Flashcards in Chapter 45 Deck (55):
Where does the central motor systems receive input?
receives incoming signals mainly from dendrites, and a little from synapses on cell body.
Where are the outputs in the central motor systems?
travels via a single axon leaving the cell body, and then the axon has many separate branches to other parts of the CNS or PNS. A special feature of most synapses is that the signal passes in the forward direction only. The signal travels in the required direction for performing specific nervous functions.
What causes sensory stimulation?
sensory experience exciting sensory receptors, whether visual receptors in the eyes, auditory receptors in the ears, or tactile receptors on body surface. The input causes brain reaction or is stored as memory
After the peripheral nerves bring information to the CNS, where do the inputs go?
(1) Spinal cord
(2) Reticular substance of medulla, pons, and mesencephalon
(5) Cerebral cx
What are the motor components of the nervous system?
i) Controls bodily movements/activities, by controlling contraction of skeletal muscle (body movement), smooth muscle (viscera), and secretion of chemical substances by exocrine and endocrine glands. The muscle and glands are called effectors b/c they perform the body function at the direction of nerve signals.
Is the main type of synapse in the CNS chemical or electrical?
WHat is a chemical synapse?
presynaptic neuron releases a NT which acts on the postsynaptic cell body, either exciting or inhibiting it (depending on NT and receptor)
Do chemical synapses travel in 1 direction or multiple?
only 1 direction
What are the main NT's at chemical synapses?
epi, NE, histamine, GABA, glycine, serotonin, glutamate
What are electrical synapses?
i) Smooth muscle and cardiac muscle cells transmit potentials via electrical synapses using gap junctions. Gap junctions conduct electricity from one cell to another, this done by the gap junctions allowing ions to flow from one cell to another.
Do electrical synapses travel in 1 direction or multiple?
they allow bi-directional transmissions
What are the steps to NT release at the synapse?
a) AP depolarizes the presynaptic terminal which opens voltage gated Ca channels, allowing Ca to enter. The entry of Ca into the presynaptic terminal allows NT vesicles to fuse with the presynaptic membrane and empty NT into the cleft. The NT diffuses across the cleft to the postsynaptic terminal where it binds to the receptors on the postsynaptic membrane.
b) Ca causes NT vesicles to fuse with the presynaptic membrane b/c Ca binds to release sites w/in the presynaptic terminal. The more Ca that enters the presynaptic terminal, the more NT released
What is the ionosphore at the postynaptic membrane?
ionosphore can be a ion channel or second messanger
What is the difference between a cation channel and an anion channel?
i) Cation channel: allows passage of sodium. Lined with negative charge, which attracts Na and repels Cl, when the diameter is large enough Na will be attracted and will move through
ii) Anion channel: allows passage of chloride ions. This channel is not charged, it is just small enough to let Cl through but not anything else (Na and Ca)
What are second messengers?
when it binds NT it activates one or more substances inside the postsynaptic cell. Important for functions that require activation longer than a few milliseconds (memory), the activated second messenger can continue the response for a long time after the NT is gone
What is the most common type of 2nd messenger proteins?
i) G-proteins are the most common, they consist of alpha (activator), beta, and gamma. When the G-prot is activated the alpha component dissociates from the other subunits and is free to act w/in the cell and performs one or more of the tasks listed in the next objective
What are four changes which can be activated by a postsynaptic receptor?
i) Opening specific ion channels through the postsynaptic cell membrane, these usually stay open longer than directly activated ion channels
ii) Activation of cAMP or cGMP in the neuronal cell, which can cause long-term changes in cell structure itself, which in turn alters long-term excitability of the neuron.
iii) Activation of one or more intracellular enzymes, the enzymes can cause any one of many specific chemical functions in the cell.
iv) Activation of gene transcription. This is one of the most important effects of activation of the second messenger systems because gene transcription can cause formation of new proteins within the neuron, thereby changing its metabolic machinery or its structure.
What is an excitatory receptor?
a rec that allows positive ions (cations) to enter the postsynaptic cell, the positive charges of the Na will excite the neuron
WHat is an inhibitory receptor?
a rec that allows entry of anions which will hyperpolarize the cell and inhibiting it
What are small molecule NT's?
are small and fast acting, causes most acute responses like transmission of sensory signals to the brain and of motor signals back to the muscles.
What are neuropeptides?
are larger and slow acting, cause more prolonged action such as long-term opening or closure of certain ion channels, or number/size of synapses
Where is the secretion of Ach?
secreted by neuron terminals of the large pyramidal cells from motor cx, different types of neurons in the basal ganglia, motor neurons that innervate the skeletal muscles, pregang neurons of the ANS, postgang neurons of parasympathetic nervous system, postgang neurons of the sympathetic nervous system
What is the polysynaptic effect of Ach?
excitatory mostly, inhibitory on heart via vagus n
Where is the secretion of NE?
secreted by neurons whose bodies are located in brainstem and hypothalamus. Specifically neurons located in the locus ceruleus in the pons which send neurons all over brain to control activity/mood/wakefulness.
What is the polysynaptic effect of NE?
excitatory and inhibitory
Where is the secretion of Dopamine?
secreted by neurons of substantia nigra, acts on striatal region of basal ganglia
What is the polysynaptic effect of dopamine?
Where is the secretion of glycine?
secreted by synapses in spinal cord
What is the polysynaptic effect of glycine?
Where is the secretion of GABA?
nerve terminals in spinal cord, cerebellum, basal ganglia, cx
What is the polysynaptic effect of GABA?
Where is the secretion of glutamate?
secreted by presynaptic terminals of sensory pathways entering the CNS and the cerebral cx
What is the polysynaptic effect of glutamate?
Where is the secretion of serotonin?
secreted by nuclei of median raphe of brainstem, projects to dorsal horns and hypothalamus
What is the polysynaptic effect of serotonin?
inhibitor of pain pathways in cord, inhibitor in higher regions of nervous system
Where is the secretion of NO?
secreted by nerve terminals in area of brain responsible for long term behavior and memory. It is not stored in vesicles but is made instantly when needed w/in presysn terminal and then diffuses out of presyn terminal and into postsyn terminal
What is the polysynaptic effect of NO?
changes intracellular metabolic functions that modify neuronal excitability, does not directly change postsyn cell potential
What are the ion concentrations of Na, K and Cl for neuronal cells?
i) Na: high outside soma, low inside soma (via Na pump continually pumping Na out)
ii) K: low outside soma, high inside soma (via K pump continually pumping K in)
iii) Cl: high outside soma, low inside soma (moves out b/c of the neg charge inside the cell)
What is the Action potential (AP) mechanism?
i) AP travels down presynaptic axon by salutatory conduction and is propagated by opening Na channels. Once the AP has passed the Na channels close and K channels open repolarizing the axon. When the AP reaches the postsynaptic terminal it opens Ca channels. Ca enters the presynaptic terminal causing vesicles packed with NT to fuse with the presyn membrane and release NT into cleft. NT diffuses across cleft and binds to receptors.
ii) If the excitatory stimulus large enough, it will cause Na channels to open in the postsynaptic terminal, if enough Na enters it will generate an AP. The AP moves down the postsynaptic axon by opening Na channels.
What is an EPSP?
i) The presyn terminal releases an excitatory NT into the cleft, the NT binds to its rec on the postsyn terminal, this causes Na channels to open, letting Na enter the postsyn cell. The increase in positive Na ions in the postsyn terminal increases the cells membrane potential depolarizing it, this is the excitatory postsynaptic potential.
What is an IPSP?
i) Inhibitory postsyn potential: increase in negativity (hyperpolarization) beyond resting membrane potential (if resting potential is -65mV and the charged is changed to -70mV, the IPSP is -5mV)
ii) Done by opening Cl channels (letting Cl- flow into the cell) or opening K channels (letting K+ flow out of cell), either way the negative charge inside the cell will become more negative, which inhibits AP
What is spatial summation?
when many presynaptic terminals, which are spread over a single postsynaptic terminal, release NT and the effect of the NT is the summation of them all. A single presyn terminal NT is usually not enough to illicit a postsyn effect b/c it only changes the postsyn cells EPSP about 0.5 to 1mV, but when 10+ presyn terminals act on the same postsyn terminal all of their effects add together to give an EPSP of 5 to 10mV, enough to cause a postsyn AP.
What is temporal summation?
it takes only 1ms to open a channel on the postsyn cell, but the change this causes can last up to 15ms. So if one NT stimulates the postsyn cell, then another NT stimulates the cell w/in that 15ms window, their effects are added together, this is temporal summation.
What is facilitation?
is when there is a postsyn potential that is excitatory but not enough to fire an AP, it doesn’t reach threshold. But it is in a depolarized state so that a signal from another source can easily cause an AP
What is the role of dendrites in neural signaling?
a) Dendrites extend out away from the soma and receive signals from large spatial area; this allows for summation of signals from many separate presyn nerve fibers. They then transmit electronic current to the soma, stimulating or inhibiting it.
What is decremental conduction?
the effect of excitatory/inhibitory inputs on dendrites depends on their distance from the soma. Since dendrites are leaky, they lose electrical charge as the current passes through them, therefore the further the excitatory/inhibitory synapse is from the soma the less effect is has on the soma
Where on the neuron do 80-95% of the presynaptic terminals synapse onto in the anterior motor neuron?
What is synaptic fatigue?
When excitatory synapses are repetitively stimulated at a rapid rate, the number of discharges by the postsynaptic neuron is at first very great, but the firing rate becomes progressively less in succeeding milliseconds or seconds.
What causes fatigue?
i) Exhaustion of stores of NT in presyn terminal
ii) Progressive inactivation of many of the postsyn membrane receptors
iii) Slow development of abnormal concentration of ions inside the postsyn neuronal cell
What is the effect of alkalosis on synaptic transmission?
i) Alkalosis greatly increases neuronal excitability. An increase in blood pH to 8.0 can cause epileptic seizures b/c of increased excitability
What is the effect of acidosis on synaptic transmission?
ii) Acidosis greatly depresses neuronal activity. A drop to 7.0 blood pH usually causes comatose. (diabetic acidosis = diabetic coma)
What is the effect of hypoxia on synaptic transmission?
i) Some neurons when they have no O2 they will be completely unexcitable. Loss of blood flow (O2 delivery) to the brain for 3-7mins will cause a person to lose consciousness
What is the effect of the excitatory drug strychinine on synaptic transmission?
by inhibiting the action of normally inhibiting glycine in the spinal cord. This allows the excitatory NT to go apeshit and excite neurons so much it causes severe tonic muscle spasm. Book also talked about caffeine, theophylline, and thebromine all increasing excitability by lowering a neurons threshold
What is the affect of anesthetics on synaptic transmission?
anesthetics increase threshold thus inhibiting the neuron by making it harder to fire an AP