Superior Cervical Ganglion Research Articles

Sympathetic motor neuron dysfunction is a missing link in age-associated sympathetic overactivity

Overactivity of the sympathetic nervous system is a hallmark of aging. The cellular mechanisms behind this overactivity remain poorly understood, with most attention paid to likely central nervous system components. In this work, we hypothesized that aging also affects the function of motor neurons in the peripheral sympathetic ganglia. To test this hypothesis, we compared the electrophysiological responses and ion-channel activity of neurons isolated from the superior cervical ganglia of young (12 weeks), middle-aged (64 weeks), and old (115 weeks) mice. These approaches showed that aging does impact the intrinsic properties of sympathetic motor neurons, increasing spontaneous and evoked firing responses. A reduction of M current emerged as a major contributor to age-related hyperexcitability. Thus, it is essential to consider the effect of aging on motor components of the sympathetic reflex as a crucial part of the mechanism involved in sympathetic overactivity.

Sympathetic motor neuron dysfunction is a missing link in age-associated sympathetic overactivity.

Overactivity of the sympathetic nervous system is a hallmark of aging. The cellular mechanisms behind this overactivity remain poorly understood, with most attention paid to likely central nervous system components. In this work, we hypothesized that aging also affects the function of motor neurons in the peripheral sympathetic ganglia. To test this hypothesis, we compared the electrophysiological responses and ion-channel activity of neurons isolated from the superior cervical ganglia of young (12 weeks), middle-aged (64 weeks), and old (115 weeks) mice. These approaches showed that aging does impact the intrinsic properties of sympathetic motor neurons, increasing spontaneous and evoked firing responses. A reduction of M current emerged as a major contributor to age-related hyperexcitability. Thus, it is essential to consider the effect of aging on motor components of the sympathetic reflex as a crucial part of the mechanism involved in sympathetic overactivity.

Anatomical Targeting of the Superior Cervical Ganglion on CT imaging for Guidance of Endovascular Transmural Intervention

Endovascular transmural targeting of cervical and cranial perivascular structures is a novel approach for minimally invasive delivery of therapeutics. Components of the autonomic nervous system are in close anatomic proximity to major cervical vasculature and, therefore, represent potential targets for intervention. The superior cervical ganglion (SCG) is a discrete structure of interest for this approach, as sympathetic blockade may have therapeutic effects for various conditions. Variability of SCG location and its relationship to large cervical vessels, and the feasibility of endovascular transmural targeting has not been elucidated. In this retrospective study, computed tomography angiography (CTA) of head and neck from patients with subarachnoid hemorrhage (SAH) or cerebral aneurysms were reviewed. SCG dimensions and spatial relationship to cervical vessels were measured. Measured anatomic parameters were used to determine endovascular transmural accessibility of the SCG from various cervical vessels. 159 SCGs were identified and measured from 314 unilateral neck images of sufficient quality. SCGs had an average radio-opacity of 49.6 Hounsfield Units, length of 1.91cm, and width of 0.71cm. Internal carotid artery (ICA) has the longest contact length with the SCG (mean=1.80cm) compared to other major cervical vessels. 95% of SCGs were accessible from ICA using an endovascular transmural approach, with the majority of SCGs located anteromedially to the ICA. This is the first anatomical study to provide pertinent targeting information for endovascular transmural access to the SCG using CTA. In most cases, endovascular transmural access to the SCG is anatomically feasible from the proximal cervical ICA.

Bilateral Correlational Behavior of Pyroglutamate Aminopeptidase I Activity in Rat Photoneuroendocrine Locations During a Standard 12:12 h Light–Dark Cycle

We previously described the circadian variation and bilateral distribution of pyroglutamate aminopeptidase I (pGluPI) activity levels in photoneuroendocrine locations of adult male rats during a standard 12:12 h light–dark cycle. However, the correlational analysis between such locations has not yet been studied. This may provide new data about the unilateral and bilateral functional interaction between photoneuroendocrine locations under light and dark conditions. We analyzed the correlations between locations of a photoneuroendocrine circuit consisting of retina, anterior hypothalamus, superior cervical ganglion, and pineal gland, as well as other related photoneuroendocrine locations: posterior hypothalamus, anterior pituitary, posterior pituitary, occipital cortex, and serum. In particular, we analyzed the correlations between the left retina or the right retina versus the rest of the locations, as well as the correlations between the left and right sides of paired structures at the different time points selected from 12 h light and 12 h dark periods. Also, the profiles of correlational results were compared with the corresponding mean levels. The results demonstrate the complexity of asymmetrical brain behavior. The correlation profile did not always parallel the profile observed with the mean activity values. The diurnal behavior of correlations with the left or right retina differed from one location to another. Likewise, the diurnal variation of correlations between the left and right sides of the paired structures differed between them. Particularly, while most correlations between the left versus right sides of paired structures showed positive values, that of the posterior hypothalamus showed a negative value at 13 h of light period. In addition, except the posterior hypothalamus, most paired locations only correlated significantly with right retina at 07 h of the light period. The results demonstrate the dynamic complexity of brain asymmetry, which represents a challenge for understanding its functional meaning.

Identification of a postnatal period of interdependent neurogenesis and apoptosis in peripheral neurons.

During neurogenesis, excessive numbers of neurons are produced in most regions of the central and peripheral nervous systems. Nonessential neurons are eliminated by apoptosis, or programmed cell death. This has been most thoroughly characterized in the peripheral nervous system (PNS) where targets of innervation play a key role in this process. As maturing neurons project axons towards their targets of innervation, they become dependent upon these targets for survival. Survival factors, also called neurotrophic factors, are produced by targets, inhibit apoptosis cascades, and promote further growth and differentiation. Because neurotrophic factors are limited, as is target size, neurons that do not correctly and efficiently innervate targets undergo apoptosis ( Levi-Montalcini, 1987; Davies, 1996). Thus, excessive neurogenesis acts to ensure that sufficient numbers of neurons are produced during development. In the superior cervical ganglion (SCG), this process of neurogenesis and subsequent apoptosis is reported to be complete by postnatal day 3-4 (P3-P4) in mice. Surprisingly, we observed significant numbers of apoptotic neurons out to P14, and neurogenesis was still present at P14 as well. In both the SCG and geniculate ganglion (GG), postnatal neurogenesis was dependent on apoptosis because little or no postnatal neurogenesis was observed in Bax-/- mice, in which apoptosis is eliminated. These results indicate that both neurogenesis and apoptosis continue to occur well after birth in peripheral ganglia, and that neurogenesis depends on apoptosis, suggesting that neurogenesis continues postnatally to replace neurons that are eliminated during synaptic refinement.

Superior cervical ganglionectomy attenuates vascular remodeling in spontaneously hypertensive rats.

Sympathetic hyperactivity contributes to the pathogenesis of hypertension. However, it is unclear whether the excessive sympathetic activity is an independent and crucial factor for vascular remodeling in hypertension. This study focused on the effect of local sympathetic denervation with superior cervical ganglionectomy (SCGx) on vascular remodeling. Surgical bilateral SCGx was performed in 9-week-old male Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Control rats received sham-operation without SCGx. All measurements were made 4 weeks after the surgery. The effectiveness of SCGx was confirmed by the eye features of Horner syndrome, greatly reduced tyrosine hydroxylase (TH) contents in the superior cervical ganglion (SCG)-innervated arteries in the head. Although SCGx had no significant effects on blood pressure and heart rate in WKY and SHR, it attenuated vascular remodeling of facial artery and superficial temporal artery in SHR, two representative SCG-innervated extracranial arteries, without significant effects on non-SCG-innervated thoracic aorta and mesenteric artery. SCGx-treated SHR had more auricular blood flow and retina microvasculature than sham-operated SHR. However, SCGx had only a mild effect in attenuating the vascular remodeling of basilar artery and middle cerebral artery, two representative SCG-innervated intracranial arteries, in SHR. SCGx-treated SHR exhibited upregulation of α-smooth muscle actin, downregulation of proliferating cell nuclear antigen, and attenuation of oxidative stress and inflammation in facial artery and superficial temporal artery. Sympathetic denervation by SCGx in SHR attenuated local vascular remodeling, suggesting that sympathetic overactivity is a crucial pathogenic factor of vascular remodeling in SHR.

Alzheimer's Disease: An Attempt of Total Recall.

This review is an attempt to compile existing hypotheses on the mechanisms underlying the initiation and progression of Alzheimer's disease (AD), starting from sensory impairments observed in AD and concluding with molecular events that are typically associated with the disease. These events include spreading of amyloid plaques and tangles of hyperphosphorylated tau and formation of Hirano and Biondi bodies as well as the development of oxidative stress. We have detailed the degenerative changes that occur in several neuronal populations, including the cholinergic neurons in the nucleus basalis of Meynert, the histaminergic neurons in the tuberomammillary nucleus, the serotonergic neurons in the raphe nuclei, and the noradrenergic neurons in the locus coeruleus. Furthermore, we discuss the potential role of iron accumulation in the brains of subjects with AD in the disease progression which served as a basis for the idea that iron chelation in the brain may mitigate oxidative stress and decelerate disease development. We also draw attention to possible role of sympathetic system and, more specifically, noradrenergic neurons of the superior cervical ganglion in triggering of the disease. We also explore the alternative possibility of compensatory protective changes that may occur in these neurons to support cholinergic function in the forebrain of subjects with AD.

Chronically Low NMNAT2 Expression Causes Sub-lethal SARM1 Activation and Altered Response to Nicotinamide Riboside in Axons.

Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is an endogenous axon survival factor that maintains axon health by blocking activation of the downstream pro-degenerative protein SARM1 (sterile alpha and TIR motif containing protein 1). While complete absence of NMNAT2 in mice results in extensive axon truncation and perinatal lethality, the removal of SARM1 completely rescues these phenotypes. Reduced levels of NMNAT2 can be compatible with life; however, they compromise axon development and survival. Mice born expressing sub-heterozygous levels of NMNAT2 remain overtly normal into old age but develop axonal defects in vivo and in vitro as well as behavioural phenotypes. Therefore, it is important to examine the effects of constitutively low NMNAT2 expression on SARM1 activation and disease susceptibility. Here we demonstrate that chronically low NMNAT2 levels reduce prenatal viability in mice in a SARM1-dependent manner and lead to sub-lethal SARM1 activation in morphologically intact axons of superior cervical ganglion (SCG) primary cultures. This is characterised by a depletion in NAD(P) and compromised neurite outgrowth. We also show that chronically low NMNAT2 expression reverses the NAD-enhancing effect of nicotinamide riboside (NR) in axons in a SARM1-dependent manner. These data indicate that low NMNAT2 levels can trigger sub-lethal SARM1 activation which is detectable at the molecular level and could predispose to human axonal disorders.

Rat Sympathetic Neuron Calcium Channels Are Insensitive to Gabapentin.

The gabapentenoids such as gabapentin (GP) and pregabalin are approved for the treatment of chronic pain, but their utility is limited by persistent side effects. These adverse effects result from GPs affecting many types of neurons and muscle cells, not just the pain-sensing neurons that are the intended targets. We have recently discovered a type of peripheral neuron, rat sympathetic neurons from the superior cervical ganglion (SCG), that is uniquely insensitive to GP effects. Currents were measured using whole-cell patch-clamp electrophysiology from cells in primary culture from either the SCG or the Nodose Ganglion (NDG) as a positive control for the effects of GP. We find that the calcium current density was dramatically reduced by GP pretreatment in NDG neurons, but that neurons from the SCG were resistant. Further, when GP was cytoplasmically injected into these neurons, the resistance of SCG neurons to GP treatment persisted. These data demonstrate that rat sympathetic neurons appear to be uniquely resistant to GP treatment. These results may help us to better understand the mechanism of action of, and resistance to, GP in altering calcium channel current density, which may help to develop future treatments with fewer side effects.

The Enigma of Basilar Artery Dissections Secondary to Vasospasm Following Subarachnoid Hemorrhage. Exploration of the Unknown Effect of Superior Cervical Ganglia: A Preliminary Experimental Study.

Life-threatening basilar artery dissection (BAD) can be seen following subarachnoid hemorrhage (SAH), but it is not clear whether SAH causes dissection, or not. This study aims to investigate the relationship between degenerative changes in the superior cervical ganglia and the dissection rate of the basilar artery. In this study, after 3 weeks of experimental SAH, animals were decapitated. Eighteen rabbits were divided into three groups according to their vasospasm indices. The basilar arteries were examined by anatomical and histopathologic methods. Basilar dissection with high vasospasm index (VSI) value (VSI > 3) was detected in six animals (group I); severe basilar edema and moderate VSI value (>2.4) were detected in seven rabbits (group II); and slight VSI value (<1.5) was detected in five subjects (group III). The degenerated neuron densities of the superior cervical ganglia were 12 ± 4 n/mm3 in group I, 41 ± 8 n/mm3 in group II, and 276 ± 78 n/mm3 in group III. The dissected surface values/lumen values were calculated as (42 ± 1)/(64 ± 11) in G-I, (21 ± 6)/(89 ± 17) in group II, and (3 ± 1)/(102 ± 24) in group III. If we look at these ratios as a percentage, it was 62% in group I, 23% in group II, and 5% in group III. Inverse relationship between the degenerated neuron densities of the superior cervical ganglia and the dissected surface values of the basilar artery was observed. Common knowledge is that BAD may lead to SAH; however, this study indicates that SAH is the cause of BAD.

Sympathetic Motor Neuron Dysfunction is a Missing Link in Age-Associated Sympathetic Overactivity.

Overactivity of the sympathetic nervous system is a hallmark of aging. The cellular mechanisms behind this overactivity remain poorly understood, with most attention paid to likely central nervous system components. In this work, we hypothesized that aging also affects the function of motor neurons in the peripheral sympathetic ganglia. To test this hypothesis, we compared the electrophysiological responses and ion-channel activity of neurons isolated from the superior cervical ganglia of young (12 weeks), middle-aged (64 weeks), and old (115 weeks) mice. These approaches showed that aging does impact the intrinsic properties of sympathetic motor neurons, increasing spontaneous and evoked firing responses. A reduction of M current emerged as a major contributor to age-related hyperexcitability. Thus, it is essential to consider the effect of aging on motor components of the sympathetic reflex as a crucial part of the mechanism involved in sympathetic overactivity.

The human-specific nicotinic receptor subunit CHRFAM7A reduces α7 receptor function in human induced pluripotent stem cells-derived and transgenic mouse neurons.

We investigated the impact of the human-specific gene CHRFAM7A on the function of α7 nicotinic acetylcholine receptors (α7 nAChRs) in two different types of neurons: human-induced pluripotent stem cell (hiPSC)-derived cortical neurons, and superior cervical ganglion (SCG) neurons, taken from transgenic mice expressing CHRFAM7A. dupα7, the gene product of CHRFAM7A, which lacks a major part of the extracellular N-terminal ligand-binding domain, co-assembles with α7, the gene product of CHRNA7. We assessed the receptor function in hiPSC-derived cortical and SCG neurons with Fura-2 calcium imaging and three different α7-specific ligands: PNU282987, choline, and 4BP-TQS. Given the short-lived open state of α7 receptors, we combined the two orthosteric agonists PNU282987 and choline with the type-2 positive allosteric modulator (PAM II) PNU120596. In line with different cellular models used previously, we demonstrate that CHRFAM7A has a major impact on nicotinic α7 nAChRs by reducing calcium transients in response to all three agonists.

Preliminary study on the role and mechanism of IL-6 receptor antagonists in improving post-infarction ventricular arrhythmia

Objective: To investigate the effect of tocilizumab (TCZ) on ventricular arrhythmias (VAs) after myocardial infarction (MI) in Sprague-Dawley rats and explore its potential mechanism. Methods: The random number table method was used to divide 32 adult male Sprague-Dawley rats into 4 groups: Sham group, TCZ group, MI group and MI+TCZ group, with 8 rats in each group. The MI model was established by ligation of the left anterior descending branch of the coronary artery in the MI and MI+TCZ groups, and only sutured without ligation in the Sham and TCZ groups. TCZ was injected into the left superior cervical ganglion (SCG) of rats in the TCZ and MI+TCZ groups after successful modeling or sham operation, and the same amount of normal saline was injected in the Sham and MI groups. 24 h after successful modeling, ECG of rats in each group was recorded, heart rate variability (HRV, including low frequency power (LF), high frequency power (HF), LF/HF ratio), QT interval, QTc interval were calculated, and left ventricular effective refractory period (ERP) and VA inducibility were measured. Myocardial infarct size and tissue changes were observed with triphenyl tetrazolium chloride staining and HE staining. Real-time PCR analysis was used to detect the messager RNA (mRNA) expression of interleukin-6 (IL-6) and signal transducer and activator of transcription (STAT) 3 in SCG and potassium voltage-gated channel subfamily D member 2 (Kcnd2) in myocardial infarction periphery. The expression of c-fos in SCG was detected by immunofluorescence staining. Results: Compared with Sham group and MI+TCZ group, rats in MI group had higher LF and LF/HF ratio, longer QT interval and QTc interval, more VAs induced, lower HF and shorter ERP (P all<0.05). Triphenyl tetrazolium chloride staining and HE staining showed that rats in the Sham and TCZ groups had normal myocardial tissue structure, those in the MI group had severe myocardial injury, and those in the MI+TCZ group had less myocardial injury than those in the MI group. Real-ime PCR analysis showed that compared with Sham group and MI+TCZ group, mRNA expression levels of IL-6 and STAT3 in SCG of rats in MI group were higher, and mRNA expression level of myocardial Kcnd2 was lower (P all<0.05). Immunofluorescence staining showed that the content of c-fos in SCG of rats in MI group was higher than that of Sham group and MI+TCZ group (P all<0.05). Conclusions: TCZ may reduce neural activity of the SCG after MI by inhibiting the IL-6/STAT3 signaling pathway, thereby alleviating myocardial injury and inhibiting VAs.

Laryngeal nerves in the cadaveric neck and its relevance to neck surgery- A descriptive study

Background Because of its close relationship with vessels that supply the thyroid gland, it is necessary to understand and document the course of the laryngeal nerves to prevent accidental damage. Otherwise it can lead to weakness in vocal cord function if ligated along with the arteries during thyroidectomy or other surgical procedures. The aim of our study was to examine and document the origin, relationship, and branching patterns of the laryngeal nerves on the side of the neck. Method The present cross sectional anatomical study was conducted on 64 dissected necks of formalin-fixed cadavers that were utilized for undergraduate teaching purposes. Different parameters were measured in the neck along with the relationship between the laryngeal nerves and their accompanying arteries. Results We observed usual and unusual course of laryngeal nerves along with some variations. Some of the novel findings were an internal laryngeal nerve piercing the thyroid cartilage lamina and an external laryngeal nerve communicating with the superior cervical ganglion. Conclusion The present study observed anatomical variations in the course of the laryngeal nerves, which are relevant for clinical practice. The potential risks of damage to these laryngeal nerves during various surgical procedures make it necessary to review and compile its relationship with the surrounding structures.

Effect of NaV1.7 blockers on post-ganglionic sympathetic nerve function

NaV1.7, also known as the sodium voltage-gated channel alpha subunit 9 (SCN9A), plays a critical role in action potential induction and conduction in pain-causing nociceptors. Accordingly, NaV1.7 blockers may be effective non-opioids analgesics. SCN9A is also expressed in autonomic neurons, but its functional role in the autonomic system is less established. We employed three highly selective NaV1.7 inhibitors to investigate the role of NaV1.7 in action potential conduction in postganglionic sympathetic nerves and in sympathetic adrenergic contractions of blood vessels. Our single neuron rt-PCR analysis revealed that nearly all neurons (32/39) isolated from guinea pig stellate ganglia expressed NaV1.7 mRNA. Genentech Pharmaceuticals provided a highly selective NaV1.7 blocker, GNE8493, which exhibits a selectivity ranging from 500 to 5000-fold for NaV1.7 over all other NaV subtypes. SiteOne Pharmaceuticals contributed another mechanistically distinct and highly selective NaV1.7 blocker, ST2262, with a selectivity of 1000-fold for human NaV1.7 over other NaV subtypes (as reported in Sci Rep. 10:14791, 2020). Unfortunately, ST2262 has little affnity for rodent and guinea pig NaV1.7. We quantified the effect of GNE8493 on postganglionic compound actional potentials (CAP) within the sympathetic trunk of superior cervical ganglia (SCG). GNE8493 inhibited the CAP in the postganglionic neurons of SCG by ~ 70% (n=5, p&lt;0.01). With such a significant impact of the NaV1.7 blocker on post-ganglionic actional potential conduction, we were prompted to explore its potential physiological relevance. Our study involved the isolated pulmonary arteries from anonymous human lung donors (obtained from IIAM) and isolated pulmonary arteries and the abdominal aorta from guinea pigs. We measured smooth muscle tension using standard tissue bath techniques. Stimulation of intrinsic nerves was achieved through electrical field stimulation (EFS) at 12V, 1msec, and 10Hz for 30 seconds, resulting in rapid contractions in all tissues. These contractions were completely prevented by the nonselective NaV1 blocker tetrodotoxin and by the alpha adrenoceptor antagonist prazosin. The contractions were quantified as a percentage of the maximum adrenergic contraction achievable, induced by the addition of 100 μM phenylephrine at the end of the experiment. In guinea pigs, GNE8493 completely blocked sympathetic contractions of the isolated pulmonary arteries (IC50 of -log (M) 5.8) and abdominal aorta (IC50 of -log (M) 6.4 ± 0.3). In human pulmonary arteries, GNE8493 (1 μM) and ST2262 inhibited the sympathetic contractions 94% and 87%, respectively (p&lt;0.01, n=6). These findings support the hypothesis that pharmacological inhibition of NaV1.7 using selective inhibitors has the potential to reduce sympathetic function in specific vascular beds. R35HL155671 - BJU F32HL170490 - JSK. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Ganglionic Local Opioid Analgesia at the Superior Cervical Ganglion: MRI-Verified Solution Spread.

Ganglionic local opioid analgesia (GLOA) at the superior cervical ganglion (SCG) is performed for pain control and is known to be an effective procedure. In this study, we evaluated the spread of the injectate in the area of the SCG. Our expectation was that there would be a correlation between the area and volume of the injectate spread and post-procedural outcome measures. This was a retrospective blinded review of magnetic resonance imaging (MRI) scans. Assessors evaluated the anatomical area of fluid spread, the furthermost spread from midline, any hampered spread and contact of contrast fluid with other structures. The efficacy of GLOA and complications were estimated. The main solution spread reached from the C1 to C3 vertebrae. The furthest spread in the lateral and sagittal planes was 21.2 and 15.2mm, respectively. The furthest craniocaudal spread was 63.5mm. In 53.3% and 33% of interventions, the solution was found in the parapharyngeal space and in its "medial compartment," respectively. A correlation was found between pain relief and both solution spread and volume of solution spread. No hampered spread was recorded. A negative correlation between pain reduction and number of GLOA was observed. Higher pre-procedural pain intensity was correlated with higher pain reduction. We estimated pain relief in 93% of procedures correctly. No correlation between post-procedural Numerical Rating Scale (NRS) scores and different needle approaches was found. For the transoral blocking technique, a strict laterodorsal needle direction is recommended to prevent possible block failures. A total volume of 2ml injected into the parapharyngeal space and its "medial compartment" is recommended. Higher volumes may lead to uncontrolled distribution patterns. Clinicaltrials.gov identifier NCT05257655; date of registration 2022-02-25; patient enrollment date from 2023-01-09 to 2023-08-31.

Arterial supply and morphological characteristics of sympathetic neurons in the human superior cervical ganglion.

The aim of this study was the micromorphological analysis of the distribution of microvessels, mast cells and ganglionic neurons in two parts, proximal and distal of the human superior cervical sympathetic ganglions (SCSGs). Statistical analyses were applied to detect the possible metric regional differences in their densities. Five injected human SCSGs with colored India ink and gelatin were microdissected and examined. Second group of five human SCSGs was prepared and serially sliced for CD34 and mast cell tryptase immunostaining. The microscopic fields of two parts of the SCSGs were analyzed for the following quantifications: microvessel density (MVD), mast cell density (MCD), and ganglionic cell count and measurements. The mean number of CD34-positive microvessels in microscopic fields, the MVD, had a value of 83 for the upper parts, and 82.7 for the lower parts of SCSGs. The mean number of tryptase-positive mast cells in microscopic fields, the MCD, was 4.5 in the proximal parts, and 4.7 in the distal parts of SCSGs. The mean number of ganglionic neurons in microscopic fields was 19.5 in the proximal parts, and 19.8 in the distal parts of SCSGs. The density of CD34-positive microvessels, the density of tryptase-positive mast cells, and the density, mean diameters and mean areas of ganglionic neurons were not significantly different in two observed parts, upper and lower of the SCSGs. In conclusion, the distributions of microvessels, mast cells, and neurons in two parts of the SCSGs were uniform with no specific micromorphological variations, there is a homogenous vascular and cellular pattern within the SCSGs.

Single-cell herpes simplex virus type 1 infection of neurons using drop-based microfluidics reveals heterogeneous replication kinetics.

Single-cell analyses of viral infections reveal heterogeneity that is not detected by traditional population-level studies. This study applies drop-based microfluidics to investigate the dynamics of herpes simplex virus type 1 (HSV-1) infection of neurons at the single-cell level. We used micrometer-scale Matrigel beads, termed microgels, to culture individual murine superior cervical ganglia (SCG) neurons or epithelial cells. Microgel-cultured cells are encapsulated in individual media-in-oil droplets with a dual-fluorescent reporter HSV-1, enabling real-time observation of viral gene expression and replication. Infection within drops revealed that the kinetics of initial viral gene expression and replication were dependent on the inoculating dose. Notably, increasing inoculating doses led to earlier onset of viral gene expression and more frequent productive viral replication. These observations provide crucial insights into the complexity of HSV-1 infection in neurons and emphasize the importance of studying single-cell outcomes of viral infection. These techniques for cell culture and infection in drops provide a foundation for future virology and neurobiology investigations.

The Interaction between ADK and SCG10 Regulate the Repair of Nerve Damage

The cytoskeleton must be remodeled during neurite outgrowth, and Superior Cervical Ganglion 10 (SCG10) plays a critical role in this process by depolymerizing Microtubules (MTs), conferring highly dynamic properties to the MTs. However, the precise mechanism of action of SCG10 in the repair of injured neurons remains largely uncertain. Using transcriptomic identification, we discovered that SCG10 expression was downregulated in neurons after Spinal Cord Injury (SCI). Additionally, through mass spectrometry identification, immunoprecipitation, and pull-down assays, we established that SCG10 could interact with Adenosine Kinase (ADK). Furthermore, we developed an excitotoxicity-induced neural injury model and discovered that ADK suppressed injured neurite re-growth, whereas, through overexpression and small molecule interference experiments, SCG10 enhanced it. Moreover, we discovered ADK to be the upstream of SCG10. More importantly, the application of the ADK inhibitor called 5-Iodotubercidin (5-ITu) was found to significantly enhance the recovery of motor function in mice with SCI. Consequently, our findings suggest that ADK plays a negative regulatory role in the repair of injured neurons. Herein, we propose a molecular interaction model of the SCG10-ADK axis to regulate neuronal recovery.

Age-Dependent Changes in the Occurrence and Segregation of GABA and Acetylcholine in the Rat Superior Cervical Ganglia.

The occurrence, inhibitory modulation, and trophic effects of GABA have been identified in the peripheral sympathetic nervous system. We have demonstrated that GABA and acetylcholine (ACh) may colocalize in the same axonal varicosities or be segregated into separate ones in the rat superior cervical ganglia (SCG). Neurotransmitter segregation varies with age and the presence of neurotrophic factors. Here, we explored age-dependent changes in the occurrence and segregation of GABA and ACh in rats ranging from 2 weeks old (wo) to 12 months old or older. Using immunohistochemistry, we characterized the expression of L-glutamic acid decarboxylase of 67 kDa (GAD67) and vesicular acetylcholine transporter (VAChT) in the rat SCG at 2, 4, 8, 12 wo and 12 months old or older. Our findings revealed that GAD67 was greater at 2 wo compared with the other ages, whereas VAChT levels were greater at 4 wo than at 12 wo and 12 months old or older. The segregation of these neurotransmitters was more pronounced at 2 and 4 wo. We observed a caudo-rostral gradient of segregation degree at 8 and 12 wo. Data point out that the occurrence and segregation of GABA and ACh exhibit developmental adaptative changes throughout the lifetime of rats. We hypothesize that during the early postnatal period, the increase in GABA and GABA-ACh segregation promotes the release of GABA alone which might play a role in trophic actions.