Neurotrophic Factors - A Tool for Therapeutic Strategies in Neurological,Neuropsychiatric and Neuroimmunological Diseases?

Schulte‐Herbrüggen, Olaf; Braun, Alena; Rochlitzer, Sabine; Jockers-Scherübl, Maria C.; Hellweg, Rainer

doi:10.2174/092986707781745578

Cited by 95 publications

(54 citation statements)

References 196 publications

(235 reference statements)

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“…Neurotrophin nerve growth factor (NGF) contributes to cutaneous innervation development and turnover (Tominaga et al, 2009) and maintains SP þ nerve fibers in the skin (Botchkarev et al, 2004;Schulte-Herbruggen et al, 2007). It is also involved in stress-induced cutaneous hyperinnervation (Peters et al, 2007) and induces keratinocyte proliferation (Botchkarev et al, 2004), mast cell degranulation (Tal and Liberman, 1997), and alterations of the cytokine balance that promote allergic inflammation (Bonini et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Nerve Growth Factor Partially Recovers Inflamed Skin from Stress-Induced Worsening in Allergic Inflammation

Peters

Liezmann

Spatz

et al. 2011

Journal of Investigative Dermatology

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Neuroimmune dysregulation characterizes atopic disease, but its nature and clinical impact remain ill-defined. Induced by stress, the neurotrophin nerve growth factor (NGF) may worsen cutaneous inflammation. We therefore studied the role of NGF in the cutaneous stress response in a mouse model for atopic dermatitis-like allergic dermatitis (AlD). Combining several methods, we found that stress increased cutaneous but not serum or hypothalamic NGF in telogen mice. Microarray analysis showed increased mRNAs of inflammatory and growth factors associated with NGF in the skin. In stress-worsened AlD, NGF-neutralizing antibodies markedly reduced epidermal thickening together with NGF, neurotrophin receptor (tyrosine kinase A and p75 neurotrophin receptor), and transforming growth factor-β expression by keratinocytes but did not alter transepidermal water loss. Moreover, NGF expression by mast cells was reduced; this corresponded to reduced cutaneous tumor necrosis factor-α (TNF-α) mRNA levels but not to changes in mast cell degranulation or in the T helper type 1 (Th1)/Th2 cytokine balance. Also, eosinophils expressed TNF receptor type 2, and we observed reduced eosinophil infiltration after treatment with NGF-neutralizing antibodies. We thus conclude that NGF acts as a local stress mediator in perceived stress and allergy and that increased NGF message contributes to worsening of cutaneous inflammation mainly by enhancing epidermal hyperplasia, pro-allergic cytokine induction, and allergy-characteristic cellular infiltration.

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Section: Introductionmentioning

confidence: 99%

Nerve Growth Factor Partially Recovers Inflamed Skin from Stress-Induced Worsening in Allergic Inflammation

Peters

Liezmann

Spatz

et al. 2011

Journal of Investigative Dermatology

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“…Neurotrophins have attracted much interest for their therapeutic potential in a range of neurologic disorders (Schulte-Herbruggen et al 2007). BDNF has also emerged as a potent synaptic modulator involved in many forms of activity-dependent synaptic plasticity (Lu 2003) and may play an important role in learning and memory (Tyler et al 2002).…”

Section: Introductionmentioning

confidence: 99%

BDNF Evokes Release of Endogenous Cannabinoids at Layer 2/3 Inhibitory Synapses in the Neocortex

Lemtiri‐Chlieh

Levine

2010

Journal of Neurophysiology

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. The neurotrophin brain-derived neurotrophic factor (BDNF) is a potent regulator of inhibitory synaptic transmission, although the locus of this effect and the underlying mechanisms are controversial. We explored a potential interaction between BDNF and endogenous cannabinoid (endocannabinoid) signaling because activation of type 1 cannabinoid (CB1) receptors potently regulates ␥-aminobutyric acid (GABA) release and both trkB tyrosine kinase receptors and CB1 receptors are highly expressed at synapses in neocortical layer 2/3. Here, we found that the effects of BDNF at inhibitory cortical synapses are mediated by the release of endocannabinoids acting retrogradely at presynaptic CB1 receptors. Specifically, acute application of BDNF rapidly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) via postsynaptic trkB receptor activation because intracellular delivery of the tyrosine kinase inhibitor K252a completely blocked the BDNF effect. Although triggered by postsynaptic trkB activation, BDNF exposure decreased presynaptic release probability, as evidenced by increases in the paired-pulse ratio and coefficient of variation of evoked responses. In addition, BDNF decreased the frequency but not the amplitude of action potential-independent miniature IPSCs and BDNF did not alter the postsynaptic response to locally applied GABA. These results suggest that BDNF induces the release of a retrograde messenger from the postsynaptic cell that regulates presynaptic neurotransmitter release. Consistent with a role for endocannabinoids as the retrograde signal, the effect of BDNF on IPSCs was blocked by CB1 receptor antagonists and was occluded by a cannabinoid receptor agonist. Furthermore, inhibiting endocannabinoid synthesis or transport also disrupted the BDNF effect, implicating postsynaptic endocannabinoid release triggered by BDNF.

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“…Evidence has implied the role of p75NTR receptor and its ligands in the regulation and modulation of neurological and behavioral functions [47][48][49] . Some prior reports have also indicated that epilepsy often shows a comorbidity with behavioral disturbances, including aggression and agitation [12,17,43] , and induction of SE by pilocarpine can also provoke seizure-associated behaviors such as aggressive and unsocial responses.…”

Section: Discussionmentioning

confidence: 99%

Blockade of p75 Neurotrophin Receptor Reverses Irritability and Anxiety-Related Behaviors in a Rat Model of Status Epilepticus

Mehrabi

Janahamdi

Joghataie

et al. 2018

IBJ

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Background: Many recent epidemiological studies have shown that epileptic patients are more likely suffer from depression, anxiety, and irritability. However, the cellular mechanisms of epilepsy-induced psychotic behaviors are not fully elucidated. Neurotrophin receptors have been suggested to be involved in epilepsy and also in psychiatric disorders. Up-regulation of p75NTR expression and activation of p75NTR signalling cascades after the seizure have been shown, but the role of the p75 receptor in epilepsy-induced psychotic behaviors has not been documented so far. Therefore, the present work aimed to investigate the effect of p75 receptor blockade on seizure activity, irritability, and anxiety-like behaviors in a rat model of status epilepticus. Methods: Rats were injected with pilocarpine (350 mg/ kg, i.p.) to induce status epilepticus. Then various behavioral tests were performed after the blockade of p75NTR alone or in combination with p75 antagonist and phenobarbital. Molecular analysis by PCR was performed to investigate the expression of p75 and pro-NGF. Results: Molecular findings indicated a high level of mRNA expression for both p75 receptors and pro-NGF in the epileptic model group. Results also showed that the administration of p75 antagonist alone or in combination with phenobarbital was able to significantly influence the behavioral responses. Furthermore, 20-hours video monitoring showed a decrease in the frequency and duration of seizures in the rat group receiving p75 antagonist. Conclusion: Taken together, the present study suggests that the blockade of the p75 receptor may affect the irritability and anxietyrelated behavior in a rat model of status epilepticus.

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Neurotrophic Factors - A Tool for Therapeutic Strategies in Neurological,Neuropsychiatric and Neuroimmunological Diseases?

Cited by 95 publications

References 196 publications

Nerve Growth Factor Partially Recovers Inflamed Skin from Stress-Induced Worsening in Allergic Inflammation

Nerve Growth Factor Partially Recovers Inflamed Skin from Stress-Induced Worsening in Allergic Inflammation

BDNF Evokes Release of Endogenous Cannabinoids at Layer 2/3 Inhibitory Synapses in the Neocortex

Blockade of p75 Neurotrophin Receptor Reverses Irritability and Anxiety-Related Behaviors in a Rat Model of Status Epilepticus

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