Unit 4: NeuroT Removal and Meds Flashcards
What is one way to stop neuroT release?
Calcium ions are pumped out of the presynaptic neuron via Ca2+ pumps or Na+/Ca2+ exchanges to prevent further release of neuroT vesicles from the presynaptic membrane.
What is a passive form of neuroT removal from the synaptic cleft?
NeuroT will diffuse away from the synaptic cleft- This is effective at low-frequency neuroT release as the rate of these transmissions can still be accurately determined by the postsynaptic dendrites. Unsuitable at a high rate of release as the NeuroT will not diffuse away quickly enough and will build up- will keep triggering ligand-gated channels. They are broken down by other proteins/enzymes.
What is enzyme breakdown of neuroT?
Ach is broken down by Acetylcholinesterase found in the synaptic cleft and on the postsynaptic membrane. The enzyme breaks Ach down/hydrolyses into acetate and choline. The choline is then taken back into the presynaptic neuron via a high-affinity choline uptake system. Acetate diffuses into the surrounding medium.
What is the reuptake of neuroT?
This happens at the presynaptic neuron where the NeuroT is taken back into the neuron via reuptake transporter proteins. The whole neuroT is taken back into the axon terminal. it is then transported back to the cell body where it is where it can be repackaged by the Golgi body and used again. intercellular repackaging into cytoplasmic vesicles. Norepi dopamine serotonin
What are astrocytes?
They are a type of glial cell in the CNS- mainly the brain and have endfeet at the synapses. transporter proteins at the membrane remove the neuroT from the synaptic cleft into the cell which is then returned to the presynaptic neuron to use. they also help maintain extracellular ion concentrations eg calcium and also are responsible for the blood-brain barrier
What is myasthenia gravis? What is the treatment?
It is an autoimmune disease that mainly effects the PNS (due to large presence of Ach at NMJ). The Immu syst attacks Ach receptors on the postsynaptic membranes at the NMJ. This results in slow movement, muscular weakness, fatigue, heavy-lidded eyes or double vision. This is due to the fine motor control in the area which needs many neurons thus many receptors.
Target the enzyme that breaks up Ach- Acetylcholinesterase inhibitors to increase the amount left in the synaptic cleft which in turn can stimulate the reduced number of receptors. (Ach is usually broken down via an enzyme so this is effective)
What are SSRI and how are they used?
Selective serotonin reuptake inhibitors are a class of antidepressants and used to treat depression and sleep regulation. These drugs block reuptake channels by binding to the receptor and block the reuptake process. This increases the number of serotonin in the synaptic cleft, increasing the effect.
What does an overproduction and underproduction of dopamine result in?
Underproduction- A result of degeneration in the substantia nigra, which produces dopamine. It also affects receptors stimulated by dopamine. Dopamine is a hormone and neurotransmitter used in parts of the brain that coordinate movement. so there may be an intention tremor, stiffness in movement, slowness. Depression in Parkinson’s can be attributed to a lack of dopamine
Overproduction- results in overstimulation of the brain and has been implicated in schizophrenia
How is norepinephrine used?
SNRI- selective norepinephrine reuptake inhibitors are used to block reuptake channels on the presynaptic membrane and used as antidepressants.
Also used in the treatment of ADHD as it has been linked to understimulation so SNRI’s can be used to increase stimulation
