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VON FREY FILAMENTS
(Model: Bio-VF-M)
A set of 20 monofilaments based on the Semmes Weinstein monofilament set - featuring retractable filaments to protect the filament and allow the investigator to carry a few around in a pocket

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! NEW RESEARCH WORK ! A recent publication by O. Kopach, V. Krotov, N. Voitenko in "Journal of Neuroscience Methods" highlights the merits of using Bioseb's Von Frey Filaments: Atlanto-occipital catheterization of young rats for long-term drug delivery into the lumbar subarachnoid space combined with in vivo testing and electrophysiology in situ

Atlanto-occipital catheterization of young rats for long-term drug delivery into the lumbar subarachnoid space combined with in vivo testing and electrophysiology in situ
O. Kopach, V. Krotov, N. Voitenko
Bogomoletz Institute of Physiology, Kiev, Ukraine
Published in "Journal of Neuroscience Methods" (2017-08-01)


Background
Catheterization has been widely used in neuroscience and pain research for local drug delivery. Though different modifications were developed, the use of young animals for spinal catheterization remains limited because of a little success rate. A reliable technique is needed to catheterize young animals aimed for in vivo testing combined with spinal cord electrophysiology, often limited by animal age, to facilitate pain research.

New methods
We describe intrathecal catheterization of young rats (3-week-old) through atlanto-occipical approach for long-lasting drug delivery into the lumbar subarachnoid space. The technique represents a surgical approach of minimized invasiveness that requires PE-10 catheter and few equipment of standard laboratory use.

Results
Behavioral assessments revealed that spinal catheterization does not change peripheral sensitivity of different modalities (thermal and mechanical) and gives no rise to locomotive deficit or anxiety-like behavior in young rats. The long-term administration of genetic material (oligodeoxynucleotides given up to 4 days), examined both in vivo and in situ, produced no adverse effects on basal peripheral sensitivity, but changed the AMPA receptor-mediated currents in sensory interneurons of the spinal cord.

Comparison with existing methods
Dissimilar to already described methods, the method is designed for the use of young rats for behavioral testing in vivo and/or spinal cord electrophysiology in situ.
This set of 20 monofilaments is based on the Semmes Weinstein monofilament set, but now features retractable filaments to protect the filament and allow the investigator to carry a few around in a pocket.

The Semmes Weinstein set of monofilaments provide an approximately logarithmic scale of actual force, and a linear scale of perceived intensity. They have a long history of effective use in clinical settings, and can be used to diagnose pathologies of hyper- or hypo-aesthesia. Subsets within the set of 20 probes distinguish pathologies on different parts of the body (foot, hand, lip, cheek, etc.).

The operating principle remains the same: when the tip of a fiber of given length and diameter is pressed against the skin at right angles, the force of application increases as long as the researcher continues to advance the probe, until the fiber bends. After the fiber bends, continued advance creates more bend, but not more force of application. This principle makes it possible for the researcher using a hand held probe to apply a reproducible force, within a wide tolerance, to the skin surface.

Size 1,652,362,442,833,223,613,844,08 4,174,314,564,744,935,075,185,46 5,886,16,456,65
Force (g) 0,0080,020,040,070,160,40,61 1,42468101526 60100180300

Rodents exhibit a paw withdrawal reflex when the paw is unexpectedly touched. The Touch Test™ Sensory Evaluator can be used on the Plantar surfaces of the foot of a rat or mouse, and the animal will indicate sensation by pulling back its paw. Replacement filaments available.

Attention : Because of the physical properties of the material making up the filaments it's recommended to work at temperature between 18°C an 24°C and hygrometry between 60 and 80 %, for a better reliability of the results.

Publications (Click on an article to show details and read the abstract)

PAIN
- General pain -
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain. (2017)
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.
Urien L, Gaillard S, Lo Re L, Malapert P, Bohic M, Reynders A, Moqrich A
"Aix-Marseille-Université, Institut de Biologie du Développement de Marseille, Marseille, France "
Published in "Scientific Reports" (2017-02-17)

Primary sensory neurons are heterogeneous by myriad of molecular criteria. However, the functional significance of this remarkable heterogeneity is just emerging. We precedently described the GINIP(+) neurons as a new subpopulation of non peptidergic C-fibers encompassing the free nerve ending cutaneous MRGPRD(+) neurons and C-LTMRs. Using our recently generated ginip mouse model, we have been able to selectively ablate the GINIP(+) neurons and assess their functional role in the somatosensation. We found that ablation of GINIP(+) neurons affected neither the molecular contents nor the central projections of the spared neurons. GINIP-DTR mice exhibited impaired sensation to gentle mechanical stimuli applied to their hairy skin and had normal responses to noxious mechanical stimuli applied to their glabrous skin, under acute and injury-induced conditions. Importantly, loss of GINIP(+) neurons significantly altered formalin-evoked first pain and drastically suppressed the second pain response. Given that MRGPRD(+) neurons have been shown to be dispensable for formalin-evoked pain, our study suggest that C-LTMRs play a critical role in the modulation of formalin-evoked pain.

- Mechanical allodynia & hyperlagesia -
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain. (2017)
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.
Urien L, Gaillard S, Lo Re L, Malapert P, Bohic M, Reynders A, Moqrich A
"Aix-Marseille-Université, Institut de Biologie du Développement de Marseille, Marseille, France "
Published in "Scientific Reports" (2017-02-17)

Primary sensory neurons are heterogeneous by myriad of molecular criteria. However, the functional significance of this remarkable heterogeneity is just emerging. We precedently described the GINIP(+) neurons as a new subpopulation of non peptidergic C-fibers encompassing the free nerve ending cutaneous MRGPRD(+) neurons and C-LTMRs. Using our recently generated ginip mouse model, we have been able to selectively ablate the GINIP(+) neurons and assess their functional role in the somatosensation. We found that ablation of GINIP(+) neurons affected neither the molecular contents nor the central projections of the spared neurons. GINIP-DTR mice exhibited impaired sensation to gentle mechanical stimuli applied to their hairy skin and had normal responses to noxious mechanical stimuli applied to their glabrous skin, under acute and injury-induced conditions. Importantly, loss of GINIP(+) neurons significantly altered formalin-evoked first pain and drastically suppressed the second pain response. Given that MRGPRD(+) neurons have been shown to be dispensable for formalin-evoked pain, our study suggest that C-LTMRs play a critical role in the modulation of formalin-evoked pain.

- Chronic pain -
Cingulate Overexpression of Mitogen-Activated Protein Kinase Phosphatase-1 as a Key Factor for Depression (2017)
Cingulate Overexpression of Mitogen-Activated Protein Kinase Phosphatase-1 as a Key Factor for Depression
F Barthas, M Humo, R Gilsbach, E Waltisperger, M. Karatas, S. Leman, L. Hein, C. Belzung, A. Boutillier, M. Barrot, I. Yalcin
University of Strasbourg, National Centre for Scientific Research, Institute of Cellular and Integrative Neuroscience, Strasbourg
Published in "Biological Psychiatry" (2017-02-14)

BACKGROUND:

Depression is frequently associated with chronic pain or chronic stress. Among cortical areas, the anterior cingulate cortex (ACC, areas 24a and 24b) appears to be important for mood disorders and constitutes a neuroanatomical substrate for investigating the underlying molecular mechanisms. The current work aimed at identifying ACC molecular factors subserving depression.

METHODS:

Anxiodepressive-like behaviors in C57BL/6J male mice were induced by neuropathic pain, unpredictable chronic mild stress, and optogenetic ACC stimulation and were evaluated using novelty suppressed feeding, splash, and forced swim tests. ACC molecular changes in chronic pain-induced depression were uncovered through whole-genome expression analysis. Further mechanistic insights were provided by chromatin immunoprecipitation, Western blot, and immunostaining. The causal link between molecular changes and depression was studied using knockout, pharmacological antagonism, and local viral-mediated gene knockdown.

RESULTS:

Under chronic pain-induced depression, gene expression changes in the ACC highlighted the overexpression of a regulator of the mitogen-activated protein kinase pathway, mitogen-activated protein kinase phosphatase-1 (MKP-1). This upregulation is associated with the presence of transcriptionally active chromatin marks (acetylation) at its proximal promoter region as well as increased cyclic adenosine monophosphate response element-mediated transcriptional activity and phosphorylation of cyclic adenosine monophosphate response element binding protein and activating transcription factor. MKP-1 overexpression is also observed with unpredictable chronic mild stress and repeated ACC optogenetic stimulation and is reversed by fluoxetine. A knockout, an antagonist, or a local silencing of MKP-1 attenuates depressive-like behaviors, pointing to an important role of this phosphatase in depression.

CONCLUSIONS:

These data point to ACC MKP-1 as a key factor in the pathophysiology of depression and a potential target for treatment development.

CENTRAL NERVOUS SYSTEM (CNS)
- Spinal Cord -
Atlanto-occipital catheterization of young rats for long-term drug delivery into the lumbar subarachnoid space combined with in vivo testing and electrophysiology in situ (2017)
Atlanto-occipital catheterization of young rats for long-term drug delivery into the lumbar subarachnoid space combined with in vivo testing and electrophysiology in situ
O. Kopach, V. Krotov, N. Voitenko
Bogomoletz Institute of Physiology, Kiev, Ukraine
Published in "Journal of Neuroscience Methods" (2017-08-01)

Background
Catheterization has been widely used in neuroscience and pain research for local drug delivery. Though different modifications were developed, the use of young animals for spinal catheterization remains limited because of a little success rate. A reliable technique is needed to catheterize young animals aimed for in vivo testing combined with spinal cord electrophysiology, often limited by animal age, to facilitate pain research.

New methods
We describe intrathecal catheterization of young rats (3-week-old) through atlanto-occipical approach for long-lasting drug delivery into the lumbar subarachnoid space. The technique represents a surgical approach of minimized invasiveness that requires PE-10 catheter and few equipment of standard laboratory use.

Results
Behavioral assessments revealed that spinal catheterization does not change peripheral sensitivity of different modalities (thermal and mechanical) and gives no rise to locomotive deficit or anxiety-like behavior in young rats. The long-term administration of genetic material (oligodeoxynucleotides given up to 4 days), examined both in vivo and in situ, produced no adverse effects on basal peripheral sensitivity, but changed the AMPA receptor-mediated currents in sensory interneurons of the spinal cord.

Comparison with existing methods
Dissimilar to already described methods, the method is designed for the use of young rats for behavioral testing in vivo and/or spinal cord electrophysiology in situ.

SENSORY SYSTEM
- Somatosensory system -
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain. (2017)
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.
Urien L, Gaillard S, Lo Re L, Malapert P, Bohic M, Reynders A, Moqrich A
"Aix-Marseille-Université, Institut de Biologie du Développement de Marseille, Marseille, France "
Published in "Scientific Reports" (2017-02-17)

Primary sensory neurons are heterogeneous by myriad of molecular criteria. However, the functional significance of this remarkable heterogeneity is just emerging. We precedently described the GINIP(+) neurons as a new subpopulation of non peptidergic C-fibers encompassing the free nerve ending cutaneous MRGPRD(+) neurons and C-LTMRs. Using our recently generated ginip mouse model, we have been able to selectively ablate the GINIP(+) neurons and assess their functional role in the somatosensation. We found that ablation of GINIP(+) neurons affected neither the molecular contents nor the central projections of the spared neurons. GINIP-DTR mice exhibited impaired sensation to gentle mechanical stimuli applied to their hairy skin and had normal responses to noxious mechanical stimuli applied to their glabrous skin, under acute and injury-induced conditions. Importantly, loss of GINIP(+) neurons significantly altered formalin-evoked first pain and drastically suppressed the second pain response. Given that MRGPRD(+) neurons have been shown to be dispensable for formalin-evoked pain, our study suggest that C-LTMRs play a critical role in the modulation of formalin-evoked pain.

MOOD DISORDERS
- Depression -
Cingulate Overexpression of Mitogen-Activated Protein Kinase Phosphatase-1 as a Key Factor for Depression (2017)
Cingulate Overexpression of Mitogen-Activated Protein Kinase Phosphatase-1 as a Key Factor for Depression
F Barthas, M Humo, R Gilsbach, E Waltisperger, M. Karatas, S. Leman, L. Hein, C. Belzung, A. Boutillier, M. Barrot, I. Yalcin
University of Strasbourg, National Centre for Scientific Research, Institute of Cellular and Integrative Neuroscience, Strasbourg
Published in "Biological Psychiatry" (2017-02-14)

BACKGROUND:

Depression is frequently associated with chronic pain or chronic stress. Among cortical areas, the anterior cingulate cortex (ACC, areas 24a and 24b) appears to be important for mood disorders and constitutes a neuroanatomical substrate for investigating the underlying molecular mechanisms. The current work aimed at identifying ACC molecular factors subserving depression.

METHODS:

Anxiodepressive-like behaviors in C57BL/6J male mice were induced by neuropathic pain, unpredictable chronic mild stress, and optogenetic ACC stimulation and were evaluated using novelty suppressed feeding, splash, and forced swim tests. ACC molecular changes in chronic pain-induced depression were uncovered through whole-genome expression analysis. Further mechanistic insights were provided by chromatin immunoprecipitation, Western blot, and immunostaining. The causal link between molecular changes and depression was studied using knockout, pharmacological antagonism, and local viral-mediated gene knockdown.

RESULTS:

Under chronic pain-induced depression, gene expression changes in the ACC highlighted the overexpression of a regulator of the mitogen-activated protein kinase pathway, mitogen-activated protein kinase phosphatase-1 (MKP-1). This upregulation is associated with the presence of transcriptionally active chromatin marks (acetylation) at its proximal promoter region as well as increased cyclic adenosine monophosphate response element-mediated transcriptional activity and phosphorylation of cyclic adenosine monophosphate response element binding protein and activating transcription factor. MKP-1 overexpression is also observed with unpredictable chronic mild stress and repeated ACC optogenetic stimulation and is reversed by fluoxetine. A knockout, an antagonist, or a local silencing of MKP-1 attenuates depressive-like behaviors, pointing to an important role of this phosphatase in depression.

CONCLUSIONS:

These data point to ACC MKP-1 as a key factor in the pathophysiology of depression and a potential target for treatment development.


Model:
Bio-VF-M
Von Frey Filaments (Modif.)
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