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Flashcards in Interneurons and Pain Deck (14):
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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.

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Inhibitory interneuron

located in the CNS, they use GABA, glycine and some peptides as transmitters

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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)

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Pain transmitters

Glutamate and substance P

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Pain pathway

through spinal cord to the brain, via the spinothalamic tract, to the sensory cortex and the limbic system.

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Myelinated A sigma fibers

Conduct fast, sharp and shooting pain

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Unmyelinated C fibers

Conduct slow, dull, aching and burning pain

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Endogenous pain reducers

Enkephalins (Enk) and beta-endorphin released from the periacqueductal and periventricular gray matter

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Opioid receptors

mu, sigma, and kappa *They are Gi/o protein coupled receptors

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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

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Anesthetic types (Ester)

Procaine, benzocaine, tetracaine

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Anesthetic types (Amide)

Lidocaine, bupivicaine, prilocaine

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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

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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