Title: BV4 / Modul 1

Q: The equilibrium potential can be determined by the Nernst equation. What characterizes the equilibrium potential in a neuron?
A: There is not net ion flow

Q: The degree of summation of synaptic inputs and synaptic integration in each neuron is determined by its passive membrane properties. Which of the following statements is correct?
A.
The passive membrane properties are specific to each neuron and do not involve activation of ion channels
B.
The shape of action potentials is determined by the passive membrane properties of neurons
C.
The time and space constant is the same for all neurons and so is the temporal and spatial summation
D.
The spatial summation depends on the resting membrane potential and is more efficient in neurons with short time constant
E.
The temporal summation depends on the resting membrane potential and is more efficient in neurons with short space constant
A: The passive membrane properties are specific to each neuron and do not involve activation of ion channels

Q: The resting membrane potential of neurons is around -65 mV. Which of the following statements gives the best description regarding the resting membrane potential?
A.
The resting membrane potential is determined by K^+ and Na^+ ion flow through leak channels
B.
The membrane potential of neurons lacking non-gated ion channels is set instead by ion flow through gated ion channels
C.
At the resting membrane potential all voltage-gated channels are activated
D.
Na/K-ATPase is not required for maintaining the resting membrane potential
E.
Leak Ca^2+ channels contribute to the resting membrane potential
A: The resting membrane potential is determined by K^+ and Na^+ ion flow through leak channels

Q: Action potential are actively generated and propagate electrical signals to presynaptic presynaptic terminals. Which of the following statements gives the best description regarding action potentials?
A.
At presynaptic terminals of chemical and electrical synapses action potentials can be converted into chemical signals.
B.
Action potentials are generated in the dendrites of neurons where they are mediated by non-gated ion channels
C.
Action potentials are generated in the dendrites of neurons where they are mediated by gated ion channels
D.
There is an influx of Ca^2+ via voltage-gated channels during action potentials
E.
Action potentials are mediated by gated and non-gated ion channels
A: There is an influx of Ca^2+ via voltage-gated channels during action potentials

Q: Which of the following statements gives the best description of ion channels?
A.
Both gated- and non-gated channels are closed at the resting membrane potential
B.
Gated channels become open only in response to specific stimuli
C.
Non-gated ion channels are not present in all neurons
D.
Ligand-gated channels can only be gated by stimuli from the outside of a neuron
E.
Both gated and non-gated ion channels become inactivated with a prolonged stimulation
A: Gated channels become open only in response to specific stimuli

Q: Which factor determines the time course of the repolarization of an action potential?
A.
Voltage-dependent K^+ channels
B.
The time constant
C.
Ca^2+-dependent K^+ channels
D.
K^+ leak channels
E.
The Na-K pump
A: Voltage-dependent K^+ channels

Q: The passive membrane properties of neurons plays an important role in the integration of activity in neural circuits. Which of the following statements gives the best description of synaptic summation.
A.
Synaptic summation is less efficient with higher time and space constants
B.
The time and space constants affects the amplitude and conduction velocity of action potentials
C.
The time and space constants affect the release of transmitters from axon terminals
D.
The time and space constants can only influence subthreshold postsynaptic potentials
E.
The resting membrane potential of a neuron determines its time and space constants
A: The time and space constants affects the amplitude and conduction velocity of action potentials

Q: Which of the following statements gives the best description of the neuron´s electrical properties?
A.
Synaptic summation is independent of the length of dendrites
B.
Synaptic summation is independent of the membrane area of the cell body
C.
Inhibitory synapses occur frequently on the soma and proximal dendrites
D.
Excitatory synapses occur frequently on the soma and proximal dendrites
E.
Inhibitory synapses do not summate
A: Inhibitory synapses occur frequently on the soma and proximal dendrites

Q: Which of the following statements gives the best description of action potential propagation?
A.
Its conduction velocity depends on K^+ leak channels
B.
Its conduction velocity depends on the axon diameter in all axons
C.
Its conduction velocity depends on the axon diameter only in unmyelinated axons
D.
Its conduction velocity depends on the axon diameter only in myelinated axons
E.
Its conduction velocity depends on Na^+ leak channels
A: Its conduction velocity depends on the axon diameter in all axons

Q: Which factor(s) determine the relative refractory period?
A.
Voltage-dependent K^+ channels and voltage-dependent Na^+ channels
B.
Ca^2+-dependent Na^+ channels and voltage-dependent K^+ channels
C.
Voltage-dependent Ca^2+ channels and voltage-dependent Cl^- channels
D.
Voltage-dependent K^+ channels and Ca^2+ -dependent K^+ channels
E.
Voltage-dependent Cl^- channels and Ca^2+ -dependent K^+ channels
A: Voltage-dependent K^+ channels and Ca^2+ -dependent K^+ channels

Q: Which of the following statements gives the best description of chemical and electrical synapses?
A.
Chemical synapses are faster than electrical synapses
B.
Chemical synapses consume more energy than electrical synapses
C.
Electrical synapses are more plastic than chemical synapses
D.
Electrical synapses propagate more complex signals than chemical synapses
E.
Electrical synapses contain synaptic vesicles
A: Chemical synapses consume more energy than electrical synapses

Q: What is the most appropriate description of the role of vATPase in synaptic transmission?
A.
It is essential for fusion of synaptic vesicles with the plasma membrane
B.
It is essential for recycling of synaptic vesicles
C.
It is essential for recycling of SNARE proteins
D.
It is essential for priming of synaptic vesicles
E.
It is essential for loading synaptic vesicles with neurotransmitter
A: It is essential for loading synaptic vesicles with neurotransmitter

Q: How would you best describe the role of NSF in synaptic transmission?
A.
) It is essential for fusion of synaptic vesicles with the plasma membrane
B.
It is essential for recycling of synaptic vesicles
C.
It is essential for recycling of SNARE proteins
D.
It is essential for priming of synaptic vesicles
E.
It is essential for loading synaptic vesicles with neurotransmitter
A: It is essential for recycling of SNARE proteins

Q: Glutamatergic synapses can be active at high rates making it critical that the supply of glutamate is efficient, and that released glutamate is properly inactivated. What is true about glutamate formation and termination of glutamate action at excitatory synapses? Be prepared to explain your answer.
A.
Glutamine synthetase is the rate-limiting enzyme in presynaptic glutamate synthesis and glutamate acts at ionotropic receptors
B.
Glutamate can be formed from tyrosine in the nerve terminal and it is inactivated by uptake into astrocytes
C.
Glutamate is inactivated by diffusion from the synaptic cleft and by uptake into astrocytes
D.
Glutamate can be formed from tyrosine in the nerve terminal and it is inactivated by uptake into astrocytes
E.
Glutamate can be formed from glutamine in the nerve terminal and is inactivated by enzymatic degradation
A: Glutamate is inactivated by diffusion from the synaptic cleft and by uptake into astrocytes

Q: What is the reversal potential for an AMPA receptor-mediated EPSP?
A: About 0 mV

Q: Which of the following statements gives the best description of dopamine receptors?
A.
D_1 receptors are coupled to inhibitory heterotrimeric Gi/o proteins
B.
D_5 receptors are coupled to inhibitory heterotrimeric Gi/o proteins
C.
D_2 receptors occur presynaptically
D.
D_2 receptors do not occur postsynaptically
E.
D_3 receptors are ionotropic
A: D_2 receptors occur presynaptically

Q: Which of the following statements gives the best description of 5-hydroxytryptamine receptors?
A.
5HT_3 receptors are coupled to inhibitory heterotrimeric Gi/o proteins
B.
5HT_3 receptors are ionotropic
C.
5HT_1 receptors increase cAMP levels
D.
5HT_2 receptors decrease IP_3 levels
E.
5HT_3 receptors are restricted to the CNS
A: 5HT_3 receptors are ionotropic

Q: Which of the following statements gives the best description of NMDA receptors?
A.
NMDA receptors are insensitive to GABA
B.
NMDA receptors are insensitive to glycine
C.
NMDA receptors consist of five subunits
D.
NMDA receptors are voltage-dependent at positive membrane potentials
E.
NMDA receptors are permeable to Cl^-
A: NMDA receptors are insensitive to GABA

Q: How would you best describe synaptic long-term depression?
A.
It exhibits specificity but not cooperativity
B.
It depends on voltage-dependent AMPA receptors
C.
It can be induced by low-frequency (e.g. 1 Hz) stimulation for long periods (e.g. 15 min)
D.
It can be induced by high-frequency (e.g. 100 Hz) stimulation for brief periods (e.g. 1 s)
E.
It typically lasts for less than 1 h
A: It can be induced by low-frequency (e.g. 1 Hz) stimulation for long periods (e.g. 15 min)

Q: Which neurotrophin acts at TrkB receptors?
A: BDNF

Q: Pharmacological activation of the parasympathetic nervous system can be induced by two principal mechanisms. Which two?
A.
Stimulation of postsynaptic muscarinic receptors and inhibition of acetylcholine esterase
B.
Stimulation of presynaptic muscarinic receptors and inhibition of presynaptic nicotinergic receptors
C.
Inhibition of cholinergic re-uptake and inhibition of acetylcholine esterase
D.
Inhibition of acetylcholine esterase and stimulation of betaadrenergic receptors
A: Stimulation of postsynaptic muscarinic receptors and inhibition of acetylcholine esterase

Q: One of the following statements about monoamines of the peripheral nervous system is wrong. Which one?
A.
Tyrosine hydroxylase is the rate-limiting enzyme of noradrenaline synthesis
B.
Dopamine decarboxylase is the rate-limiting enzyme of adrenaline synthesis
C.
Tryptophan is the precursor of the serotonin synthesis
D.
The rate-limiting steps in ACh synthesis are the availability of choline and acetyl-CoA.
A: Dopamine decarboxylase is the rate-limiting enzyme of adrenaline synthesis

Q: Administration of Atropine will induce one of the following effects. Which one?
A.
Diarrhea
B.
Decreased blood pressure
C.
Tachycardia
D.
Bronchial constriction
A: Tachycardia

Q: Administration of a selective beta2 adrenoceptor agonist will produce one of the following effects. Which one?
A.
Uterus relaxation
B.
Decreased saliva secretion
C.
Constriction of bronchi
D.
Obstipation
A: Uterus relaxation

Q: One of the following drugs can block the nicotinic acetylcholine receptor at the neuromuscular junction. Which one?
A.
Carbacholine
B.
Metoprolol
C.
Curare
D.
Physostigmine
A: Curare

Q: One of the following statements about serotonin is wrong. Which one?
A.
Serotonin is the primary transmitter of the enteric nervous system.
B.
Serotonin can act on 5-hydroxytryptamine -receptors in the area postrema to induce vomiting.
C.
Serotonin can be produced by gut microbiota
D.
Serotonin inhibits peristaltic contractions
A: Serotonin inhibits peristaltic contractions

Q: One of the following statements about the control of bronchial tonus by the peripheral nervous system is correct. Which one?
A.
Blood adrenaline contracts the bronchial tubes
B.
Neuronal acetylcholine contracts the bronchial tubes
C.
Blood serotonin dilatates the bronchial tubes
D.
Neuronal noradrenaline contracts bronchial tubes
A: Neuronal acetylcholine contracts the bronchial tubes

Q: One of the following substances can release noradrenaline from nerve terminals. Which one?
A.
Cocaine
B.
Atropine
C.
Amphetamine
D.
Adrenaline
A: Amphetamine

Q: Several dopamine pathways exist in the brain. Which of the following is not considered as a dopamine pathway?
A.
The Mesolimbic Pathway projects from the ventral tegmental area (VTA) to the nucleus accumbens in the limbic system.
B.
The locus coeruleus to dorsal reticular nucleus pathway
C.
The Mesocortical Pathway projects from the VTA to the prefrontal cortex.
D.
The Nigrostriatal Pathway projects from the substantia nigra to the striatum.
E.
The Tuberoinfundibular (TI) Pathway projects from the arcuate nucleus (a.k.a. the “infundibular
A: The locus coeruleus to dorsal reticular nucleus pathway

Q: How do you define the term ligand efficacy?
A.
The efficacy of the ligand is defined by the position of the concentration response on the x axis
B.
The efficacy of the ligand is defined by the amplitude of the concentration response curve
C.
The efficacy of a neutral antagonists is set to 1.
D.
Inverse agonists have no efficacy.
E.
Full agonists have the highest potency.
A: The efficacy of the ligand is defined by the amplitude of the concentration response curve

Q: Which property separates the anaesthetic drug ketamine from other intravenous anaesthetics?
A.
1. Induces respiratory depression
B.
Induces drop in blood pressure
C.
Induces vasodilation
D.
Can be administered by intramuscular injection
E.
Lacks analgetic effects
A: Can be administered by intramuscular injection

Q: Which is the pharmacological mechanism of action of ketamine?
A.
Activates dopamine receptors in the brain
B.
Activates acetylcholine receptors in the brain
C.
Inhibits GABA receptors in the brain
D.
Inhibits serotonin receptors in the brain
E.
Inhibits NMDA receptors in the brain
A: Inhibits NMDA receptors in the brain

Q: Which property of an inhalation anaesthetic gives a fast onset of anaesthesia and a quick recovery?
A.
Low blood solubility
B.
Low diffusion coefficient
C.
Low fat solubility
D.
High fat solubility
E.
High blood solubility
A: Low blood solubility

Q: Which is the pharmacological mechanism of action of the antidote neostigmine, often used to reverse the effect of non-depolarizing muscle relaxants at the neuromuscular junction?
A.
Acetylecholine receptor agonist
B.
Acetylecholine receptor antagonist
C.
Acetylcholine esterase inihibitor
D.
Inhibition of acetylcholine release
E.
Stimulation of acetylcholine release
A: Acetylcholine esterase inihibitor

Q: The effects of one of the drugs below can be inhibited by an antidote. Which one
A.
Diazepam
B.
Ketamin
C.
Klonidin
D.
Propofol
E.
Tiopental
A: Diazepam

Q: At the end of surgery administration of inhalation anaesthetics is stopped but before that you sometimes must reverse the effects of the non-depolarizing muscle relaxants. We use the antidote Neostigmin. What is the mode of action?
A: Acetylcholinesterase inihibitor

Q: Which is the pharmacological mechanism of action of ketamine?
A: Inhibits NMDA receptors in the brain

Q: In neurophysiology it is common to refer to different types of potential, including equilibrium potential, reversal potential, and resting membrane potential. Which statement gives the best description of these different types of potential? Be prepared to explain your answer.
A
There is typically no equilibrium potential in a real neuron, and at the reversal potential for Na^+ there is no flux of Na^+. At the resting membrane potential there is a flow of Na^+ but no flow of K^+
B
At the equilibrium potential for K^+ there is only a flow of K^+. At the reversal potential of an EPSP both Na^+ and K^+ flows, while at resting membrane potential there is only a flow of Na^+
C
At the equilibrium potential for K^+ there is no flow of K^+, and at the reversal potential of an EPSP there is no ion flow, while at resting membrane potential there is flow of both K^+ and Na^+
D
An equilibrium potential can typically not be calculated for a real neuron. At the reversal of an EPSP both Na^+ and K^+ flows, and at the resting membrane potential there is also a flow of both Na^+ and K^+.
E
The reversal potential of an excitatory postsynaptic potential is equal to the equilibrium potential for Na^+, and at resting membrane potential there is flow of both Na^+ and K^+.
A: An equilibrium potential can typically not be calculated for a real neuron. At the reversal of an EPSP both Na^+ and K^+ flows, and at the resting membrane potential there is also a flow of both Na^+ and K^+.

Q: Vilken equation använder man för att räkna fram equilibrium potentialen för 1 jon?
A: Man räknar fram equilibrium potentialen med Nernst equationen (som bara kan hantera en ekvation)

Q: Vilken ekvation använder man för att räkna fram membranpotentialen (för flera joner)?
A: Goldman equationen räknar ut membranpotentialen - räknar ut för flera joner

Q: If the stimulus you gave above was not an injected current but a synaptic current, it would have given rise to an EPSP. If two EPSPs reach the neuron via the same synapse, but are separated by a short time interval they summate. Which factor(s) will then determine the efficacy of the summation?
A: The time constant and the membrane resistance
- Membran resistansen är rätt för att den ingår i ekvationen för tidskonstanten

Q: Two EPSPs evoked by different synapses can also reach a neuron simultaneously to summate. Which factor(s) will then determine the efficacy of the summation?
A: The length constant and the membrane resistance

Q: Vad avgörs membranresistansen utav?
A: Membranresistansen avgörs av antalet läckkanaler

Q: Varför får man en kortare längdkonstant vid inhibitoriska synapser
A: Inhibitoriska synapser ligger ofta nära cellkroppen och när de öppnas får man en misnkad membranresistans, så man får därför en kortare längdkonstant

Q: När kan man använda ordet reversal potential?
A: Reversal potential används för synaptiska potentialer

Q: Which factor(s) determine the relative refractory period?
A: Voltage-dependent K^+ channels in axon and soma, Ca^2+ -dependent K^+ channels in soma

Q: How do changes of the Na^+ and K^+ conductance relate to the action potential and to each other?
A: The K^+ conductance peaks after the peak of the action potential

Q: Vad är skillnaden mellan ström och spänning?
A: Det är skillnad mellan ström och spänning - ström är momental, medan spänning ändras med tidskonstanten

Q: What is the most correct regarding the location of the hippocampus in humans?
A: It is located medial to the inferior horn of the lateral ventricle with the rostral end at the same level as mesencephalon

Q: Baserat på dina kunskaper om synaptisk transmission misstänker du att Susannes problem kan vara orsakade av BoTx – vilken verkningsmekanism har detta ämne?
A: Det klyver SNARE proteiner

Q: Ett annat tillstånd har en underliggande patofysiologi som liknar BoTx - vilket? Vilka är symtomen och varför skiljer de sig från tillståndet ovan?
A: Tetanus - motsatta symtom mot BoTx (kramper, ökad muskeltonus)

Q: Hur liknas BoTx och TeTx vid varandra?
A: De båda klyver SNARE proteiner men på olika ställen

Q: Vilken är den troligaste orsaken till TeTx?
A: Kontaminering av ett sår med jord (ffa gödslad jord)

Q: Hur förebygger man bäst TeTx?
A: Genom vaccination

Q: Alzheimers sjukdom kan inte botas men det finns symtomlindrande mediciner. Vilken neurotransmittor påverkas av det läkemedel du skulle välja i första hand till en Alzheimerpatient?
A: Acetylkolin

Q: Vad är verkningsmekanismen för att ge acetylkolinesteras inhibitor vid Alzheimers?
A: För att bryta icke-depolariserande muskelrelaxantia - ACh är ett av neurotransmittorerna som är viktiga flr minnesinlagring så genom att tilföra det tänker man att man minskar effekten

Q: Vilken annan sjukdom kan behandlas med ACh?
A: Myasthenia gravis

Q: ACh kan ge upphov till flera biverkningar men sannolikt inte denna:
A: Takykardi

Q: Om biverkningarna vid Alzheimerbehandling blir besvärande finns ett alternativt läkemedel - vilken neurotransmittor är då i fokus?
A: Glutamat

Q: Ångest är ett vanligt symptom som i första hand behandlas med SSRI preparat (Modul 4). Tidigare var dock behandling med ett annat läkemedel vanligt förekommande – vilket?
A: Benzodiazepiner (GABAa-receptorn) så GABA faciliteras och man får en ångestdämpande effekt

Q: Vad är det viktigaste skälet till att benzodiazepin inte primärt används till behandling av ångest?
A: Det kan orsaka beroende

Q: Vad är verkningsmekanismen hos benzodiazepin?
A: Det binder allosteriskt till och potentierar GABA_A receptorer

Q: Vilket av följande läkemedel är ett möjligt alternativ vid behandling av ångest?
A: Sederande antihistaminer

Q: Vad är en vanlig biverkan för sederande antihistaminer?
A: Antikolinerg effekt - det är vanligt att dessa preparat spiller över på muskarinreceptorer

Q: Dopamin är en annan farmakologiskt viktig transmittor i fokus vid bla Parkinsons sjukdom (Modul 3) och psykoser (Modul 4). Vilket ytterligare tillstånd kan behandlas med läkemedel som påverkar dopamintransmission?
A: Hyperprolaktinemi

Q: Cannabis är ett omdiskuterat preparat som i viss utsträckning används medicinskt vid smärtbehandling. Vilket av följande påståenden är mest rimligt när det gäller cannabis och endocannabinoider?
A. De verkar på neuronens CB_2 receptorer
B. De frisätts från neuronens presynaptiska terminaler
C. De verkar på neuronens TRP kanaler
D. De frisätts från mikroglia
E. De verkar på neuronens opioidreceptorer
A: De verkar på neuronens TRP kanaler - de finns i sensoriska nervtrådar som reagerar på smärta och värmen men man har kommit på att det är en av de viktigaste kanalerna för endocannabinoider (snabb transmisson med endocannabinoider går via TRP kanaler, medan modulerande går via CB1 receptorer)

Q: Vad är funktionen hos mikroglia?
A: Mikroglia är med i nästa alla hjärnfunktioner, i bilninen och upprätthållande av neuroner

Q: Before starting the administration of drugs, you let the patient breath 100 % oxygen via a mask for a couple minutes. This procedure is called preoxygenation and is a security measure. It prolongs the time to keep oxygen saturation during apnéa. What is the main physiological mechanism that provides this effect?
A: Replacement of nitrogen with oxygen in the lung alveoli

Q: You induce anaesthesia by intravenous administration of propofol. After approximately 30 seconds you find that the patient has fallen asleep, by not responding to your call and loss of eye reflexes. What is the main pharmacological mechanism by which propofol (and also thiopental) induces sleep?
A: Potentiate GABA action on its receptor

Q: In another patient thiopental was used as inducer of anaesthesia. The onset is similar to propofol (30 s) and the duration of action is about 5-6 minutes. However, in contrast to propofol the half-life of thiopental is several hours. How come that the duration of action is only minutes?
A: Redistribution

Q: Vad innebär redistribution?
A: När det ges intravenöst kommer läkemedlet först hamna i organen som genomblöds mycket, som hjärna, njure, muskel och fett - när allt har fördelats och konc. i blodet börjar sjunka så sjunker konc. i hjärnan så man vaknar

Q: When the patient has fallen asleep it is time to add drugs to facilitate intubation. In this procedure a tube is applied via the mouth to the trachea in order to control the ventilation of the patient during surgery. You first give a fast-acting opioid followed by a non-depolarizing muscle relaxant that works on the neuromuscular junction. How does the muscle relaxant work?
A: Competitive inhibition of the nicotinergic acetylcholine receptor

Q: The physiochemical properties of an inhalation anaesthetic decide the speed of onset and recovery. Which property leads to the fastest onset and recovery?
A: Low blood solubility
Ju mer svårlöslig en gas är i blodet ju lättare och snabbare byggs det upp ett partialtryck som vill lämna blodet och ju snabare kommer dessa molekyler gå in i hjärnan
Dessa gasen har ingen metabolism i kroppen, allt som ges måste man andas ut igen
Lustgas är en av de gaserna med lägst blodlöslighet

Q: Inhalation anaesthetics have cardiovascular side effects which sometimes causes clinical problems. Which is the most common and what is the main underlying mechanism?
A: Hypotension due to vasodilation

Q: In patients that have suffered a major trauma and arrive to the trauma center in the state of hemorrhagic shock we often use the anaesthetic ketamine due to its beneficial profile during these circumstances. Which one of the following statements is false regarding ketamine?
A. Does not no cause respiratory depression
B. Does not cause hypotension
C. Has psychomimetic side effects
D. Has potent analgetic effects
E. Can be reversed by flumazenil
A: Can be reversed by flumazenil

Q: Which statements about ketamine are correct?
A: A. Does not no cause respiratory depression
B. Does not cause hypotension
C. Has psychomimetic side effects
D. Has potent analgetic effects

Q: How does ketamine affect the NMDA receptor?
A: Antagonism of the NMDA receptor (glutamate) is responsible for the anesthetic

Q: Vad kan ketamin vara ett alternativ till?
A: Ketamin kan vara ett alternativ till ECT vid svår depression

Q: Postoperative analgesia is extremely important, not only to reduce discomfort and pain but also to facilitate mobilization after surgery. The most commonly used opioid in the postoperative ward is still morphine. Which is not a common side effects of morphine?
A: Oedema

Q: What is respiratory distress?
A: (Hypoventilation) is a breathing disorder characherized by slow and ineffective reathing

Q: Vad är inotropi?
A: Inotropi avser hjärtats kontraktilitet - en förändring av kontraktiliteten i hjärtats muskulatur kallas inotrop effekt