Journal of Clinical & Experimental Pharmacology

A Note on Neurological Responses through Mechanical Inputs

Sanista Nandez^* Department of Medical Pharmacology, Carol Davila University, Bucharest, Romania
^*Correspondence: Dr. Sanista Nandez, Department of Medical Pharmacology, Carol Davila University, Bucharest, Romania, Email:

Received: 10-Sep-2021 Published: 01-Oct-2021, DOI: 10.35248/2161-1459.21.s9.e005

Editorial Note

The conversion of mechanical inputs into neuronal responses is known as mechanosensation. The senses of light touch, hearing, proprioception, and pain are all based on mechanosensation. The sense of touch is controlled by cutaneous mechanoreceptors, which are mechanoreceptors present in the skin. Hearing and balance are controlled by hair cells, which are tiny cells in the inner ear. Mechanosensation is also linked to neuropathic pain states such as hyperalgesia and allodynia. In the process of mechanosensation, a wide range of factors are involved, many of which are still unidentified.

Thin axons and myelin sheaths differentiate A-fibres, which are either D-hair receptors or nociceptive neurons. The resistance of A-fibres can reach up to 25 m/s. D-hair receptors are the most sensitive of all known cutaneous mechanoreceptors, with wide receptive fields and low mechanical thresholds. A-fiber Mechanoreceptors (AM) is notable for their "free" nerve terminals and minimal myelination. A-fiber mechanonociceptors are thought to be responsible for fast mechanical and heat pain due to their high mechanical sensitivity and large receptive fields.

Because they lacked a myelin covering, C fibres have modest conduction rates of less than 1.3 m/s. 60-70 percent of primary afferent neurons that innervate the skin are C fibres. Mechanical and heat stimuli activate C fibres, which also respond to algesic drugs like capsaicin. Mechanical stimuli are the only ones that some C fibres respond to. As a result, the classification of C fibres is further broken down. C-Mechano Heat (C-MH), CMechano Cold (C-MC), and C-mechanoheatcold are C-fiber nociceptors that respond to both mechanical and thermal stimuli (C-MHC). C-mechanonociceptors are C-fiber nociceptors that only respond to stimulations (C-M).

Mechanically Insensitive Afferents (MIA), which lack mechanosensitivity and are also known as "silent" or "sleeping" nociceptors, are two other types of C fibres. C-fiber Low Threshold mechanoreceptors (C-LT) are involved in nondiscriminative touch. C-fibres categorized as "C-Mechano Insensitive Heat Insensitive" (C-MIHI) make up 15 to 25% of all C-fibres.

These molecular mechanisms causing cutaneous mechanosensitivity are currently unknown. Most likely, there's not a single unifying transduction method that all sensory neurons use. Sensory neurons, on the other hand, are thought to use rapid, mechanically gated cation channels, with the resulting depolarization being followed by the production of a sodium-dependent action potential at the transduction site. Rapid, mechanically gated cation channels are thought to be present in all sensory neurons. The depolarization of the membrane causes a sodium-dependent action potential to form at that region.

Mechanical strain is also considered to be recognised by ion channels via cytoplasmic and extracellular components. It's highly unlikely that all sensory neurons have their own transduction pathway. The attachment of ion channels to cytoplasmic and extracellular components is thought to be important for detecting mechanical strain on the cell membrane, and cell curvature may not directly gate these ion channels. Mechanosensation also aids cell growth and development by connecting with the Extracellular Matrix (ECM) and tractioning integrin receptors, which aid adhesion.

There is evidence that the lipid bilayer, which contributes to stretch issues that act the channel to open, may be regulated in whole or in part by mechanosensitive channels. While the lipid bilayer properties of cell membranes are known to contribute to mechanosensation, the amount to which the protein interacts with the lipid head groups is unknown. The formation of phosphatidic acid in a quick two-step process was directly linked to the mechanosensitivity of TREK-1 channels in a biological membrane.