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Nociceptive effect in mice (Process (1)Transduction (Peripheral terminals…
Nociceptive effect in mice
Nociception
Somatic nociceptive pain is sharp, crushing, tearing pain that usually follows a dermatomal pattern.
Visceral nociceptive pain is dull, cramping, or colicky pain associated with peritoneal irritation, dilation of smooth muscle or a tubular passage.
Nociceptors that respond to noxious stimuli and converting them into electrical signals toward the spinal cord, thalamus, and the cerebral cortex
Associated with inflammation, which is a primary response essential for maintaining homeostasis
Acetic acid
Measuring peripheral antinociceptive activity by induced abdominal writhing according to Koster et al. (Koster et al., 1959) test.
Causes pain by the release of endogenous substances such as serotonin, histamine, prostaglandins (PG), bradykinins, and substance P (Bentley et al., 1983)
Also associated with prostanoid, that increased the level of PGE2, PGF22 and PGF2,which increased level lipoxygenase product (Deraedt et al., 1980).
Provoke abdominal contractions, movements of the body as a whole (particularly of the hind paws) , twisting of dorsal abdominal muscles, reduction in motor activity and coordination.
The number of writhing were recorded for 30 min, starting 5 min after the injection of acetic acid intraperitoneally.
Formalin test
Formaldehyde 2.5% (v/v in distilled water) were injected subcutaneously into the plantar surface of the left hind paw of the mice.
The behavioral responses to nociception including biting, licking, and scratching of the injected paw were observed
The time spent was recorded in 2 phases, 0-5 min (early phase), and 15-30 min (late phase) after formalin injection.
The first phase (neurogenic pain) involves direct stimulation of sensorial afferent C- fibers by formalin.
Second phase (infl ammatory pain) involves a peripheral inflammatory process and is believed to arise from nociceptive spinal neuron hyperactivity (Tjolsen et al., 1992; and Le Bars et al.,2001).
Process
1)Transduction
Peripheral terminals of nociceptive C fibers and A-delta (Aδ) fibers are depolarized by noxious mechanical, thermal, or chemical energy and create action potential (AP).
3) Transmission
AP reaches the presynaptic terminal in the dorsal horn and cause realisation of a variety of pro-nociceptive substances into the synaptic cleft which activates postsynaptic receptors
Ion influx and depolarize second order neurons and interneurons. When a secondary neuron is depolarized it generates an action potential that is relayed through the medulla and brain stem or to the hypothalamus.
2) Conduction,
AP is conducted across the peripheral process to the central process were it depolarizes the presynaptic terminal that interfaces with a network of interneurons and second order neurons in the dorsal horn.
Interneurons can facilitate or inhibit transmission to second order neurons.
4) Modulation
Adaptive process involving both excitory and inhibitory mechanisms.
Using peripheral modulation & central modulation
5) Perception
An unpleasant sensation that can be localized to a specific region of the body
Capsaicin
Targeting TRPV1 (transient receptor potential vanilloid type 1
Chemically-gated non-specific cation channel with high calcium permeability.
Causing sharp and burning sensation
Effect of capsaicin was observed 10 min post-injection of intraplantar.