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
what kind of junction mediates electrical transmission
gap junctions
which part of the ANS is dominant in moment-to-moment modulation of HR and why?
parasympathetic. M2 cause direct stim of K+ channels to open, causing hyperpol whereast B1 stimulate through a G-coupled 2nd messenger system of cAMP activation (this takes longer)
older men can have hyperactive internal bladder sphincters. What kind of med is given for this?
alpha-1 blocker to normalize tone of internal bladder sphincter
what neuropeptide is lacking in narcolepsy?
orexin
organs of limbic system
amygdala, thalamus, hypothalamus, basal nuclei, prefrontal cortex, hippocampus, olfactory bulbs