar spinal cord. This is the first demonstration of the effects of sexual experience on molecular expressions in the neural circuits controlling male sexual activity in the spinal cord.

Does Motor Learning Occur in the Spinal Cord?

1997 ◽  
Vol 3 (5) ◽  
pp. 287-294 ◽  
Author(s):  
V. Reggie Edgerton ◽  
Roland R. Roy ◽  
Ray De Leon Niranjala Tillakaratne ◽  
John A. Hodgson
Keyword(s):  
Spinal Cord ◽  
Motor Task ◽  
Lumbar Spinal Cord ◽  
Lumbosacral Spinal Cord ◽  
Patterns Of Use ◽  
The Neural Network ◽  
The Central Nervous System ◽  
Network Plasticity ◽  
Lumbar Spinal ◽  
The Brain

It is becoming clear that the plasticity of the sensory-motor networks of the adult mammalian lumbosacral spinal cord is much greater than and is more dependent on the specific patterns of use than has been previously assumed. Using a wide variety of experimental paradigms in which the lumbar spinal cord is isolated from the brain, it has been shown that the lumbosacral spinal cord can learn to execute stepping or standing more successfully if that specific task is practiced. It also appears that the sensory input associated with the motor task and/or the manner in which it is interpreted by the spinal cord are important components of the neural network plasticity. Early evidence suggests that several neurotransmitter systems in the spinal cord, to include glycinergic and GABAergic systems, adapt to repetitive use. These studies extend a growing body of evidence suggesting that memory and learning are widely distributed phenomena within the central nervous system. NEUROSCIENTIST 3:287–294, 1997

scholarly journals High-Voltage Electron Microscopy Reveals Direct Synaptic Inputs from a Spinal Gastrin-Releasing Peptide System to Neurons of the Spinal Nucleus of Bulbocavernosus

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 417-421 ◽  
Author(s):  
Hirotaka Sakamoto ◽  
Tatsuo Arii ◽  
Mitsuhiro Kawata
Keyword(s):  
Electron Microscopy ◽  
Spinal Cord ◽  
High Voltage ◽  
Lumbar Spinal Cord ◽  
Sexually Dimorphic ◽  
High Voltage Electron Microscopy ◽  
Synaptic Inputs ◽  
Gastrin Releasing Peptide ◽  
Voltage Electron ◽  
Lumbar Spinal

Abstract The spinal nucleus of bulbocavernosus (SNB) is a sexually dimorphic motor nucleus located in the anterior horn of the fifth and sixth lumbar segments of the spinal cord that plays a significant role in male sexual function. We recently found that a sexually dimorphic expression of gastrin-releasing peptide (GRP) in the lumbar spinal cord regulates male copulatory reflexes. Although it is reported that these systems are both profoundly regulated by circulating androgen levels in male rats, no direct evidence has been reported regarding GRP synaptic inputs onto SNB motoneurons. The aim of the current study was to determine the axodendritic synaptic inputs of spinal GRP neurons to SNB motoneurons. Immunoelectron microscopy, combined with a retrograde tracing technique using high-voltage electron microscopy (HVEM), provided a three-dimensional visualization of synaptic contacts from the GRP system in the lumbar spinal cord onto SNB motoneurons. HVEM analysis clearly demonstrated that GRP-immunoreactive axon terminals directly contact dendrites that extend into the dorsal gray commissure from the SNB. These HVEM findings provide an ultrastructural basis for understanding how the spinal GRP system regulates male sexual behavior.

scholarly journals Spinal Cord Injury Causes Reduction of Galanin and Gastrin Releasing Peptide mRNA Expression in the Spinal Ejaculation Generator of Male Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
James W. Wiggins ◽  
Jonathan E. Sledd ◽  
Lique M. Coolen
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Gastrin Releasing Peptide ◽  
Cord Injury ◽  
Contusion Injury ◽  
Spinal Contusion ◽  
Lumbar Spinal ◽  
Injury Causes

Spinal cord injury (SCI) in men is commonly associated with sexual dysfunction, including anejaculation, and chronic mid-thoracic contusion injury in male rats also impairs ejaculatory reflexes. Ejaculation is controlled by a spinal ejaculation generator consisting of a population of lumbar spinothalamic (LSt) neurons that control ejaculation through release of four neuropeptides including galanin and gastrin releasing peptide (GRP) onto lumbar and sacral autonomic and motor nuclei. It was recently demonstrated that spinal contusion injury in male rats caused reduction of GRP-immunoreactivity, but not galanin-immunoreactivity in LSt cells, indicative of reduced GRP peptide levels, but inconclusive results for galanin. The current study further tests the hypothesis that contusion injury causes a disruption of GRP and galanin mRNA in LSt cells. Male rats received mid-thoracic contusion injury and galanin and GRP mRNA were visualized 8 weeks later in the lumbar spinal cord using fluorescent in situ hybridization. Spinal cord injury significantly reduced GRP and galanin mRNA in LSt cells. Galanin expression was higher in LSt cells compared to GRP. However, expression of the two transcripts were positively correlated in LSt cells in both sham and SCI animals, suggesting that expression for the two neuropeptides may be co-regulated. Immunofluorescent visualization of galanin and GRP peptides demonstrated a significant reduction in GRP-immunoreactivity, but not galanin in LSt cells, confirming the previous observations. In conclusion, SCI reduced GRP and galanin expression in LSt cells with an apparent greater impact on GRP peptide levels. GRP and galanin are both essential for triggering ejaculation and thus such reduction may contribute to ejaculatory dysfunction following SCI in rats.

scholarly journals Androgen Regulates the Sexually Dimorphic Gastrin-Releasing Peptide System in the Lumbar Spinal Cord that Mediates Male Sexual Function

Endocrinology ◽  
2009 ◽  
Vol 150 (8) ◽  
pp. 3672-3679 ◽  
Author(s):  
Hirotaka Sakamoto ◽  
Keiko Takanami ◽  
Damian G. Zuloaga ◽  
Ken-ichi Matsuda ◽  
Cynthia L. Jordan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Real Time ◽  
Quantitative Pcr ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Testicular Feminization ◽  
Western Blots ◽  
Gastrin Releasing Peptide ◽  
Real Time Quantitative Pcr ◽  
Lumbar Spinal

A collection of neurons in the upper lumbar spinal cord of male rats projects to the lower lumbar spinal cord, releasing gastrin-releasing peptide (GRP) onto somatic and autonomic centers known to regulate male sexual reflexes such as erection and ejaculation. Because these reflexes are androgen dependent, we asked whether manipulating levels of androgen in adult rats would affect GRP expression in this spinal center. We found that castration resulted, 28 d later, in a profound decrease in the expression of GRP in the spinal cord, as reflected in immunocytochemistry and competitive ELISA for the protein as well as real-time quantitative PCR for the transcript. These effects were prevented if the castrates were treated with testosterone propionate. Genetically male (XY) rats with the dysfunctional testicular feminization allele for the androgen receptor (AR) displayed GRP mRNA and protein levels in the spinal cord similar to those of females, indicating that androgen normally maintains the system through AR. We saw no effect of castration or the testicular feminization allele on expression of the receptor for GRP in the spinal cord, but castration did reduce expression of AR transcripts within the spinal cord as revealed by real-time quantitative PCR and Western blots. Taken together, these results suggest that androgen signaling plays a pivotal role in the regulation of GRP expression in male lumbar spinal cord. A greater understanding of how androgen modulates the spinal GRP system might lead to new therapeutic approaches to male sexual dysfunction.

scholarly journals A Novel Anti-Inflammatory d-Peptide Inhibits Disease Phenotype Progression in an ALS Mouse Model

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1590
Author(s):  
Julia Post ◽  
Vanessa Kogel ◽  
Anja Schaffrath ◽  
Philipp Lohmann ◽  
Nadim Joni Shah ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Mouse Model ◽  
Brain Stem ◽  
Motor Coordination ◽  
Therapeutic Potential ◽  
Lumbar Spinal Cord ◽  
Motor Deficits ◽  
Disease Phenotype ◽  
Lumbar Spinal ◽  
The Brain

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by selective neuronal death in the brain stem and spinal cord. The cause is unknown, but an increasing amount of evidence has firmly certified that neuroinflammation plays a key role in ALS pathogenesis. Neuroinflammation is a pathological hallmark of several neurodegenerative disorders and has been implicated as driver of disease progression. Here, we describe a treatment study demonstrating the therapeutic potential of a tandem version of the well-known all-d-peptide RD2 (RD2RD2) in a transgenic mouse model of ALS (SOD1*G93A). Mice were treated intraperitoneally for four weeks with RD2RD2 vs. placebo. SOD1*G93A mice were tested longitudinally during treatment in various behavioural and motor coordination tests. Brain and spinal cord samples were investigated immunohistochemically for gliosis and neurodegeneration. RD2RD2 treatment in SOD1*G93A mice resulted not only in a reduction of activated astrocytes and microglia in both the brain stem and lumbar spinal cord, but also in a rescue of neurons in the motor cortex. RD2RD2 treatment was able to slow progression of the disease phenotype, especially the motor deficits, to an extent that during the four weeks treatment duration, no significant progression was observed in any of the motor experiments. Based on the presented results, we conclude that RD2RD2 is a potential therapeutic candidate against ALS.

Descending inhibitory influences from periaqueductal gray, nucleus raphe magnus, and adjacent reticular formation. I. Effects on lumbar spinal cord nociceptive and nonnociceptive neurons

1983 ◽  
Vol 49 (4) ◽  
pp. 932-947 ◽  
Author(s):  
B. G. Gray ◽  
J. O. Dostrovsky
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Periaqueductal Gray ◽  
Spinal Cord Dorsal Horn ◽  
Lumbar Spinal Cord ◽  
Nucleus Raphe Magnus ◽  
Nucleus Reticularis ◽  
Raphe Magnus ◽  
Lumbar Spinal ◽  
The Brain

1. This study examined the inhibitory effects of conditioning stimuli delivered to the periaqueductal gray (PAG), nucleus cuneiformis (CU), nucleus raphe magnus (NRM), nucleus reticularis gigantocellularis (NGC), and nucleus reticularis magnocellularis (NMC) on functionally identified neurons of the lumbar spinal cord dorsal horn in chloralose-anesthetized or decerebrate cats. 2. Neurons were classified according to their responses to a variety of cutaneous stimuli as low-threshold mechanoreceptive (LTM), wide dynamic range (WDR), or nociceptive specific (NS). The major aim of this study was to determine whether there was a difference in the effectiveness of the brain stem stimulation-produced inhibition of nociceptive (noci) neurons (consisting of both WDR and NS neurons) and the LTM non-nociceptive (nonnoci) neurons. There were no statistical differences in the susceptibility of WDR and NS neurons to brain stem-induced inhibition. 3. Most neurons tested could be inhibited by stimulation of any of the brain stem regions tested. In all cases the percentage of noci neurons inhibited from a given region was higher than the percentage of nonnoci neurons; however, this difference was only statistically significant in the case of NMC stimulation. 4. Threshold current intensities necessary to produce inhibition were determined for each neuron from each stimulation site. Although there was a trend for noci neurons to require slightly lower current intensities, there was in fact no statistically significant difference in the inhibitory thresholds between noci and nonnoci neurons for any of the regions tested. 5. A comparison of the mean threshold currents for the five regions studied revealed that the lowest stimulation currents were obtained in NMC with NRM, CU, NGC, and PAG, each requiring progressively higher current intensities in order to produce inhibition. 6. These results indicate that stimulation in PAG and NRM not only inhibits the responses of noci neurons but also those of nonnoci neurons. Moreover, stimulation in reticular regions adjacent to these two regions is effective in inhibiting the responses of both noci and nonnoci neurons.

Sexually dimorphic gastrin-releasing peptide system in the lumbar spinal cord controls masculine reproductive functions in rats

2009 ◽  
Vol 65 ◽  
pp. S41
Author(s):  
Hirotaka Sakamoto ◽  
Ken-Ichi Matsuda ◽  
Damian G. Zuloaga ◽  
Hisayuki Hongu ◽  
Etsuko Wada ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Lumbar Spinal Cord ◽  
Sexually Dimorphic ◽  
Gastrin Releasing Peptide ◽  
Peptide System ◽  
Lumbar Spinal

scholarly journals Retrograde Transport of Transmissible Mink Encephalopathy within Descending Motor Tracts

2002 ◽  
Vol 76 (11) ◽  
pp. 5759-5768 ◽  
Author(s):  
Jason C. Bartz ◽  
Anthony E. Kincaid ◽  
Richard A. Bessen
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Neuronal Damage ◽  
Red Nucleus ◽  
Disease Onset ◽  
Retrograde Transport ◽  
Lumbar Spinal Cord ◽  
Transmissible Mink Encephalopathy ◽  
Lumbar Spinal ◽  
The Brain

ABSTRACT The spread of the abnormal conformation of the prion protein, PrPSc, within the spinal cord is central to the pathogenesis of transmissible prion diseases, but the mechanism of transport has not been determined. For this report, the route of transport of the HY strain of transmissible mink encephalopathy (TME), a prion disease of mink, in the central nervous system following unilateral inoculation into the sciatic nerves of Syrian hamsters was investigated. PrPSc was detected at 3 weeks postinfection in the lumbar spinal cord and ascended to the brain at a rate of approximately 3.3 mm per day. At 6 weeks postinfection, PrPSc was detected in the lateral vestibular nucleus and the interposed nucleus of the cerebellum ipsilateral to the site of sciatic nerve inoculation and in the red nucleus contralateral to HY TME inoculation. At 9 weeks postinfection, PrPSc was detected in the contralateral hind limb motor cortex and reticular thalamic nucleus. These patterns of PrPSc brain deposition at various times postinfection were consistent with that of HY TME spread from the sciatic nerve to the lumbar spinal cord followed by transsynaptic spread and retrograde transport to the brain and brain stem along descending spinal tracts (i.e., lateral vestibulospinal, rubrospinal, and corticospinal). The absence of PrPSc from the spleen suggested that the lymphoreticular system does not play a role in neuroinvasion following sciatic nerve infection. The rapid disease onset following sciatic nerve infection demonstrated that HY TME can spread by retrograde transport along specific descending motor pathways of the spinal cord and, as a result, can initially target brain regions that control vestibular and motor functions. The early clinical symptoms of HY TME infection such as head tremor and ataxia were consistent with neuronal damage to these brain areas.

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