Interneurons and Pain Flashcards
Inhibitory interneuron
located in the CNS, they use GABA, glycine and some peptides as transmitters
Excitatory interneuron
Stretch receptor sensory neurons of the quadricep muscles makes excitatory connection with the extensor motor neuron of the same muscle and an inhibitory interneuron projecting to the flexor motor neurons supplying the antagonist hamstring muscle, results in kick reflex.
Function of interneurons
In the brain: interneurons form circuitry, integrate neuronal activity, and synchronize activity and large principal cells
In the spinal cord: the regulate the reflex (exciting extensor and inhibiting flexor muscles)
Pain transmitters
Glutamate and substance P
Pain pathway
through spinal cord to the brain, via the spinothalamic tract, to the sensory cortex and the limbic system.
Myelinated A sigma fibers
Conduct fast, sharp and shooting pain
Unmyelinated C fibers
Conduct slow, dull, aching and burning pain
Endogenous pain reducers
Enkephalins (Enk) and beta-endorphin released from the periacqueductal and periventricular gray matter
Opioid receptors
mu, sigma, and kappa *They are Gi/o protein coupled receptors
Mechanism of opioids
Stimulation of opioid receptors inhibits adenylyl cyclase (AC), decreases cAMP/PKA cascading, and decreases activity of voltage gated Ca channels in presynaptic terminals reducing the release of glutamate/substance P
- Also activate K channels in postsynaptic membrane = hyperpolarization of both presynaptic and postsynaptic terminals (stoppage of signal transduction)
- opioids decrease the release of glutamate/substance P from presynaptic terminals and reduces activity of Post-syn neurons to conduct pain to brain
Anesthetic types (Ester)
Procaine, benzocaine, tetracaine
Anesthetic types (Amide)
Lidocaine, bupivicaine, prilocaine
Mechanism of Local Anesthetics
All block VG Na channels.
Blockade is voltage and time dependent
*Higher affinity for Na channels in the open-state (depolarized Vm) than those at close-state (hyperpolarized Vm)
*Slower recovery than those than normal inactivation
Toxicity of local anesthetics
CNS: Sleepiness, depression, headache, restlessness, seizure.
Lidocaine can cause transient neuropathy symptoms (loss of sensations, prickling, pain) when used for spinal anesthesia
Cardiovascular system: block Na channels in cardiac cells, high doses can also block Ca channels and reduce cardiac contraction.
*Allergic reactions caused by metabolites of procaine