Flashcards in 11/10 Synapses Deck (33)
two main types of the huge diversity of neurotransmitter receptors on postsynaptic neurotransmitters
Describe Channel-Linked (ionotropic) Receptors
ligand gated ion channels. Action is immediate and brief. Excitatory receptors are channels for small cations. Inhibitory receptors allow Cl- or K+ to hyperpolarize.
Examples of Ionotropic receptros
AMPA (glutamtate), nicotinic Ach, GABAa
Describe G Protein-linked (metabotropic) Receptors.
Transmembrane protein complex that binds the neurotransmitter, triggering intracellular cascade. Slow, indirect, complex, and prolonged and widespredead.
examples of G protein-linked metabotropic receptors
muscarinic Ach, GABAb, dopamine (D2 receptors
what is the second messenger for the G-protien receptors?
activated G-protien activates adenylate cyclase that makes cAMP that brings about the cell signal change by opening/closing ion channels and activating enzymes and activating genes.
Atropine (metabotropic receptor drug)
muscarinic Ach antagonis (treatment for bradychardia) increases SA node fireing
Propanolol (metabotropic receptor drug)
(beta blockers) beta-adrenergic antagonist --treatment for hypertension, tachycardia
opiates (metabotropic receptor drug)
(morphine, oxycodone, etc.) target opioid receptors.
What do most post synaptic receptors have for a class of recepotor molecule?
both the ionotropic and metabotropic receptors.
what really decides what the action at a synapse will be?
the postsynaptic receptor does!! it interprets the signal and responds...
what will decide the strength of a postsynaptic potential?
the amount of neurotransmitter released; the time the neruortrnamitter is in the adrea; the density and conductance of postsynaptic receptors.
what type of post-synaptic transmitter would usually lead to an IPSP due to Cl-?
IPSP triggered by ionotropic receptors (GABA) due to Cl- conductance
what type of post-synaptic transmitter would usually lead to an IPSP due to K+
usually metabotropic receptors like mGluRs
compare the spacial oriention of EPSP neurons and IPSPs
typically the IPSPs will be on the cell body and the EPSPs will be on the dendrites of the cell
why would the spacial orientation of EPSPs and IPSPs neurons be significant
spacial summation occurs at the start of the axon and the IPSPs don't have as much magnitude, but by being closer they can still overcome the EPSPs
what is a dendritic spine?
these are specialized sites for synaptic input, they are the post synaptic sites for axon synapse.
what is a dendritic spine do
it amplifies the electrical signals and can act as a small indipendent biochemical compartment. theis can allow for independent modulation at individual synapses
what is common with genetci defects of dendritic spines?
defects that result in lackk of porper spine formation typically lead to severe mental retardation, congitive deficits
how does the use of a synapse chage its character
repeated use increases the efficiency of neurotransmission, and disuse can reduce efficiency!!! this can be seen as an increase in release of neurotransmitter and neurotransmitter receptors; this could be function of memory.
What might be the bio-molecular mechanism of long-term potentiation (highly used synapses become more efficient)
It seems to be related to the NMDA glutamate receptor. This receptor is both ligand and voltage gated. Glutamate will be released to the synapse and bind both the normal AMPA receptor and NMDA receptor. the AMPA opens for Na+ and depolarize the cell. This will then open the NMDA receptor and allow Ca+ to come in that will change the cell to lead to more AMPA receptors. therefore we need both the glutamate release and a good depolarizatio of the post synaptic to lead to more receptors. It also leads to remodeling of the cytoskeleton of the synapse to make it larger!
Repeated use increased the -------- of neurotransmission
what will brief, high frequency stimulation partially depolarizing the postsynaptic neuron do to the neuron?
chemically gated channesl (NMDA receptors) allow Ca2+ entry and this activates kinase enzymes that promote more effective responses to subsequent stimuli
You wish to design a drug to erase particular memoris would you....1. NMDA receptor antagonist; 2. Kinase inhibitor; 3. Inhibitor of presynaptic glutamate release; 4. inhibitor of protein synthesis
target a Kinase inhibitor itself since this is what is driving and maintaining the post-synaptic signalling.
what will Kinase activation do in a post-synaptic receptor region to alter memory or learning?
it can also lead to changes in receptor expression
what is epilepsy like a fat kid on a teater-totter?
it is a loss in the balance of excitation and inhibition signals ... excitation runaway is what would lead to a seizure, just like the fat kid would lead to an imbalance in the teater totter,
how can alzhimers lead to loss of memory
by having the amyloid plaques that end up blocking the dendrites and the synapse even before they break down the cell in other ways.
why type of receptor could I block in a neuron to simulate a tonic-clonic seizure?
block the GABAa receptros. since these are the IPSP signals, if they are absent then the cell will be over-excited and seizure!
what type of drugs are used for seizure control?
use drugs that enhance GABA-ergic transmission and block Na+, and Ca+ channels. in essence blocking the channels for EPSPs and promoting the channels for IPSPs
what is the major protein to point a finger at for alzhiemers?
newest evidence is not so implicative of the amyloid plaques...what then could lead to nerve signal problems?
excess Ab peptide even before it forms an amyloid plaque. this will cause internilaztion of AMPA, NMDA, Glu receptors, nAchR blockade, spine retraction and loss of synaptic plasticity.
what is the result of the damage caused by Ab peptide even before it makes an amyloid plaque?
synaptic depression at glutamatergic synapses, loss of cholinergic neurons.