Flashcards in Neural & Hormonal Communication (230 #4) Deck (46):
can rapidly alter their membrane permeabilities and undergo rapid transient membrane potentials when excited.
- or + signifies the charge on the INSIDE of the membrane (typically -70mV in a neuron)
a reduction in the magnitude of the negative membrane potential, i.e. membrane is LESS polarized than at resting potential (-60 instead of -70mV)
the membrane returns to resting potential after being depolarized
increase in the magnitude of the negative membrane potential
1) change in electrical field in vicinity of excitable tissues
2) interaction of a chemical messenger with a surface receptor on a nerve or muscle cell membrane
3) stimulus like sound waves
4) spontaneous change of potential caused by inherent imbalances in the leak/pump cycle
open all the time, permitting unregulated leakage of their chosen ion across membrane through channels
2) chemically gated (change conformation from binding of messenger with receptor)
3) mechanically gated (respond to stretching or mechanical deformation)
4) thermally gated
local changes in membrane potential that occur in varying strengths (10-20mV). Usually chemically or mechanically-gated channels that open and let Na+ into the cell, causing depolarization. Strength and duration of potential is directly related to that of the triggering event. Starts at Na+ channel, then depolarization spreads as current flows away from the initial site of the potential change - diminishes as it spreads (few mm) - involves only small portion of the entire membrane. Can function as signals for very short distances
brief, rapid, large (100mv) changes in membrane potential during which potential actually reverses. Involves only small portion of membrane, but doesn't diminish in strength as it travels from site of initiation to rest of membrane (like the wave in a stadium). When depolarization of area reaches 'threshold potential', explosive depolarization takes place (from -70 mV to +30mV - 'overshoot') then back to resting, quickly. A.K.A. firing, spiking. Result from triggered opening and subsequent closing of voltage-gated Na+ and K+ channels.
either the membrane is depolarized to threshold and an action potential takes place that spreads non-decrementally throughout the membrane, or threshold is not reached in response to the depolarizing event and no action potential occurs.
protein with number of charged groups - sensitive to small changes in potential which cause distortions in channel shape, which makes them flip from one conformation to another. Na+ has activation and inactivation gate, can be:
1) closed, but capable of opening
2) open, or activated
3) closed and incapable of opening
K+ has only one gate that can be either closed or open.
Na+/K+ Action Potential Sequence
Depolarization of the membrane to threshold potential triggers sequential changes in permeability caused by conformational changes in voltage-gated Na+ and K+ channels.
1) Na+ influx (into the cell) causes the rising phase (to +30mV)
2) K+ efflux (out of the cell) causes the falling phase
3) before returning to resting, the action potential regenerates a new action potential by current flow away from it, which brings next area to threshold.
4) 'The Wave' - the self-perpetuating cycle continues down the axon until it has spread over the entire cell membrane undiminished.
5) restoration by Na+/K+ pumps over time, but it need not be fully restored before another AP can occur.
non-myelinated fibres - the action potential spreads along every portion of the membrane
myelinated fibres - the impulse jumps over the sections of the fibre covered with insulating myelin. more rapid than contiguous.
covered with myelin at regular intervals. Myelin is mostly lipids making it a good insulator - cells wrap around axons in a jelly-roll fashion. In the brain and spinal cord these are OLIGODENDROCYTES, and in the peripheral they are SCHWANN cells. In between nodes are NODES OF RANVIER there the axonal membrane is bare, each 1mm, where the bare space is 2 micrometers. Na+ channels are concentrated at the NOR, with sparse Na+ channels under the myelin. Non-myelinated fibres have Na+ channels throughout the entire length.
Regeneration of Nerve Fibres
1) non-myelinated: Schwann cells phagocytize the debris, while the Schwann cells themselves form a regeneration tube - nerve axon grows back and moves through tube by amoeboid movement.
2) myelinated: oligodendrocytes actually inhibit axonal growth by producing nerve-growth-inhibiting proteins (produced late in fetal devlpmnt) and myelin serves as guardrails to keep nerve endings from straying during fetal growth.
junction between two neurons. Axon terminal of one is the PRE-SYNAPTIC NEURON and dendrocytes/cell body of the second is the POST-SYNAPTIC NEURON. Synaptic KNOB of first contains synaptic vesicles that store a neurotransmitter (usually the same, sometimes 2) that will be sent across the synaptic CLEFT. So electric current does not pass from one to the other (since axon terminal does not contain channels for charged Na+ or K+) but instead, the postsynaptic neuron's potential is altered chemically.
1) AP in presynaptic neuron goes through axon terminal, local potential change triggers voltage-gated Ca2+ channels in synaptic knob.
2) influx of Ca2+ into synaptic knob
3) Ca2+ triggers exocytosis of synaptic vesicles through synaptic cleft
4) neurotransmitter binds with protein receptors on sub-synaptic membrane
5) changes opening of CHEMICALLY-gated channels in post-synaptic neuron.
Binding of neurotransmitter triggers opening of nonspecific cation channels that allow Na+ and K+ through them simultaneously. Results in small depolarization (lots of Na+ in, bit of K+ out), brings membrane potential closer to threshold. Called EXCITATORY POSTSYNAPTIC POTENTIAL or EPSP. Graded potential!
Binding of neurotransmitter increases permeability of K+ or Cl- (more K+ out or Cl- in), which brings about a small hyperpolarization. Moves the membrane potential FURTHER from threshold. Called INHIBITORY POSTSYNAPTIC POTENTIAL or IPSP. Graded potential!
conversion of the electrical signal (AP in presynaptic neuron) to an electrial signal in the postsynaptic neuron (EPSP or IPSP) takes 0.5-1msec. Chains of neurons may also need traversing - more time.
1) always leads to the same change in permeability/potential.
2) some typically bring EPSPs (glutamate in brain), and some are IPSPs (GABA, glycine), while some are variable (norepinephrine).
3) as long as neurotransmitter is bound to receptor, the response continues. Sometimes NT diffuses away, by inactivated by enzymes or postsynaptic membrane, or be taken back up by presynaptic membrane.
grand postsynaptic potential (GPSP)
summation of all EPSPs and IPSPs occurring at approximately the same time.
1)temporal summation - a second EPSP of the same origin is applied before the first one dies off.
2) spatial summation: EPSPs from more than one origin occur simultaneously.
The summation of changes in potentials at dendrocytes or cell body spread to axon hillock, where threshold is lowest (most density of voltage-gated Na+ channels). So AP originates in axon hillock and propagates from there to end of axon.
small rapid-acting molecules that trigger within a few milliseconds. Synthesized and packaged in the synaptic vesicles in the cytosol of the axon terminal - typically amino acids or closely-related compounds.
larger molecules made up of 2-40 amino acids, synthesized in cell body in the ER and Golgi, moved by axonal transport along microtubular highways to axon terminal. Packaged in DENSE-CORE vesicles, which undergo Ca2+-induced exocytosis and are released at the same time as neurotransmitters. Axon terminal may release one or more neuropeptide types. Bring about slower, more prolonged responses.
chemical messengers that do not cause EPSPs or IPSPs, but subtly depress or enhance the action of the synapse at either presynaptic or postsynaptic sites.
neuronal integration where one neuron binds to another to alter the amount of neurotransmitter that is secreted in response to an AP.
1) altering synthesis, axonal transport, storage or release of neurotransmitter.
2) modifying neurotransmitter interaction with postsynaptic receptor
3) influencing neurotransmitter re-uptake or destruction
4) replacing a deficient neurotransmitter with a substitute transmitter.
blocks reuptake of neurotransmitter dopamine at presynaptic terminals by binding with reuptake transporter. So dopamine remains in synaptic cleft longer than usual and continues to interact with postsynaptic receptor sites. Prolonged activation along emotional 'pleasure' pathways. Postsynaptic cells become used to high levels of stimulation and need increasingly higher doses. The number of dopamine receptors in brain decreased. When drug molecules diffuse away, the good feeling evaporates because the normal level of dopamine activity does not sufficiently satisfy the overly needy demands of the postsynaptic cells for stimulation.
desensitization to an addictive drug so that the user needs greater quantities for the same effect.
deficiency of dopamine in the basal nuclei - controls complex movements. Muscular rigidity and involuntary tremors. Levodopa (lDopa) is administered, converted to dopamine in brain and substitutes for deficiency.
tetanus & strychnine
prevention of IPSPs
Tet: prevents release of GABA neurotransmitter
Str: competes with glycine neurotransmitter at receptor site.
unchecked excitatory inputs to neurons result in uncontrolled spasms, convulsions, etc.
a given neuron has many other neurons synapsing on it - a single cell is influenced by many
branching of axon terminals so that a single cell synapses with and influences many other cells.
extracellular chemical messangers
1)paracrines - locally secreted, distributed by diffusion, short distance action, no intro to bloodstream (histamine).
2) neurotransmitters - diffuse and act locally on adjoining target cell
3) hormones - long-range, secreted into blood
4) neurohormones - released by neurosecretory neurons, which releases chemicals into blood instead of innervating a target cell.
binding of messanger to matching receptor brings about desired intracellular response:
1) opening/closing channels (like in an EPSP or IPSP)
2) activating second messanger systems (hormones)
binding of first messenger serves as a signal for activating an intracellular second messenger, who ultimately relays the orders through a series of biochemical intermediaries.
rapid response synapse, where neurotransmitter functions by changing the conformation of chemically-gated channels and producing EPSPs or IPSPs.
lead to responses mediated by second messengers, because they take longer and often last longer
the study of homeostatic chemical adjustments and other activities accomplished by hormones secreted by endocrine glands.
1)highly water-soluble - can dissolve & be transported in plasma
2) peptide (shorter) or protein (longer) hormones are produced in ER and packaged by Golgi. Secreted by exocytosis (insulin, catecholamines from tyrosine)
3) receptors on outside of target cell
4) change channels or activate second-messengers to alter activity of pre-existing proteins that produce the effect.
5) majority of hormones are this type. Hormones from the ADRENAL MEDULLA makes catecholamines.
1) high lipid solubility - cannot dissolve in plasma so must bind to plasma proteins (like albumin).
2) cholesterol or tyrosine derivative - made with help of enzymes limited to specific steroidogenic organs - not stored, but immediately diffuse through lipid plasma membrane
3) diffuse into target cell's lipid plasma membrane.
4) activate specific genes to make new proteins to produce the effect.
5) made in thyroid follicular cells, the adrenal cortex and the gonads.
Cyclic AMP Second-Messenger Pathway (cAMP)
1) binding of first messenger activates enzyme adenylyl cyclase in cytoplasm, through membrane-bound 'middleman' G protein.
2) induces the conversion of intracellular ATP for cAMP by cleaving off two phosphates.
3) cAMP activates intracellular protein kinase A
4) protein kinase A phosphorylates a specific protein XXX
5) XXX changes shape/function to inhibit/activate it
6) XXX brings about change in cell function.
Ca2+ Second-Messenger System
1) binding of first messenger activates enzyme phospholipase C in cytoplasm, through membrane-bound 'middleman' G protein.
2) enzyme breaks down PIP2 into DAG and IP3.
3) IP3 mobilizes Ca2+
3) Ca2+ activates intracellular calmodulin
4) calmodulin phosphorylates a specific protein XXX
5) XXX changes shape/function to inhibit/activate it
6) XXX brings about change in cell function.