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Nerve Endings

Nerve Endings: The termintaions of sensory nerves that detect various stimuli, inclduding touch, temperature, and pain.
These specialized receptors transmit signals to the central nervous system, allowing for the perception and interpretation of sensations.
Understanding nerve endings is crucial for research on pain management, sensory disorders, and the development of new therapies targeting the peripheral nervous system.
PubCompare.ai's AI-driven platform can optimize the reproducibility and accuracy of nerve endings research by locating the best protocols from literature, pre-prints, and patents using intelligent comparisons, enhancing the research process with cutting-edge technology and streamlined workflows.

Most cited protocols related to «Nerve Endings»

1
Visualizing Neuromuscular Junctions in Mice

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Publication 2014
Antibodies Argon Axon Cholinergic Receptors Cross Reactions Denervation Dental Plaque Dyes Fluorescence Forceps Helium Neon Gas Lasers IgG1 Immunoglobulins Laser Scanning Microscopy Light Mice, House Microscopy Muscle Tissue Nerve Endings Nerve Tissue Neurofilaments Neuromuscular Junction Submersion Synapses Synaptic Vesicles Synaptophysin tetramethylrhodamine Triton X-100 Z 300
2
Velocity and Fidelity of Spike Propagation in Purkinje Cells
Sequential spikes in Purkinje cells propagate on their main axons. The experiments were conducted by whole-cell recordings on their somata to induce spikes and by loose-patch recordings on the remote ends of their main axons (Figure 1A) to record the propagated spikes. The electrical signals were recorded by a MultiClapm-700B amplifier (Axon Instrument Inc, CA USA) and inputted into a pClamp-10 with 50 kHz sampling rate. The transient capacitance was compensated and output bandwidth was 3 kHz. The pipette solution for recording spikes in whole-cell model included (mM) 150 K-gluconate, 5 NaCl, 0.4 EGTA, 4 Mg-ATP, 0.5 Tris- GTP, 4 Na-phosphocreatine and 10 HEPES (pH 7.4 adjusted by 2 M KOH). The solution for axonal loose-patch recording was ACSF. The osmolarity of pipette solution made freshly was 295–305 mOsmol, and pipette resistance was 8 ~ 10 MΩ.
In the study of spike propagation on the main axons of Purkinje cells, we injected depolarization pulses in various durations and intervals into the somata to induce the spikes at 100 ~ 200 Hz, and recorded spike propagation at the remote ends of their main axons. In addition to fluorescent tracing, the spikes at soma and axonal bleb with phase-locking indicated the signals from a Purkinje cell. The fidelity of spike propagation on the axonal branches of Purkinje cells was assessed by a ratio of spikes recorded at axonal terminals to spikes induced on somata. The velocity of spike propagation on the axons of Purkinje cells was calculated by the formula that the lengths from somata to axonal blebs were divided by the peak-time intervals between axonal spikes and somatic ones, in which the somatic spikes were converted into dV/dt [17 (link),76 (link)]. As spike propagation was time-dependent, the fidelity and velocity of spike propagation at every 50 ms were averaged from ten spikes. This calculation method was also used to quantify spike-rising slope (maximal dV/dt). As the lengths of axons may be variable in our experiments, the presentation of spike propagation velocity was normalized.
The influence of VGSC’s functional status on spike propagation was studied. The inactivation of VGSCs was prevented by using anemone toxin (ATX), a blocker of VGSC inactivation [45 (link),46 (link)], or hyperpolarization pulses [34 (link),42 (link)]. 5 μM ATX was puffed onto the middle segment of main axons by ATX-containing pipette, while using whole-cell recording on soma and loose-patch recording on axonal bleb. The inactivation of VGSCs was made by using a steady depolarization [34 (link),42 (link)].
The data were analyzed if the recorded neurons had resting membrane potentials negatively more than −60 mV and action potentials above 70 mV. The criteria for the acceptation of each experiment also included less than 5% changes in resting membrane potential, spike magnitude, input and seal resistance. The values of the spike propagation velocity, fidelity and maximal dV/dt are presented as mean ± SE. The comparisons between groups are done by t-test.
Yang Z., Gu E., Lu X, & Wang J.H. (2014). Essential role of axonal VGSC inactivation in time-dependent deceleration and unreliability of spike propagation at cerebellar Purkinje cells. Molecular Brain, 7, 1.
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Publication 2014
Action Potentials Anemone Axon Cells Diploid Cell Egtazic Acid Electricity gluconate HEPES Membrane Potentials Nerve Endings Neurons Osmolarity Phocidae Phosphocreatine Presynaptic Terminals Pulses Purkinje Cells Resting Potentials Signal Transduction Sodium Chloride Toxins, Biological Transients Tromethamine
3
Quantification of Motor Neuron Innervation
Sections were imaged using an SP5 Leica confocal microscope and analyzed using LASAF software (Leica). For all immunohistochemical analysis, at least three animals were used for each genotype. For SMN quantification, the number of motor and proprioceptive neurons with either present or absent nuclear Gems from L1 – L3 spinal segments were counted using a ×40 objective from z-stacks (0.5 μm steps) scans. At least 30 motor and proprioceptive neurons were included from each animal for each genotype. For motor neuron counts, we analyzed z-stacks images (at 3 μm intervals) collected for each section that contained a fluorescent signal from L2 retrogradely labeled motor neurons as previously described for L1 motor neurons13 (link). Sections were scanned using a ×20 objective. Only motor neurons (ChAT+) that contained the nucleus were counted in order to avoid double counting of adjoining sections.
Quantitative analysis of VGluT1 immunoreactive synaptic densities on motor neurons at P4 and P11 were performed on stacks of optical sections scanned using an ×40 objective throughout the whole section thickness at 0.35 μm z-steps to include the whole cell body and dendrites of retrogradely labeled and ChAT+ motor neurons. To obtain density estimates, we measured all VGluT1+ contacts on dendritic segments at 50 μm sequential distances (0–50, 50–100, 100–150) from the cell body and divided this number by the total linear length of all dendritic segments in each compartment as described previously13 (link). For VGluT1 motor neuron soma counts, only motor neurons with a whole cell body present within the z-stack were included.
To determine the extent of NMJ innervation, NMJ synapses were acquired using an ×20 objective and z-stack images were scanned at 2 μm intervals. Images were analyzed off-line using LASAF software. NMJs were only considered innervated if the presynaptic nerve terminal completely co-localized with the postsynaptic endplate.
Analysis of Kv2.1 and Kv2.2 channels were performed from single optical plane images acquired with an ×63 oil objective at 4096×4096 dpi resolution using an SP5 Leica confocal microscope. Only motor neuron somata (identified by ChAT immunoreactivity) in which the nucleus was present were included in the analysis. To calculate the coverage by Kv channel on motor neuron soma, a line was drawn along the soma perimeter to acquire the fluorescence intensity (expressed in arbitrary units), avoiding the area in which primary dendrites were present using LAS X software (Leica). A baseline fluorescence intensity measurement was achieved by drawing a straight line within the cytoplasm. The fluorescence intensity measurements were exported into Excel as x–y coordinates (x: distance in μm; y: fluorescence intensity in arbitrary units). The fluorescence signal above 3 Standard Deviations (SD) of the baseline intensity measurement was considered expression of Kv immunoreactivity along the soma perimeter (Supplementary Fig. 14C), whereas the signal below was considered as background. The distance with fluorescence intensity above 3 standard deviations was calculated for each motor neuron and Kv channel coverage was expressed as a percentage of the total perimeter of the motor neuron soma.
Fletcher E.V., Simon C.M., Pagiazitis J.G., Chalif J.I., Vukojicic A., Drobac E., Wang X, & Mentis G.Z. (2017). Reduced sensory synaptic excitation impairs motor neuron function via Kv2.1 in spinal muscular atrophy. Nature neuroscience, 20(7), 905-916.
Publication 2017
Animals Cell Body Cell Nucleus Cytoplasm Dendrites Fluorescence Gemini of Coiled Bodies Genotype Microscopy, Confocal Motor Neurons Nerve Endings Neuromuscular Junction Neurons Perimetry Proprioception Synapses
4
Mouse Corneal Nerve Density Quantification
The adult mouse corneas (22 mice) have a radius of approximately 1.5 mm. To calculate the subbasal epithelial nerve densities, we divided the mouse cornea into central and peripheral zones. The central zone was defined by a radius of 0.5 mm starting at the apex, and the peripheral zone with a radius of 0.5 mm beginning at the limbus. To avoid overlap, approximately 0.5 mm of space between the two zones was left uncounted.
To get a better contrast, the fluorescent images were changed to grayscale mode and placed against a white background using imaging software (Photoshop; Adobe Systems, Inc., Mountain View, CA, USA). The subbasal nerve fibers in each image were carefully drawn with 4-pixel lines following the course of each fiber by using the brush tool in the imaging software (Adobe Systems, Inc.). The nerve area and the total area of the image were obtained by using the histogram tool. The percentage of total nerve area was quantified for each image as described previously.25 (link)–28 (link, link, link) To compare nerve densities in the central and peripheral areas, eight images for each zone were randomly chosen from each cornea (two images/quadrant). A total of 80 images for each zone from 10 corneas of 10 mice (5 mice/sex) were averaged. Nerve terminals in the superficial epithelia within the central and peripheral zones were calculated by directly counting the number of terminals in each image. Twenty-four images per zone from six corneas were analyzed. The terminal numbers in each image were counted directly. Since each image comprised an area of 0.335 mm2, the terminal numbers per square millimeter were calculated.
To examine the relative content of neuropeptides in the subbasal nerves, 12 corneas that had been stained with anti-βIII-tubulin were double-stained with CGRP or SP. For each neuropeptide, a total of 24 whole-mount images from the central zone (one image/quadrant) were taken, and then the same numbers of images were taken for βIII-tubulin. In the same visual field, the percentage of βIII-tubulin equaled that of the total nerve area, and the ratio of the peptide-positive nerve area against βIII-tubulin represented the relative content.
To calculate CGRP- and SP-positive neurons in the TG, 20 images were selected randomly from 10 mice (1 section/ganglion) and counted in a blind fashion. Differences in central and peripheral corneal nerve densities, terminal numbers, and the relative content of neuropeptides in the central cornea and TG were expressed as means ± SEM and t-test was performed; P < 0.05 was considered a statistically significant difference between two groups.
He J, & Bazan H.E. (2016). Neuroanatomy and Neurochemistry of Mouse Cornea. Investigative Ophthalmology & Visual Science, 57(2), 664-674.
Publication 2016
Adult Blindness Cornea Epithelium Fibrosis Ganglia Mice, Laboratory Nerve Endings Nerve Fibers Nervousness Neurons Neuropeptides Peptides Peripheral Nerves Radius Tubulin
5
Quantifying Axonal Projections and Symmetry

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Publication 2019
Axon Brain Cells Conferences Cortex, Cerebral Nerve Endings Neurons Parent Thalamus Trees

Most recents protocols related to «Nerve Endings»

1
Pressure-Clamped Single-Fiber Recordings of Mechanosensation
The pressure-clamped single-fiber recording was performed in the similar manner described in our previous studies [22 (link), 23 (link)] to measure impulses evoked by blue light and mechanical stimulation. In brief, recording electrodes for pressure-clamped single-fiber recordings were made by thin-walled borosilicate glass tubing without filament (inner diameter 1.12 mm, outer diameter 1.5 mm, World Precision Instruments, Sarasota, FL). They were fabricated by using P-97 Flaming/Brown Micropipette Puller (Sutter Instrument Co., Novato, CA) and the tip of each electrode was fire polished by a microforge (MF-900, Narishige) to final size of 4 to 8 μm in diameter. The recording electrode was filled with Krebs bath solution, mounted onto an electrode holder which was connected to a high-speed pressure-clamp (HSPC) device (ALA Scientific Instruments, Farmingdale, NY) for fine controls of intra-electrode pressures. Under a 40 × objective, the end of individual afferent nerve was visualized and separated by applying a low positive pressure (~ 10 mmHg or 0.19 Psi) from the recording electrode. The end of a single nerve fiber was then aspirated into the recording electrode by a negative pressure at approximately 10 mmHg. Once the end of the nerve fiber entered into the recording electrode in approximately 10 µm, the electrode pressure was readjusted to − 3 ± 2 mmHg and maintained at the same pressure throughout the experiment. Nerve impulses on the single afferent fiber were recorded under the I0 configuration and amplified using a Multiclamp 700B amplifier (Molecular Devices, Sunnyvale, CA). Electrical signals were amplified 500 times and sampled at 25 kHz with AC filter at 0.1 Hz and Bessel filter at 3 kHz under AC membrane mode (Digidata 1550B, Molecular Devices). All experiments were performed at 30 ± 2 °C.
To determine conduction velocity of recorded afferent fibers, action potential (AP) impulses were initiated by electrical stimulation using a bipolar stimulation electrode positioned on the tibial nerve bundle. The distance between the electrical stimulation site and the recording site was approximately 12 mm. Electrical stimuli were monophasic square pulses that were generated by an electronic stimulator (Master-9, A.M.P.I, Israel) with a stimulation isolator (ISO-Flex, A.M.P.I, Israel) and delivered to the stimulation electrode. The duration of each stimulation pulse was 200 μs for A-fibers and 2 ms for C-fibers, and the stimulation intensities for evoking impulses were 0.3–1.7 mA for A-fiber and 0.65–2.5 mA for C-fibers.
Yamada A., Yamada A.I., Ling J., Furue H., Luo W, & Gu J.G. (2023). Properties of Nav1.8ChR2-positive and Nav1.8ChR2-negative afferent mechanoreceptors in the hindpaw glabrous skin of mice. Molecular Brain, 16, 27.
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Publication 2023
Action Potentials A Fibers Bath C Fibers Cytoskeletal Filaments Electric Conductivity Electricity Fibrosis Light Medical Devices Nerve Endings Nerve Fibers Pressure Pulse Rate Stimulations, Electric Tibial Nerve Tissue, Membrane
2
Skin-Nerve Preparation for Single-Fiber Recording
Nav1.8ChR2 mice of both males and females aged 8–11 weeks were used. Animals were anesthetized with 5% isoflurane and then sacrificed by decapitation. The hindpaw glabrous skin including plantar and finger regions together with medial planter nerve and tibial nerve before the branch from sciatic nerves were dissected out. The skin-nerve preparation was then placed in a Sylgard Silicone-coated bottom of a 60-mm recording chamber. The fat, muscle and connective tissues on the nerves and the skin were carefully removed with a pair of forceps. The skin was affixed to the bottom of the chamber by tissue pins with epidermis side facing up, and the nerve bundle was affixed by a tissue anchor in the same recording chamber. The cutting end of the nerve bundle was briefly exposed to a mixture of 0.05% dispase II plus 0.05% collagenase for 30–60 s, and the enzymes were then washed off by the normal Krebs solution (see below). This gentle enzyme treatment was to help separating individual afferent fibers at the cutting end of the nerve bundle so that a single fiber could be aspirated into the recording electrode and pressure-clamped for single-fiber recordings (see below). The recording chamber was then mounted on the stage of the Olympus BX51WI upright microscope. The skin-nerve preparation was superfused with a normal Krebs bath solution that contained (in mM): 117 NaCl, 3.5 KCl, 2.5 CaCl2, 1.2 MgCl2, 1.2 NaH2PO4, 25 NaHCO3, and 11 glucose (pH 7.3 and osmolarity 325 mOsm) and was saturated with 95% O2 and 5% CO2. The Krebs bath solution in the recording chamber was maintained at 28–32 °C during experiments.
Yamada A., Yamada A.I., Ling J., Furue H., Luo W, & Gu J.G. (2023). Properties of Nav1.8ChR2-positive and Nav1.8ChR2-negative afferent mechanoreceptors in the hindpaw glabrous skin of mice. Molecular Brain, 16, 27.
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Publication 2023
Animals Bath Bicarbonate, Sodium Collagenase Decapitation dispase II Enzymes Epidermis Females Fibrosis Fingers Forceps Glucose Isoflurane Krebs-Ringer solution Magnesium Chloride Males Mice, House Microscopy Muscle Tissue Nerve Endings Nerve Fibers Nerve Tissue Nervousness Osmolarity Pressure Sciatic Nerve Silicones Skin Sodium Chloride Tibial Nerve Tissues
3
Two-Photon Imaging of Neural Stimulation
Two-photon (2P) imaging was performed using a laser scanning microscope (Ultima 2p plus Bruker, MA) equipped with a 16’ water immersion objective (numerical aperture of 0.8, Nikon, NY) and an ultrafast laser tuned to 920 nm for fluorescence Ca2+ excitations (InSight X3, Spectra-Physics). After initial habituation, z-stack 2P imaging was performed, for which mice were awake and head-restrained on a home-constructed low-friction rodent-driven belt treadmill following the design of HHMI Janelia (https://www.janelia.org/open-science/low-friction-rodent-driven-belt-treadmill). Each imaging session lasted up to 3 hours and contained multiple replicants. Each replicant contained alternating stimulation and baseline (no stimulation) trials from randomized stimulation sites and currents. 512 × 512 images of a field of view up to 1 mm × 1 mm were acquired at 30 fps using galvo-resonant scanners. The duration of a typical z-stack, referred to as an imaging trial, was about 30 s for a depth of 400 μm at the z-spacing of 2 μm. An inter-trial period of 2 to 5 seconds was implemented for data saving. Electrical stimulation was delivered via a custom Pico32+Stim front end with a Grapevine neural interface processor (Ripple Neuro, Salt Lake City, UT). During stimulation trials, 50 Hz electrical stimulation pulse trains of biphasic, charge-balanced cathode-leading square pulses at 167 μs per phase and 67 μs inter-phase interval were provided. The current amplitudes were 2, 5, 7, and 10 μA, resulting in a maximum charge injection of 1.67 nC/ph per phase and a maximum charge density of 369.5 μC/cm2. According to the Shannon criteria, the largest stimulation current gave a K=0.48, smaller than the threshold of 1.85 for tissue compatible/safe neural stimulation. Customized MATLAB (MathWorks, MA) scripts were developed to randomize stimulation parameters and control data acquisition. Stimulation and 2P imaging were synchronized via TTL signals generated by a PulsePal (Sanworks, NY) unit.
Lycke R., Kim R., Zolotavin P., Montes J., Sun Y., Koszeghy A., Altun E., Noble B., Yin R., He F., Totah N., Xie C, & Luan L. (2023). Low-threshold, high-resolution, chronically stable intracortical microstimulation by ultraflexible electrodes. bioRxiv.
Publication Preprint 2023
Conditioning, Psychology Fluorescence Friction Head Laser Scanning Microscopy Mus Neoplasm Metastasis Nerve Endings Nervousness Pulse Rate Pulses Rodent Sodium Chloride Stimulations, Electric Submersion Tissues
4
Dual SMAD-Mediated Neural Differentiation of hiPSCs
Once hiPSC reached approximately 90% confluence, neural differentiation was performed according to a modified dual SMAD protocol (Shi et al., 2012 (link)). Neural induction was initiated by changing the media into neural induction media containing 50% DMEM/F12 (Thermo Fisher Scientific, 11330057), 50% advanced neurobasal medium (Thermo Fisher Scientific, 21103049), 1% N2 (Thermo Fisher Scientific, 17502048), 1% B27 without retinoic acid (Thermo Fisher Scientific, 1258010), 1% Glutamax™ (Thermo Fisher Scientific, 35050061), 1% non-essential amino acid (NEAA, Thermo Fisher Scientific, 11140-050), 0.1% Pen/Strep (Sigma-Aldrich, United States, P0781-100ML), supplemented with the inhibitors 10 μM SB431542 (SMAD inhibitor, SMS-gruppen, S1067) and 0.1 μM LDN193189 (Noggin analog, Sigma-Aldrich, SML0559). The cells were maintained in induction media for 12 days with daily media change. On day 12, a uniform neuroepithelial sheet appeared, and the neural progenitor cells (NPCs) were passaged with Accutase (Thermo Fisher Scientific, A1110501) into neural expansion media containing growth factors 10 ng/ml FGF2 (ProSpec, CYT-557) and 10 ng/ml EGF (ProSpec, CYT-217) instead of the inhibitors. NPCs were expanded and banked. Following expansion, NPCs were plated onto Poly-L-Ornithine (PLO, Sigma-Aldrich, P4957)/laminin (Sigma-Aldrich, L2020-1 mg) coated dishes with a seeding density of 50,000 cells/cm2, and terminal neural differentiation was performed in neural maturation media, supplemented with 50 μM db-cAMP (Sigma Aldrich, D0627-100 mg), 200 μM Ascorbic acid (Sigma Aldrich, A4403-100MG), 20 ng/ml BDNF (ProSpec, CYT-207) and 10 ng/ml GDNF (ProSpec, CYT-305). The maturation process was carried out for 5 weeks for MitoTracker™ and Golgi ICC analysis and 7 weeks for assessment of Aβ secretion and Tau phosphorylation as well as MitoTracker™, Golgi and synaptic evaluation, with partial media change every third day, before the neurons were fixed or harvested for further analyses.
Haukedal H., Corsi G.I., Gadekar V.P., Doncheva N.T., Kedia S., de Haan N., Chandrasekaran A., Jensen P., Schiønning P., Vallin S., Marlet F.R., Poon A., Pires C., Agha F.K., Wandall H.H., Cirera S., Simonsen A.H., Nielsen T.T., Nielsen J.E., Hyttel P., Muddashetty R., Aldana B.I., Gorodkin J., Nair D., Meyer M., Larsen M.R, & Freude K. (2023). Golgi fragmentation – One of the earliest organelle phenotypes in Alzheimer’s disease neurons. Frontiers in Neuroscience, 17, 1120086.
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Publication 2023
4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide accutase Amino Acids, Essential Ascorbic Acid Cells Factor X Fibroblast Growth Factor 2 Glial Cell Line-Derived Neurotrophic Factor Golgi Apparatus Human Induced Pluripotent Stem Cells Hyperostosis, Diffuse Idiopathic Skeletal inhibitors Laminin LDN 193189 Nerve Endings Nerve Expansion Nervousness Neural Stem Cells Neurogenesis Neurons noggin protein Phosphorylation polyornithine Prospec secretion Streptococcal Infections Tretinoin
5
Direct nerve stimulation for BsM and PcM
For direct nerve stimulation, the BsN and PcN were identified by their direct anatomical innervation to the BsM and PcM, respectively. The BsN, for example, was found lateral to the clitoralis nerve and the terminal nerve endings were observed innervating the BsM. Both nerves, BsN and PcN, were surgically exposed using blunt microdissection scissors and glass rods. Hooked tungsten wire electrodes were implanted in the BsN (n = 2) and the PcN (n = 2) and secured in place using a sealant (Kwik-Cast Silicone Sealant, World Precision Instruments). In addition, a wired neural stimulator (wired NeuroClip, RBI) was implanted directly in the BsN (n = 1).
Hernandez-Reynoso A.G., Rahman F.S., Hedden B., Castelán F., Martínez-Gómez M., Zimmern P, & Romero-Ortega M.I. (2023). Secondary urethral sphincter function of the rabbit pelvic and perineal muscles. Frontiers in Neuroscience, 17, 1111884.
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Publication 2023
CD3EAP protein, human Microdissection Nerve Endings Nervousness Operative Surgical Procedures Rod Photoreceptors Silicones Tungsten

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More about "Nerve Endings"

Nerve endings, also known as sensory receptors or peripheral nerve terminals, are specialized structures that detect various stimuli, including touch, temperature, and pain.
These receptors are the terminations of sensory nerves that transmit signals to the central nervous system, allowing for the perception and interpretation of sensations.
Understanding the biology and function of nerve endings is crucial for research on pain management, sensory disorders, and the development of new therapies targeting the peripheral nervous system.
Researchers studying nerve endings can benefit from PubCompare.ai's AI-driven platform, which can optimize the reproducibility and accuracy of their work.
The platform utilizes intelligent comparisons to locate the best protocols from scientific literature, pre-prints, and patents, enhancing the research process with cutting-edge technology and streamlined workflows.
This can be particularly useful when working with techniques and reagents such as DMEM/F12 cell culture medium, 6-OHDA (6-hydroxydopamine) for inducing nerve damage, GlutaMAX for supporting neuronal growth, and LabChart 8 software for data analysis.
Additionally, the platform can assist researchers in exploring key subtopics related to nerve endings, such as the role of neurotrophic factors like NGF (nerve growth factor) and BDNF (brain-derived neurotrophic factor) in nerve regeneration, the use of Neurobasal A media for culturing and maintaining neuronal cells, and the application of GAPDH (glyceraldehyde 3-phosphate dehydrogenase) as a reference gene in gene expression studies.
By incorporating these insights, researchers can strengthen their understanding of the complex mechanisms underlying nerve endings and develop more effective therapies and diagnostic tools.
OtherTerms: sensory receptors, peripheral nerve terminals, touch, temperature, pain, central nervous system, pain management, sensory disorders, DMEM/F12, 6-OHDA, GlutaMAX, LabChart 8, NGF, Neurobasal A, GAPDH, BDNF, GraphPad Prism 5