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Neuro Exam 2 > N2 > Flashcards

N2 Flashcards

0
Q

Axon endings have…

A

Presynaptic terminals= Presynaptic knobs.

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1
Q

Binding of the NT to the receptor

A

Opening/closing of a specific ion channel(cl, na, k, ca)> allows SIMPLE DIFFUSION of ions DOWN their electrochemical gradients>EPSP (when Na or Ca moves in) OR IPSP (when K moves out or Cl moves IN).

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2
Q

Synaptic knobs contain

A

Transmitter vesicles

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3
Q

Transmitter vesicles

A

Membrane enclosed structures containing neurotransmitter molecules

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4
Q

Postsynaptic cell

A

Has receptors for the chemical messenger

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5
Q

Axo-dendritic

A

Most typical chemical synapse

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6
Q

Axo-somatic

A

MOST POWERFUL excitatory chemical synapses as local current flow experiences little resistance due to large surface area of the cell body…(NONDECREMENTAL CONDUCTION).

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7
Q

Axo-axonic

A

inhibitory when the axon is on the axon hillock.
-can veto excitatory effects of axo dendritic & axo somatic synapses & block/decrease the frequency of action potentials generated by an EPSP on the soma.

Exert PRESYNAPTIC FACILITATION OR INHIBITION when the synapse is onto the synaptic ending of the postsynaptic cell.

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8
Q

Dendro-dendritic

A

NO NT TO RELEASE- can only be ELECTRICAL synapses due to gap junctions bt dendrites of different neurons.

  • can allow a NT that has receptors on only 1 of the neurons to influence the activity of the other neuron.
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10
Q

PRESYNAPTIC EVENTS

A

1) Arrival of an AP at the membrane of the SYNAPTIC KNOB on the PRESYNAPTIC CELL
2) OPENING of voltage gated CA channels in the synaptic knob membrane
3) entry of CA+ into the SYNAPTIC KNOB
4) CA+ binds to CALMODULIN
5) CA/CALMODULIN activates a PROTEIN KINASE
6) . Protein Kinase phosphorylates SYNAPSINS
7) vesicles are moved to the cell membrane -involves contraction of cytoskeleton proteins
8) vesicle membrane fuses with the cell membrane and releases the NT into the cleft by EXOCYTOSIS
9) NT diffuse across the cell.

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11
Q

POSTSYNAPTIC EVENTS

A
  1. Neurotransmitters bind to specific receptors on the postsynaptic cell membrane
  2. Open or close ligand gated ion channels (or cause other changes in neuron cell function)
  3. Whether an EPSP or IPSP is produced depends on the type of receptor rather than the identity of the neurotransmitter. Each neurotransmitter has different types of receptors that work in different ways
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12
Q

VARIATIONS IN PRESYNAPTIC FUNCTIONS:

Regulation of Ca++ entry and the number of vesicles releasing neurotransmitters

A

The more Ca++ in the cytoplasm  the more vesicles release their neurotransmitters.

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13
Q

Increased frequency of action potentials

A

INCREASES the amount increases the amout of Ca++ entering the synaptic knob> increasing release of NT

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14
Q

PREsynaptic Inhibition

A

Neurotransmitters from neurons with axo-axonic synapses onto the synaptic endings of the presynaptic cell can activate a biochemical pathway that phosphorylates the voltage gated Ca++ channels and makes them harder to open in response to an action potential. As a result fewer Ca++ channels open/AP –> less Ca++ enters the synaptic ending  less NT’s released / AP

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15
Q

Presynaptic Facilitation

A

Neurotransmitters from neurons with axo-axonic synapses onto the synaptic endings of the presynaptic cell can activate a biochemical pathway that alter the voltage gated Ca++ channels and makes them easier to open in response to an action potential. As a result more Ca++ channels open/AP –> more Ca++ enters the synaptic ending  more NT’s released / AP

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16
Q

Long Term Potentiation

A

NO released from the excited Postsynaptic cell diffuses back across the synapse to the Presynaptic knob enhancing Ca++ entry

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17
Q

Long term Potentiation appies to

A

any process that improves the effectiveness of a synapse

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18
Q

Neurotransmitters are synthesized in the

A

SYNAPTIC KNOB

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19
Q

Inhibition of synthesis of neurotransmitters

A

Negative feedback regulation of the concentration of Neurotransmitter in the synapse

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20
Q

In response to an elevated concentration of the neurotransmitter in the synapse,

A

In response to an elevated concentration of the neurotransmitter in the synapse, the receptors activate a biochemical pathway that inhibits the synthesis of new molecules of the neurotransmitters. This process can cause addiction to drugs (such as Cocaine) that increase the release of a neurotransmitter.

Decreased synthesis of Nt’s –> deficiency of Nt’s for release.

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21
Q

Re-uptake of neurotransmitters.

A

Some NT are taken back into the presynaptic cell by endocytosis and re- packaged into vesicles or destroyed. Reuptake reduces the concentration of NT in the synapse and its ability to influence the post synaptic cell

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22
Q

Inhibition of re-uptake

A

prolongs the length of time neurotransmitters are in the synapse  increases the concentration of NT –> increased binding to the post synaptic cell.

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23
Q

After reuptake

A

the neurotransmitter may be destroyed by enzymes

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24
Q

Mono amine oxidase (MA0) enzymes

A

oxidize the mono amines : Serotonin, Dopamine and Norepinephrine

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25
Q

MAO inhibitors

A

block the destruction of the monoamine NT’s inside the presynaptic cell and increase the availability of monoamines to be released.

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26
Q

Synaptic Fatigue.

A

The cell has no more NT to release.

  • stops the neural pathways that cause the convulsions and allows the person to recover.
    ex. epileptic convulsions
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27
Q

Blockage of Neurotransmitter release due to Destruction of the Cytoskeleton.

A

ex. botox can block the release of a NT and can lead to paralysis..

specifically prevents the release of Acetylcholine from skeletal motor neurons at the neuromuscular junction of skeletal muscles paralysis.

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28
Q

Enzymatic Destruction of neurotransmitters by enzymes in the synaptic cleft

A

prevents NT’s from reaching their receptors.

  • Catecholamine -O- methyl transferase (COMT) destroys Norepinephrine and Dopamine
  • Acetyl cholinesterase- converts Acetyl Choline to Acetate and Choline
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29
Q

Drugs that inhibit COMT

A

can increase the effectiveness of the synapse.

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30
Q

Antibodies against neurotransmitter receptors in the synaptic cleft.- produced by autoimmune diseases

A

AB’s bind to receptors and prevent NT’s from binding

ex. Myasthenia gravis - Ab’s against Nicotinic Acetyl Choline receptors
on skeletal muscle –> muscle weakness, and paralysis.

31
Q

Low dose of Anti-acetyl cholinesterase drugs are used to

A

increase the number of Ach molecules that reach the post synaptic cell membrane to compete with the Ab’s.

32
Q

Variations in Post synaptic events

A
  1. Blockage of Neurotransmitters’ actions by molecules that bind to Nt’s receptors
    • Curare
    • Alpha and Beta Adrenergic blockers
33
Q

Curare

A

(plant product) binds to Nicotinic Acetyl Choline receptors on skeletal muscle –> paralysis

34
Q

Alpha and Beta Adrenergic blockers (drugs) block Norepinephrine action

A

(drugs) block Norepinephrine action

35
Q

Different types of receptors for each neurotransmitter

A

• The response of a cell to a NT depends on the type of receptor it has and which signal transduction mechanism the receptor activates.

36
Q

• Most Nt’s can cause either

A

EPSP’s or IPSP’s.

37
Q

• Some NT’s function as

A

Neuromodulators when bound to specific receptors

38
Q

a) Receptors that are ion channels

A
  • open rapidly
  • short acting
  • stay open for a brief time
  • generally excitatory - Na+ or Ca++ channels
  • few sites for regulation of activity
39
Q

High doses of Anti Acetyl cholinesterase

A

block the action of Achase on the cell membrane and render the Ach receptors useless.

40
Q

Nicotine

A

binds to Ach receptors, opens the ion channel and then remains bound, also inactivating the Ach receptor

41
Q

Addiction to Nicotine

A

increasing the number of Nicotinic Ach receptors on cells to compensate for blocked Ach receptors

42
Q

deprived of Nicotine

A

Nicotine –> increased receptors –> increased sensitivity to Ach–> increased skeletal muscle response to Ach and also interferes with autonomic nervous system function due to the presence of Nicotinic Ach receptors in both the Parasympathetic and Sympathetic N.S.

43
Q

Receptors that open/close ion channels by working through G proteins

G proteins are regulatory proteins they are not second messenger molecules).

A

may be a direct interaction of the G proteins with the ion channel or depend on the G proteins altering the rate of production of second messenger molecules.

Open Na+ or Ca++ channels  Na+ or Ca++ entry  EPSP
Open K+ or Cl- channels  K+ exit, Cl- entry  IPSP

44
Q

G protein related channels often remain opened or closed

A

for longer periods of time than receptor ion channels – up to a number of seconds.

45
Q

Receptors that open/close ion channels by working through G proteins

A

Norepinephrine binds to Beta 2 receptors to increase cyclic AMP production&raquo_space; activation of a cyclic AMP dependent protein kinase&raquo_space; phosphorylates and opens the Na+ and Ca++ channels on heart muscle&raquo_space;EPSP –>increased heart rate and strength of contraction.

46
Q

Acetylcholine binds to muscarinic receptors in the heart»

A

activates G proteins that bind directly to the K+ channels of pace maker cells and opens the K+ channels –> hyperpolarizes the cells –> slower heart rate.

47
Q

Diacylglycerol (DAG)

A

DAG activates DAG dependent protein kinases that open Ca++ channels&raquo_space; increased Ca++ entry into the cell&raquo_space; activation of Ca++ dependent protein kinases and binding to Calmodulin or other Calcium binding proteins&raquo_space;activation of enzymes and structural changes in proteins.

48
Q

Inositol triphosphate (IP3)

A

causes the release of internal stores of Ca++ from the endoplasmic reticulum  increased cytoplasmic Ca++  binding to Calmodulin and activation of a variety of enzymes.

49
Q

Enzyme linked receptors.

A

One protein structure extends from the inside of the cell membrane to the outside. The portion on the outside binds the primary messenger and the portion on the inside is an enzyme
EX. Guanyl Cyclase

50
Q

An example is an enzyme linked receptor with Guanyl Cyclase activity.

A

This enzyme converts GTP into cyclic Guanosine monophosphate (cyclic GMP).
Cyclic GMP binds to Cyclic GMP dependent protein kinases  phosphorylation of specific proteins  physiological effects. Enzyme linked receptors.

51
Q

Some neurotransmitters block the actions of other neurotransmitters by

A

receptors that cause the activation or inhibition of enzymes that block the mechanism of action of the other neurotransmitters.

52
Q

Phosphodiesterases

A

destroy second messenger molecules whose structure contains two phospho- esters C-O-P

53
Q

Phosphodiesters

A

Cyclic AMP and Cyclic GMP

54
Q

. The Phosphodiesterase enzymes are specific for either

A

cyclic AMP or cyclic GMP and different forms of these enzymes are found in different tissues.

55
Q

Phosphodiesterase

A

Cyclic Adenosine Mono Phosphate —»Adenosine Mono Phosphate AMP

Cyclic Guanosine Mono Phosphate ——> Guanosine Mono Phosphate AMP

56
Q

drugs such as caffeine and theophylline, that act

A

act as phosphodiesterase inhibitors increase the amount of cyclic AMP that remains in the cell after an NT stimulates cyclic AMP production

57
Q

Increased cyclic AMP accumulation

A

increases the number of protein kinase enzymes that can be activated –> an increased response to the NT.

58
Q

An NT that increases cyclic AMP- phosphodiesterase activity can

A

diminish the effectiveness of Norepinephrine when it binds to Beta 2 receptors and stimulates the production of cyclic AMP

59
Q

Viagra blocks the action of

A

cyclic GMP phosphodiesterases, leading to an increase of cyclic GMP in specific blood vessels  increase release of Nitric oxide  local vasodilation in the external genitals and in the head, amongst other effects.

60
Q

Addiction to phosphodiesterase inhibitors

A

the body adapts to partial inhibition of Cyclic AMP phosphodiesterase enzymes by making more copies of the enzyme.

61
Q

Neuromodulators

binds to receptors

A

alter the ability of the neuron to respond to a neurotransmitter

62
Q

Neuromodulators can be

A

neuropeptides produced by the nervous system or steroid hormones, prostaglandins and other molecular structures) Often involved in process of Long term potentiation.

63
Q

Actions of NM on neurons:

SHORT TERM actions

A

temporary chemical changes -> short term memory

64
Q

Short term actions:

A

Some neuromodulators bind to the same receptor as the neurotransmitter, but at a different site  change in shape of the receptor&raquo_space;increased binding affinity of the receptor for the NT&raquo_space; more NT will bind to receptors in the presence of a lower concentration of NT’s. i.e. fewer molecules of NT > greater EPSP or IPSP. This only lasts as long as the neuromodulator binds. (Valium’s action on GABA receptors). It is also possible for a NM to decrease binding affinity.

65
Q

Long term

A

strengthens specific synaptic pathways so that once initiated, they transmit information more effectively and reliably to specific regions of the nervous system.

66
Q

Long term memory requires

A

protein synthesis as well as gene expression, and causes lasting anatomical changes in the synapses.

67
Q

Other actions of neuromodulators

A

– changes in the number of ion channels,
– changes in the number or type of receptors
– changes in the number/and or type of enzymes present
– retention of synapses,
– formation of additional synapses

68
Q

Examples of Mechanisms of Long Term Potentiation that occur on the Postsynaptic cell

A
  1. There are 2 types of receptors for the neurotransmitter Glutamate: NMDA and AMPA.
    Glutamate binding to AMPA&raquo_space;>EPSP
    Glutamate binding to NMDA&raquo_space;>opening of Ca++ channels on post synaptic cellstimulates production of AMPA receptors&raquo_space;increased EPSP response to Glutamate
69
Q

Examples of Mechanisms of Long Term Potentiation that occur on the Postsynaptic cell

A
  1. When an action potential occurs on the axon, the local electrical current flow can spread backwards to the cell body and open Voltage gated Calcium channels on the cell membrane. This enhances the entry of Ca++ into the postsynaptic cell. Ca++ entry into the postsynaptic cell&raquo_space; activates the enzyme that produces Nitric Oxide and Nitric oxide diffuses out of the cell into the synapse. Nitric oxide can diffuses into the presynaptic cell&raquo_space;interact with molecules in the presynaptic cell and increase release of glutamate in response to an action potential.
70
Q

Neurotransmitters

A
  • small molecules
  • act rapidly for a short time
  • cause IPSP OR EPSP
  • major function is transmission of motor and sensory signals
71
Q

Classical v. non-classical NT

A

all are classical except NO

72
Q

Nuerotransmitters are synthesized in the

A

CYTOSOL of synaptic ending and repackaged into vesicles

73
Q

Some NT are destroyed in the

A

SYNAPTIC CLEFT, others are taken back into the cell to be recycled for future use (REUPTAKE).

Neuro Exam 2 (1 decks)

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