Sensory processing in Huntington’s disease

Mirallave, Ana; Morales, Merche; Cabib, Christopher; Muñoz, Esteban; Santacruz, Pilar; Gasull, Xavier; Valls‐Solé, Josep

doi:10.1016/j.clinph.2017.01.009

Cited by 3 publications

(5 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…12,34 Patients with HD also had a shortage of negative emotions and pain responses, such as increased latency after laser stimuli. 11,37,41…”

Section: Discussionmentioning

confidence: 99%

“…12,34 Patients with HD also had a shortage of negative emotions and pain responses, such as increased latency after laser stimuli. 11,37,41 Identifying new therapeutic methods to manage neuropathic pain is a vital medical goal. In this study, we revealed the function of neuronal HAP1 during pain progression and the potential mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…1,34 Obvious nociceptive afferent delay and abnormal spinal cord pain reaction were discovered in patients with HD. 37,41,42,44 Meanwhile, HD mice were also reported to display weaker pain behavior and painassociated chemokine reactions of the spinal cord in inflammatoryinduced pain models. 34 It seems that pain dysfunctions in HD have a strong relationship with HAP1.…”

Section: Discussionmentioning

confidence: 99%

“…Many patients with HD exhibited obvious nociceptive afferent delay and abnormal spinal cord pain reaction, but they rarely complained of pain to even drink hot water. 37,41,42,44 According to these studies, obviously, HAP1 has a potential role in nociceptive pathways. However, HAP1's role in pain processing is still unknown.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Huntington-associated protein 1 inhibition contributes to neuropathic pain by suppressing Cav1.2 activity and attenuating inflammation

Pan

Zhao

Sang

et al. 2022

Pain

View full text Add to dashboard Cite

show abstract

“…12,34 Patients with HD also had a shortage of negative emotions and pain responses, such as increased latency after laser stimuli. 11,37,41…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Huntington-associated protein 1 inhibition contributes to neuropathic pain by suppressing Cav1.2 activity and attenuating inflammation

Pan

Zhao

Sang

et al. 2022

Pain

View full text Add to dashboard Cite

show abstract

“…Neuropathic pain is a type of intractable pain caused by injury to the sensory nervous system, the pathogenesis of which is related to peripheral hyperexcitability and central sensitization (Finnerup et al, 2021). Existing studies have shown that many HD patients exhibit large afferent delays and abnormal spinal pain responses (Mirallave et al, 2017;Li et al, 2023). The same phenomenon can also be observed in mouse models of HD, as these animals exhibit diminished pain responses in response to inflammatory stimuli (Lin et al, 2018).…”

Section: Painmentioning

confidence: 95%

Research advances in huntingtin-associated protein 1 and its application prospects in diseases

Wu,

Wang,

et al. 2024

Front. Neurosci.

View full text Add to dashboard Cite

Huntingtin-associated protein 1 (HAP1) was the first protein discovered to interact with huntingtin. Besides brain, HAP1 is also expressed in the spinal cord, dorsal root ganglion, endocrine, and digestive systems. HAP1 has diverse functions involving in vesicular transport, receptor recycling, gene transcription, and signal transduction. HAP1 is strongly linked to several neurological diseases, including Huntington’s disease, Alzheimer’s disease, epilepsy, ischemic stroke, and depression. In addition, HAP1 has been proved to participate in cancers and diabetes mellitus. This article provides an overview of HAP1 regarding the tissue distribution, cell localization, functions, and offers fresh perspectives to investigate its role in diseases.

show abstract

Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington’s Disease

Rodríguez-Urgellés,

Casas-Torremocha,

Sancho-Balsells

et al. 2023

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Background Huntington's Disease (HD) is a disorder that affects body movements. Altered glutamatergic innervation of the striatum is a major hallmark of the disease. Approximately 30% of those glutamatergic inputs come from thalamic nuclei. Foxp2 is a transcription factor involved in cell differentiation and reported low in patients with HD. However, the role of the Foxp2 in the thalamus in HD remains unexplored. Methods We used two different mouse models of HD, the R6/1 and the HdhQ111 mice, to demonstrate a consistent thalamic Foxp2 reduction in the context of HD. We used in vivo electrophysiological recordings, microdialysis in behaving mice and rabies virus-based monosynaptic tracing to study thalamo-striatal and thalamo-cortical synaptic connectivity in R6/1 mice. Micro-structural synaptic plasticity was also evaluated in the striatum and cortex of R6/1 mice. We over-expressed Foxp2 in the thalamus of R6/1 mice or reduced Foxp2 in the thalamus of wild type mice to evaluate its role in sensory and motor skills deficiencies, as well as thalamo-striatal and thalamo-cortical connectivity in such mouse models. Results Here, we demonstrate in a HD mouse model a clear and early thalamo-striatal aberrant connectivity associated with a reduction of thalamic Foxp2 levels. Recovering thalamic Foxp2 levels in the mouse rescued motor coordination and sensory skills concomitant with an amelioration of neuropathological features and with a repair of the structural and functional connectivity through a restoration of neurotransmitter release. In addition, reduction of thalamic Foxp2 levels in wild type mice induced HD-like phenotypes. Conclusions In conclusion, we show that a novel identified thalamic Foxp2 dysregulation alters basal ganglia circuits implicated in the pathophysiology of HD.

show abstract

Sensory processing in Huntington’s disease

Cited by 3 publications

References 60 publications

Huntington-associated protein 1 inhibition contributes to neuropathic pain by suppressing Cav1.2 activity and attenuating inflammation

Huntington-associated protein 1 inhibition contributes to neuropathic pain by suppressing Cav1.2 activity and attenuating inflammation

Research advances in huntingtin-associated protein 1 and its application prospects in diseases

Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington’s Disease

Contact Info

Product

Resources

About