Neurons, brain, cell membrane, NT Flashcards
midterm prep
3 classes of neurons
1) Afferent convey info from tissues and organs toward CNS
2) Efferent convey info away from CNS to effector cells
3) Interneurons connect neurons w/in CNS
astrocyte function
- Regulate compositn xtracellular fluid in CNS via removal of K+ and neurotransmitters around synapses
- Stimulate fxn of tight junctions between cells that make up walls of capillaries in the CNS
o Blood brain barrier - Sustain neurons metabolically
o Provide glucose, remove ammonia - In embryos, astrocytes guide CNS neurons as they migrate to their ultimate destination and stimulate neuronal growth via secretion of growth factors
- Have ion channels – can generate weak electrical responses
ACh
- Synthesized from choline and acetyl coA in the cytosol of pre-synaptic terminals and stored in synaptic vesicles. Neurons that release ACh are cholinergic neurons.
- RECEPTORS: Nicotinic receptors (ion channel) and muscarinic receptors (metabotropic and couple with G proteins)
- INACTIVATION: Enzyme acetylcholinesterase (located in pre and postsynaptic membranes destroying ACh releasing choline and acetate)
- PHARMACOLOGY: Atropine is a naturally occurring antagonist of muscarinic receptors (eg. Eyedrops) that relax the smooth muscle of the iris, thereby dilating the pupils for eye exam.
Biogenic Amines
Catecholamines: dopamine, norepinephrine, epinephrine
- Dopamine is precursor of epinephrine and norepinephrine.
- Synthesis begins with uptake of tyrosine by the axon terminals and its conversion to another precursor L-dopa (by rate limiting enzyme tyrosine hydroxylase). Then, depending on the enzyme expressed in a given neuron, any one of the three catecholamines may be released. Phenylethanolamine N-methyltransferase (PNMT) is the enzyme that converts norepinephrine to epinephrine.
- INACTIVATION: Enzymes monoamine oxidase (MAO) & Catechol-O-methyltransferase (COMT)
- PHARMACOLOGY: drugs known as monoamine oxidase (MAO) inhibitors increase the amount of norepinephrine and dopamine in a synapse by slowing their metabolic degradation, used in treatment of depression.
What do beta-blockers do (ie: which receptor do they bond to)?
Beta blockers lower blood pressure by binding to beta-adrenergic receptors, preventing epi and NE from binding since they raise BP
what do stimulated alpha-1 receptors do to visceral organs?
widen pupil, constrict arterioles to coronary / skin / skeletal / abdominal viscera / kidney / salivary gland, contract urinary bladder sphincter
what do stimulated beta-1 receptors do to visceral organs?
increase HR, contractility, conduction
what do stimulated beta-2 receptors do to visceral organs?
relax bronchiole muscle and bladder wall
what is the effector enzyme for IP3 / DAG?
phospholipase C
what does Botulinum do?
blocks SNARE protein, preventing release of neurotransmitter and causing flaccid paralysis
what does atropine do?
It is a muscarinic antagonist; it blocks the muscarinic receptor on the postsynaptic membrane and results in decreased secretions
where electron potentials are generated
axon hillock
lidocaine action
blocks Na+ voltage-gated channels, preventing action potential
tetrodoxin
created by pufferfish
similar to lidocaine in that it blocks voltage-gated Na+ channels to prevent action potential
how are NT removed from synaptic cleft?
reuptake, diffusion, enzyme degrades, degraded by nearby glial
