chapter 4 Flashcards
describe the resting membrane potential
polarized
-70mV
How can you record membrane potential?
comparisons of intracellular and extracellular electrode readings
what did Hodgkin and Huxley experiment on?
-giant squid motor neurons
how are sodium ions distributed?
- higher outside the cell
describe the resting membrane in relation to chloride ions
- concentration is higher outside the cell but only slightly resisted
describe the potassium concentrations in relation to resting potential
concentration is higher inside driven inside by electrostatic pressure but driven out by concentration gradient
what is concentration gradient?
tends to equally distrubute by moving high to low concentration
what is electrostatic pressure?
attractive forces between opposite charges and repelling forces between like charges
what are non-homogenizing factors to maintain resting potential?
passive and active movement
what is passive movement?
random motion due to selectively permeable ion channels
what is active transport?
sodium potassium pumps that maintain stability of resting potential in spite of random motion
what do post synaptic potentials do?
create signals in neurons
what do excitatory neurotransmitters do?
depolarization to make the membrane potential less negative
what do excitatory post synaptic potentials do?
increase the likelihood of an action potentials
what do inhibitory neurotransmitters do?
hyperpolarize the cell and make membrane potential more negative
what do inhibitory post synaptic potentials do?
decrease the likelihood of action potentials
what is the rate of EPSPs and IPSPs?
instantaneous rate of transmission with variable duration
describe amplitude of grade potentials
proprotional to signal intensity
describe transmission of graded potential
decremental transmission that is from weakening passive spread
what is responsible for generation of EPSPs?
sodium influx
what is responsible for IPSPs?
chloride influx
how are postsynaptic potentials integrated?
adding or combining signals into one overall output
what is spatial summation?
integration across post synaptic locations when local EPSPs and IPSPs occur simultaneously
what is temporal summation?
integration across time on the same synapse in rapid succession
what ae action potentials?
massive reversal of membrane potential that does not degrade over space
how are action potentials generated?
voltage-gated sodium ion channels that open or close in response to the membrane potential
when threshold of activation for action potentials is reached what happens?
voltage-gated sodium channels open and sodium rushes in due to electrostatic and concentration gradient
what is the second step during an action potential?
voltage-gated potassium channels open and potassium is driven out due to electrostatic and concentration gradient to repolarize cell
what is the absolute refractory period?
brief post initiation where it is impossible to to initiate new action potentials due to inactive sodium channels
what does the absolute refractory period do?
prevents backwards motion of action potentials and limits firing rate
what is the relative refractory period?
follows absolute period and requires larger than threshold stimulus to initiate new action potentials
describe conduction of an AP
active and passive nondecremental
anterograde conduction
from hillock to boutons
retrograde conduction
boutons to hillock
orthodromic conduction
anterograde
antidromic conduction
retrograde conduction
describe conduction in myelinated axons
instant conduction along myelin with passive, saltatory conduction
when is axonal conduction fater?
in larger, myelinated neurons
describe conduction in interneurons
passive and decremental that functions to integrate neural activity in brain structure
what are some differences in cerebral neurons from squid motor neurons?
fire AP continually, duration, frequency, and amplitude differ, dendrites can conduct APs
directed synapse
site of neurotransmitter release close to post synaptic contact
undirected synapse
site of release and contact for varicosities that is common for monoamines and neuroendocrine system
first step of chemical transmission of signals
AP reaches end of axon terminal
second step of chemical transmission of signals
calcium enters the cell
third step of chemical transmission
release of neurotransmitter into the cell
fourth step of chemical transmission
receptors influnece post synaptic neurons
inotropic refers to
ion permeability
metabotropic refers to
intracellular signalling
sixth step of chemical transmission
neurotransmitter degradation and recycling
small molecule neurotransmitter synthesis
enzymatic conversion of amino acid precursors
large molecule neurotransmitter synthesis
peptides that are processed by enzymes
where are small molecule NT synthesized
cytoplasm and golgi apparatus
how are small molecules NT’s released?
in pulses for each action potential
where are large molecule NT’s released?
into extracellular fluid and ventricles for bloodstream
where are large molecule NT’s synthesized?
cell body, packaged in vesicles and trasported with cytoskeletons to terminal
describe packaging of NT’s
proteins are syntehsized in rough endoplasmic reticulum then transported to the golgi where they bud off the golgi to form vesicles and transporter proteins actively pump NT’s into them after anterograde axonal transport
what are small clear core vesicles?
contain the small molecule NT’s
what are large dense core vesicles?
contains the neuropeptides of 90-250 diameter
what is coexistence?
when more than one type of NT is synthesized and released in neurons
what is anterograde to axon terminal transport of neurotransmitters?
motor proteins of kinesin use steps of attachment/ detachment; microtubules highway system
what does transport of NT require?
energy and calcium
how are NT’s released?
AP in axon terminals that opens voltage-gated calcium channels clustered in the active zone and activate proteins
what do the active proteins in neurotransmitters release do?
mobilize vesicles and fuse vesicles with synaptic membrane
what is vesicle recapturing?
local resynthesis of synaptic vesicles
where are NT receptors?
in presynaptic and postsynaptic cells
how do NT receptors work?
each is specific for the NT and there are multiple receptor sub-types for each but act differently in different areas of the brain
what are ionotropic receptors?
ligand-gated ion channels that are fast-acting and can generate EPSPs and IPSPs and are found post synaptically
what are metabolic receptors?
slow acting and long lasting changes that have more varied and diffuse effects
what are neuropeptide receptors?
metabotropic receptors
where are metabotropic receptors found?
pre and post synaptically for inhibition and facilitation at the presynaptic site
what is the anatomy of an ionotropic channel?
an ion channel with action lasting as long as the NT is around
what is the anatomy of a metabotropic channel?
it crosses the cell membrane seven time and has a pocket for the NT to bind to the G protein to be activated
how do ionotropic receptors act?
through EPSPs or IPSPs summated to initiated or inhibit AP generation in post synaptic cell
how do metabotropic systems act?
with a NT as a first messenger and then initiate a second messenger which initiates intracellular cascades
what are the effects of metabotropic receptors?
long lasting changed and various effects due to the types of G protein coupled to the receptor
what is often the presynaptic effect of metabotropic receptors?
an increase in NT’s
what is often the postsynaptic effect of metabotropic receptors?
increase in proteins that go do things
what are autoreceptors?
metabotropic receptors that auto respond to their own NT released from the presynaptic site
what is the function of autoreceptos?
providing feedback to NT concentrations
what are the ways of stopping NT’s
reuptake or enzymatic degradation
what is responsible for reuptake?
transporters on cell neurons/ glia that pick up the NT from synapse
what happens after reuptake?
repackaging into vesicles or intracellular degradation to execute monoamines
what could precursors be used for?
NT synthesis or energy
what does NT degradation happen?
when NTs do not have transporters for reuptake
what is the effect of pesticides?
inhibiting the ability of acetylcholinesterase to degrade acetylcholine
what is the effect of low doses to inhibit acetylcholine?
helps alzheimer’s patients to have more acetylcholine
what is an example of an NT that is degraded intracellularly?
dopamine
what is NT recycling?
reuptake can provide more NT to be repackaged and released immediately or can be broken down into different NTs
what is the distribution of astrocytes?
even distribution of domains with very little overlap
how do astrocytes act in synaptic transmission?
through coordinated activity with gap junctions that allows them to modulate NT activity
what does the tripartic synapse refer to?
presynaptic, post synaptic and astrocyte cell
what is a specific example of astrocyte involvement in synaptic transmission?
uptakes glutamate to reduce excitotoxicity, and stimulate energy provision to nuron which produces locatate that maintains activity.
what are gap junctions made of?
a protein called connexin
what is the function of gap junctions?
to connect cytoplasm of two adjacent cells and allow electrical synapse
what are amino acid NTs?
small molecule NTs that allow for fact acting directed synapses and are byproducts of intermediary metabolism
what are excitatory amino acids NTs?
NTs carrying 2 negative charged
where do excitatory amino acid NTs act
dendrites
what are examples of excitatory amino acid NTs?
glutamate and aspartate
where is glutamate found?
most commonly in the CNS
what is the effect of glutamate on ionotopic receptors?
induce EPSP through sodium, potassium, and calcium
where does glutamate act metabotropically?
Gs and Gq proteins
Describe normal NMDA receptor transmission
presynaptic glutamate and post synaptic depolarization as it displaces the magnesium block, allowing calcium into the cell
describe inhibition of NMDA receptor through ketamine
Channel is blocked by ketamine and calcium cannot enter the cell
what is the evidence for depression being a disease of plasticity?
after ketamine blockage of NMDA channels, the cell is forced to make a bunch of changes to allow calcium into the cell
describe inhibitory amino acid NTs?
carry one negative charge
where do inhibitory amino acid ATs act?
the soma is the major receiving area
what are examples of inhibitory amino acid NTs?
GABA, glycine
where is GABA found?
CNS
what receptors does GABA act on?
interneurons, ionotropic, and metabotropic
what is the effect of GABA on ionotropic receptors?
inhibitory through chloride influx or potassium efflux
what does GABA act on metabotropically?
Gi proteins
where is glycine found?
spinal cord
what is epilepsy due to?
too much glutamate and not enough GABA
what are glutamates and GABA important for?
learning and memory
what are the categories of monoamine NTs?
catecholamines, indolamines, histamines
what are examples of catecholines?
dopamine, norepinephrine, epinephrine
what is characteristic of catecholines?
precursor is tyrosine
what are indolamines?
melatonin, serotonin
what is characteristic of indolamine?
tryptophan precursor
how do monoamine NTs act?
diffused effects through metabotropic receptors that are released by varicosities
what is the role of catecholamines?
modulators in PNS and CNS
where is epinephrine found?
only released in PNS sympathetic to increase energy availability
where are norepinephrine and dopamine found?
CNS and PNS but cannot cross the blood brain barrier
what is norepinephrine for?
modulatory effects related to stress/anxiety , vigilance, vigilance, and attention
where is norepinephrine found?
locus coereleus
where is dopamine found?
nigrostriatal system, dorsal mesostriatal pathway, mesolimbic cortical, periventricular, tuberal hypophyseal
what is the effect of dopamine in nigrostriatal system?
movement and reward
what is the effect of dopamine on dorsal mesotriatal pathways?
movement initiation
what is the effect of dopamine on dorsal mesotriatal pathways?
movement initiation
what is the effect of dopamine on ventral nigrostriatal pathways?
positive incentive/ reward
what is the effect of dopamine of mesolimbic pathways?
projections to limbic structures with a role in schizophrenia and parkinsons
what is the effect of dopamine on periventricular pathways?
motivated behaviours, originates in hypothalamus
what is the effect of dopamine on tuberal hypophyseal pathways?
lactation
not enough dopamine in PFC results in what?
negative cognitive symptoms associated with PD
what is the effect dopamine in PFC results in what?
positive symptoms related to schizophrenia
where do dopamine neurons carry signals?
brainstem to midbrain and PFC
where is serotonin located?
Raphe nuclei and caudal system
what does raphe nuclei do with serotonin?
provides 80% to forebrain
what does the caudal system do with serotonin?
sensory and motor function in spinal cord
what does serotonin have a role in
appetite, sleep and aggression
what does melatonin do?
regulates circadian rhythms by fluctuating with light cycles to signal seasonal day length
where does ACh predominantly act?
Neuromuscular junction
what is the effect of botox?
inhibits the release of ACh to inhibit muscle contraction
what does curare do?
inhibitor of ionotropic receptors of ACh that causes paralysis
what are receptors of ACh?
Nicotinic and muscarinic
What is the nicotinic receptor
motor receptor NMU
what is the muscarinic receptor?
metabotropic receptor in ANS
what does ACh have a role in?
learning and memory including alzheimer’s and dietary choline
what is atropine?
mAchR antagonist that inhibits the parasympathetic system causing memory disorders
what are unconventional NT’s?
soluble gases
where are soluble gases synthesized?
neural cytoplasm
what do soluble gases do?
retrograde transmission with rapid diffusion to extracellular fluid with a role in controlling brain blood flow
describe endocannabinoid?
inhibitory metabotropic receptors with a role in pain reduction, increased appetite, and retrograde transmission
what are the groups of neuropeptides?
pituitary, hypothalamus, brain-gut opioid, misc
what do pituitary neuropeptides do?
release from pituitary gland and do not reenter brain
what do hypothalamus neuropeptides do?
release into pituitary and throughout brain to control behaviour
what do brain-gut neuropeptides do?
feeding behaviours and can cross bbb
what do opioid neuropeptides do?
endorphins released from periaqueductal gray to regulate pain and stress
what does behavioural pharmacology do?
provides treatments for neurological or neuropathological disorders by drugs targeting specific receptors
what does drug addiction depend on?
ease of crossing the bbb
where does drug addiction act?
mesotelencephalic dopamine system
what are endogenous opiods?
endorphin and enhephalin
what are exogenous opioid?
from opium poppy
where do opioid act?
periqueductal gray, hypothalamus, limbic system
