Primary sensory afferents of the dorsal root ganglia and trigeminal ganglia innervate the skin, mucous membrane and muscles, and detect a wide range of stimuli, such as mechanical force, temperature and endogenous chemical mediators, through its specific sensors. The detected information triggers impulses, conducts to the central terminals in the dorsal horn or trigeminal nucleus, and then transmits to secondary neurons in the spinal cord or the medulla, which finally provides various sense: warm, cold, touch, pressure, pain and itch.
The excitabilities of primary sensory neurons are markedly influenced by the neurotropic factor, inflammatory mediators and other neuroactive agents generated under pathological condition, which transiently and/or persistently induces hyper- and hyposensitivity to various stimuli. Recent researches were shown the abnormal excitabilities of plasma membrane and sensors in addition to a structural abnormality of primary sensory afferents in cancer, diabetes and chronic inflammation of skin, joint, oral cavity and ocular surface. Furthermore, the changes in the efficacy and the number of synapses at the central terminals have also been reported under these conditions, which might be involved in the induction of sensory dysfunction. The prominent examples of these neurological changes are allodynia and hyperalgesia induced by chronic inflammation and peripheral nerve injury; sensitization of membrane excitability and nociceptor in peripheral afferents and enhancement of synaptic transmission in the central terminals. Therefore, understanding the regulatory mechanisms of neural activities and structures in primary sensory neurons is important for the evaluation of sensory abnormalities. However, the changes in neuronal properties and its underlying mechanisms has not fully understood.
To explore the molecular bases of sensory dysfunction, this Research Topic aims to receive Original Research or Review articles reporting novel finding on
(1) regulation of membrane excitability and sensory receptors in primary sensory neurons and
(2) changes in the feature of primary sensory neurons including central terminals and peripheral afferents under pathological condition.
We also welcome biological and pharmacological studies about potential therapeutic targets for abnormalities of primary sensory neurons.
Primary sensory afferents of the dorsal root ganglia and trigeminal ganglia innervate the skin, mucous membrane and muscles, and detect a wide range of stimuli, such as mechanical force, temperature and endogenous chemical mediators, through its specific sensors. The detected information triggers impulses, conducts to the central terminals in the dorsal horn or trigeminal nucleus, and then transmits to secondary neurons in the spinal cord or the medulla, which finally provides various sense: warm, cold, touch, pressure, pain and itch.
The excitabilities of primary sensory neurons are markedly influenced by the neurotropic factor, inflammatory mediators and other neuroactive agents generated under pathological condition, which transiently and/or persistently induces hyper- and hyposensitivity to various stimuli. Recent researches were shown the abnormal excitabilities of plasma membrane and sensors in addition to a structural abnormality of primary sensory afferents in cancer, diabetes and chronic inflammation of skin, joint, oral cavity and ocular surface. Furthermore, the changes in the efficacy and the number of synapses at the central terminals have also been reported under these conditions, which might be involved in the induction of sensory dysfunction. The prominent examples of these neurological changes are allodynia and hyperalgesia induced by chronic inflammation and peripheral nerve injury; sensitization of membrane excitability and nociceptor in peripheral afferents and enhancement of synaptic transmission in the central terminals. Therefore, understanding the regulatory mechanisms of neural activities and structures in primary sensory neurons is important for the evaluation of sensory abnormalities. However, the changes in neuronal properties and its underlying mechanisms has not fully understood.
To explore the molecular bases of sensory dysfunction, this Research Topic aims to receive Original Research or Review articles reporting novel finding on
(1) regulation of membrane excitability and sensory receptors in primary sensory neurons and
(2) changes in the feature of primary sensory neurons including central terminals and peripheral afferents under pathological condition.
We also welcome biological and pharmacological studies about potential therapeutic targets for abnormalities of primary sensory neurons.
