PSY 260 EXAM 1
Release
- action potential opens voltage-gated Ca2+ channels for it to go into the neuron
Exocytosis
- pushing the synaptic vesicles out of the cytoplasms
What happens to the NT once it is released into the synaptic cleft?
- receptor activation, aka the NT binds to the receptor like a key in a lock
Inactivation
- when the NT goes back into deactivation, either degredation or reuptake
Degradation
- when the enzymes simply destroy it to stop the NT action
Reuptake
- pumping the NT back into the terminal button, whether it is either recycled or destroyed
Receptors
- there are two primary receptors: inotropic and metabotropic
Ionotropic
- attached to an ion channel that is controlled by a chemical, which will open or close the
channel (very fast and short-lived action)
Metabotropic
,- attached to a G-protein, where it can open/close/modulate ion channels, activate enzymes
that produce a second messenger inside the cell (slower effects, but also bigger effects)
Second messenger
- can cause channels to change or alter biochemical processes in the neuron itself
Question: how can activation of an ionotropic receptor lead to EPSPs and IPSPs?
- Answer: It can open up an ion channel for charged ions, which can depolarize or hyper-
polarize the cell
Where are the receptors
- in the postsynaptic neuron, which is receiving the neurotransmitter with the message (we
can also see receptors in the presynaptic neuron aka. autoreceptors)
Autoreseptors
- in the presynaptic neuron that acts as a negative feedback system, and send messages down
neurotransmission when there are too many neurotransmitters (synthesis or release)
activated by the neurotransmitter released by that presynaptic neuron
Acetylcholine
- first neurotransmitter initially called Vagusstoff, and sows the heart down (aka inhibitory)
necessary for the synthesis of a neurotransmitter (neuron cholinergic)
-made from choline + acetyl enzyme
- two classes of receptors: nicotinic and muscarinic
Nicotinic receptor
- ionotropic, nicotine binds to these, and opens up ion channel
Muscarinic receptor
- metabotropic, activate a gene protein and cause chain reactions
, Myasthenia gravis
- severe muscle weakness caused by an immune disorder, system attacks acetylcholine
receptors in the muscles so the muscle can't respond well, leading to muscle weakness (we
have neurotransmitters, but no receptors)
Acetylcholinesterase
- destroys acetylcholine and the remaining choline is taken back up
Monoamies
- two categories are catecholamines and serotonin
Catecholamines
- generated from substances we get from our diet (ex. tyrosine, which can be converted to
dopa and then dopamine, which leads to norepinephrine and enpinephrine), they can't inject
pure dopamine because it won't make it past the blood barriers, but they can inject dopa that
is converted to dopamine inside your system, Catecholamines are inactivated and taken back
to the presynaptic terminal button where it is recycled OR destroyed by MAO or COMT
enzymes.
Serotonin
- generated from a substance from our diet called tryptophan
Amino acids
- glutamate and GABA
Glutamate
- excitatory neurotransmitter in the brain and spinal cord, Important with memory and
disease states(maybe schizophrenia)
GABA
Release
- action potential opens voltage-gated Ca2+ channels for it to go into the neuron
Exocytosis
- pushing the synaptic vesicles out of the cytoplasms
What happens to the NT once it is released into the synaptic cleft?
- receptor activation, aka the NT binds to the receptor like a key in a lock
Inactivation
- when the NT goes back into deactivation, either degredation or reuptake
Degradation
- when the enzymes simply destroy it to stop the NT action
Reuptake
- pumping the NT back into the terminal button, whether it is either recycled or destroyed
Receptors
- there are two primary receptors: inotropic and metabotropic
Ionotropic
- attached to an ion channel that is controlled by a chemical, which will open or close the
channel (very fast and short-lived action)
Metabotropic
,- attached to a G-protein, where it can open/close/modulate ion channels, activate enzymes
that produce a second messenger inside the cell (slower effects, but also bigger effects)
Second messenger
- can cause channels to change or alter biochemical processes in the neuron itself
Question: how can activation of an ionotropic receptor lead to EPSPs and IPSPs?
- Answer: It can open up an ion channel for charged ions, which can depolarize or hyper-
polarize the cell
Where are the receptors
- in the postsynaptic neuron, which is receiving the neurotransmitter with the message (we
can also see receptors in the presynaptic neuron aka. autoreceptors)
Autoreseptors
- in the presynaptic neuron that acts as a negative feedback system, and send messages down
neurotransmission when there are too many neurotransmitters (synthesis or release)
activated by the neurotransmitter released by that presynaptic neuron
Acetylcholine
- first neurotransmitter initially called Vagusstoff, and sows the heart down (aka inhibitory)
necessary for the synthesis of a neurotransmitter (neuron cholinergic)
-made from choline + acetyl enzyme
- two classes of receptors: nicotinic and muscarinic
Nicotinic receptor
- ionotropic, nicotine binds to these, and opens up ion channel
Muscarinic receptor
- metabotropic, activate a gene protein and cause chain reactions
, Myasthenia gravis
- severe muscle weakness caused by an immune disorder, system attacks acetylcholine
receptors in the muscles so the muscle can't respond well, leading to muscle weakness (we
have neurotransmitters, but no receptors)
Acetylcholinesterase
- destroys acetylcholine and the remaining choline is taken back up
Monoamies
- two categories are catecholamines and serotonin
Catecholamines
- generated from substances we get from our diet (ex. tyrosine, which can be converted to
dopa and then dopamine, which leads to norepinephrine and enpinephrine), they can't inject
pure dopamine because it won't make it past the blood barriers, but they can inject dopa that
is converted to dopamine inside your system, Catecholamines are inactivated and taken back
to the presynaptic terminal button where it is recycled OR destroyed by MAO or COMT
enzymes.
Serotonin
- generated from a substance from our diet called tryptophan
Amino acids
- glutamate and GABA
Glutamate
- excitatory neurotransmitter in the brain and spinal cord, Important with memory and
disease states(maybe schizophrenia)
GABA
