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Neurochemical Transmission & Anesthetic Affects Flashcards

1
Q

VOCAB:

NEURON

A

structural and functional unit of the nervous system

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2
Q

VOCAB:

SYNAPSE

A

connection between two neurons where information is transferred from one neuron to another

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3
Q

HOW DO NEURONS COMMUNICATE WITH EACH OTHER?

  1. TRANSDUCER/convert
  2. CONDUCTOR
  3. SECOND TRANSDUCER/convert
A
  1. energy of stimulus from environment

converted to

electrical signal in dendrite

  1. electrical signal in dendrite

conducted to

cell body - axon - axon terminal

  1. electrical signal in axon terminal

converted INTO

chemical message at synapse

thereby transmit signal to another neuron

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4
Q

VOCAB

ELECTRICAL POTENTIAL

A

Sum of all ion gradients.

Neg inside and positive outside

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5
Q

ION CONCENTRATION INSIDE & OUTSIDE THE CELL

  1. Na+
  2. K+
  3. Cl-
  4. Ca+2
A
  1. 15 vs 150
  2. 150 vs 5
  3. 5 vs 120
  4. 0.001 vs 2.5
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6
Q

Ion channel regulation

4 types

A
  1. voltage gated:

membrane potention

  1. ligand-gated

nuerotransmitter

  1. mechanically gated

touch

  1. thermally gated

temperature

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7
Q

VOCAB

ACTION POTENTIAL

A

picture of the change in membrane potential over a very short period of time

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8
Q

RESTING MEMBRANE POTENTIAL

A

-70mV

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9
Q

DEPOLARIZATION

ion movement

membrane potential

A

Na+ into cell

less negative

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10
Q

HYPERPOLARIZATION

ion movement (2 types)

membrane potential

A

K+ out

Cl- in

more negative

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11
Q

HOW IS ACTION POTENTIAL GENERATED

A

graded membrane potentials must be strong enough to reach threshold (approx -60)

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12
Q

ACTION POTENTIAL

CHARACTERISTICS (4)

A
  1. a change in electrical potential that travels down the surface of the axon
  2. “all or none” - pass threshold or not
  3. result from rapid opening & closing of Na+ & K+ channels in nerve membrane
  4. propagated in one direction down nerve fiber to synapse
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13
Q

PARTS OF A SYNAPSE

1

2a,b,c

A
  1. presynaptic axon terminal
  2. postsynaptic target
    a. dendrite (axodendritic)
    b. cell soma (axosomatic)
    c. another axon (axoaxonal)
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14
Q

MAJORITY OF SYNAPSES in the MAMMALIAN BRAIN are

A

Chemical Synapses

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15
Q

HOW DOES COMMUNICATION OCCUR BETWEEN CHEMICAL SYNAPSES

A

the electrical signal (carried by the actin potential) is converted into a chemical signal that can be transmitted to next neuron

by diffusion of a neurotransmitter across the synaptic cleft.

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16
Q

7 STEPS IN RELEASE OF NEUROTRANSMITTER

A
  1. action potentials arrive at axon terminal
  2. voltage-gated Ca2+ channels open
  3. CA2+ enters the cell
  4. Ca2+ signals to vesicles
  5. Vesicles move to the membrane
  6. Docked vesicles release NT by exocytosis
  7. NT diffuses across synaptic cleft and binds to receptors
17
Q

POSTSYNAPTIC RECEPTORS

2 TYPES

A
  1. Ionotropic - ligand gated - allows for ions to move directly through channel into cell
  2. Metabotropic - ligand gated - liked to 2nd membrane protein. NT binds then there is indirect effect on ion movement OR the effect will be on other 2ndary signaling pathways in the cell - 2nd messenger
18
Q

POSTSYNAPTIC RESPONSE

Na2+ vs Cl-

A
  1. EPSP - excitatory postsynaptic potential

If receptor allows Na+ in, then the membrane potential closer to threshold.

  1. IPSP - inhibitory

if receptor allows Cl- in, then membrane potential move away from threshold - hyperpolarize

19
Q

SUMMATION OF EPSP & IPSP

2 TYPES

the cummulative effect of thousands of synapses are needed to reach threshold and fire an action potential in the CNS

A
  1. Spatial - multiple synapses fire at same time
  2. Temporal - one synapse fires repeatedly
20
Q

NEUROTRANSMITTERS

AMINO ACIDS (2)

EXCITE OR INHIBIT

A
  1. Glutamate - excite
  2. GABA - inhibit
21
Q

NEUROTRANSMITTERS

BIOGENIC AMINES (4)

EXCITE OR INHIBIT

A
  1. Dopamine - excite via D1 receptors
    - inhibit via D2 receptors
  2. Norepinephrine - excite
  3. epinephrine - excite
  4. Serotonin - excite
22
Q

NEUROTRANSMITTERS

NEUROPEPTIDES (1)

EXCITE OR INHIBIT

A

Opiods - inhibit

23
Q

EFFECT OF GLUTAMATE ON ION CHANNELS

  1. TYPE OF RECEPTORS (a & b)
  2. TYPE OF IONS (2)
A
  1. ionotrophic glutamate receptors
    a. NMDA - N-methyl-D-aspartate
    b. AMPA - quisqualate receptor

alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid

  1. Na+ & Ca2+
24
Q

EFFECT OF GABA ON ION CHANNELS

TYPES OF RECEPTORS (3)

TYPES OF ION (1) AFFECTED BY 1ST TWO

TYPES OF CHANNELS (2) AFFECTED BY 3RD

RESULT OF ALL 3

A
  1. ionotrophic GABAAallow Cl- in
  2. ionotrophic GABACallow Cl- in
  3. metabotrophic GABABactivate K+ & block 2+

RESULT - net loss of positive charge inside cell = IPSP

25
STRUCTURE OF LOCAL ANESTHETICS 2 TYPES (name 3 GROUPS of each type) PURPOSE OF 1ST & 3RD GROUP
1. ester-linked: aromatic ring/ester/amine 2. amide-linked: aromatic ring/amide/amine 1. aromatic ring - determines drug's hydrophobic (lipophillic) characteristics so can bind to membrane 2. amine group determines onset of action with it's H ions.
26
WHAT IS THE EFFECT OF LOCAL ANESTHETICS when injected into the vicinity of central or peripheral nerves
rapid and temporary disruption of nerve conduction. block conduction of action potentials in sensory & motor neurons by blocking voltage gated Na+ channels neuron will not depolarize and not transmit action potential
27
WHICH NERVE FIBERS ARE THE MOST SENSITIVE TO LOCAL ANESTHETICS
small unmyelinated conduct pain, temp nerves of autonomic nervous system
28
INHALED GASES (4) administered after administration of an IV agent
isoflurane desflurane sevoflurane nitrous oxide
29
MECHANISM OF ACTION OF INHALED ANESTHETICS
increase sensitivity of the GABAA receptor to GABA. this will cause a prolongation of Cl- ions to enter the cell. this causes hyperpolarization of the membrane this will inhibit the ability of the postsynaptive neuron to fire an action potential
30
OTHER RECEPTORS THAT MAY BE AFFECTED BY INHALED ANESTHETICS (2)
1. Glycine - inhibitory ionotrophic receptor in spinal cord or brain stem receptor activity (modulating Cl- channels) is increased 2. Nicotinic acetylcholine receptors in peripheral nervous system block excitatory postsynaptic current of these receptors
31
MECHANISMS OF ACTION (4) OF INTRAVENOUS ANESTHETICS SUCH AS PROPOFOL
1. potentiate GABAA receptor - slow closing of Cl- channels - hyperpolarize membrane 2. Na+ channel blocker - prevent conduction of action potential 3. uses endocannabinoid system to induce amnesia & reduce postoperative vomiting 4. may enchance traumatic memories from preop events
32
MECHANISM OF ENDOCANNABINOIDS (5 steps) HOW DOES THIS RELATE TO PROPOFOL (2 points)
1. NT like glutamate or GABA is released from presynaptic terminal & binds to postsynaptic receptor 2. this binding causes influx of Ca2+ 3. this influx causes productin of anandamide in some cells 4. anandamide is released back into synaptic cleft & binds to presynaptic cannabinoid1 (CB1) receptors 5. this binding leads to inhibition of presynaptic CA2+ channels & inhibits release of NT from presynaptic terminals 1. propofol inhibits FAAH that degrades anadamide 2. propofol can inhibit either excitatory or inhibitory transmission based on what is released from the presynaptic terminal
33
MECHANISM OF ACTIN OF BARBITURATES & BENZODIAZEPINES (2) TYPES OF BARBS (1) TYPES OF BENZOS (2)
1. for both - interact with GABAA receptor so open Cl- channel - hyperpolarization of membrane 2. Barbs only - block excitatory glutatmate AMPA receptors to reduce flow of Na+ across membrane - inhibit membrane depolarization 1. thioental 2. diazepam lorazepam
34
MECHANISM OF ACTIN OF KETAMINE - 3 points about ketamine
1. short acting nonbarbiturate anesthetic 2. noncompetitive glutamate NMDA receptor antagonist - blocks Ca2+ influx into cell preventing depolarization 3. stimulates central sympathetic system to INC HR, BP via inhibition of catecholamine reuptake
35
OPIODS 6 FACTS 1-PROPERTY 2-USED WITH 3-RECEPTORS 4-SPECIFICITY 5-PRIMARY RECEPTOR 6-ION CHANNELS AFFECTED (2)
1. anagelsic properties 2. commonly used in combo w/ inhalation agents 3. bind to opiod receptors (mu, kappa, delta) in CNS & PNS 4. each receptor exhibits a diff specificity for drug it binds 5. analgesic properties primarily mediated by mu receptor 6. all are G-coupled receptors assoc w/ ion channels - Increase K+ efflux - hyperpolarization - postsynaptic - decrease presynaptic Ca2+ to impede vesicle fustion
36
WHAT ARE THE PHASES OF AN ACTION POTENTIAL (6)
1. Na+ channels open & Na+ begins to enter cell 2. K+ channels open, K+ begins to leave cell 3. Na+ channels become refractory to more Na+ entering 4. K+ continues to leave cell causing membrane potential to return to resting level 5. K+ channels close, Na+ channels reset 6. Extra K+ outside diffuse away
37
ACTION POTENTIAL CHARACTERISTICS (4)
1. a change in electrical potential that travels down the surface of the axon 2. "all or none" - pass threshold or not 3. result from rapid opening & closing of Na+ & K+ channels in nerve membrane 4. propagated in one direction down nerve fiber to synapse

ANATOMY (4 decks)

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