What neurotransmitter do motor neurons release at the neuromuscular junction?
Acetylcholine
Glutamate
Dopamine
Glycine
Question 7.1.2
Increases in cytosolic calcium concentration in muscle cells cause contraction. How do these calcium signals come about in skeletal muscle?
Nicotinic receptors are activated postsynaptically causing an influx of cations into the muscle and action potential firing in the muscle. The action potentials propagate across the muscle cells activating voltage-gated calcium channels, which induce a rise in cytosolic calcium concentration.
Nicotinic receptors are activated postsynaptically causing an influx of cations into the muscle. Some of these cations are calcium ions and these drive muscle contraction.
The action potential invading the synaptic boutons of the motor neuron causes an increase in cytosolic calcium concentration which diffuses into the muscle
Motor neurons secrete a growth factor which induces calcium signals
Question 7.1.3
A muscle is controlled by a group of motor neurons termed the "motor pool". How can we map the premotor neurons of a given "motor pool"?
Injecting anatomical anterograde tracers into different areas of the brainstem and following the axonal trajectories
Injecting anterograde transynaptic viral tracers into brainstem, and following the subsequent spread of virus to motor neurons
Injecting retrograde transynaptic viral tracers into muscles, first infecting motor neurons and subsequently spreading to their presynaptic inputs
Injecting anterotrograde transynaptic viral tracers into muscles, first to infect motor neurons and subsequent spread to their presynaptic inputs expressing a complement factor
Question 7.1.4
Why is motor control critical for sensory perception?
We move our eyes and heads, and therefore what our eyes see depends upon movements
We move our hands and body, and therefore what we feel depends upon movements
We sniff in order to enhance odor perception
All of the above
Question 7.1.5
Why might one propose that the motor function of whisker sensory cortex (wS1) is a negative feedback motor command, while the motor function of whisker motor cortex (wM1) is a motor command to enhance sensory input?
Stimulation of wS1 drives sustained whisker protraction, while stimulation of wM1 drives rhythmic whisker protraction
Stimulation of wS1 drives rhythmic whisker protraction, while stimulation of wM1 drives sustained whisker retraction
Stimulation of wS1 drives sustained whisker retraction, while stimulation of wM1 drives sustained whisker protraction
Stimulation of wS1 drives sustained whisker retraction, while stimulation of wM1 drives rhythmic whisker protraction
Question 7.2.1
Which of the following statement about sensory percepts is not correct?
Sensory percepts are learned through experiences
Sensory percepts are subjective
Sensory percepts are actively acquired
Sensory percepts are independent of the observer
Question 7.2.2
Psychometric curves plot the relationship between stimulus strength and behavioral performance. What is meant by the term "psychometric threshold"?
The stimulus strength at which performance is half-maximal
The stimulus strength at which performance is just above chance
The behavioral performance when stimulus strength is half maximal
The behavioral performance when stimulus strength is just above noise level
Question 7.2.3
What are the minimal requirements for experimental investigation of subjective sensory percepts?
Human subjects are needed for subjective sensory percepts
Complex stimuli are needed for subjective sensory percepts
Behavioral report of subjective percept by motor output
Visual stimuli are needed for subjective sensory percepts
Question 7.2.4
Which experiment tests for the sufficiency of neuronal activity in the C2 barrel column of primary somatosensory cortex (S1) to drive licking in a mouse trained in a detection task in which a 1 ms impulse is applied to the C2 whisker, and the mouse is trained to lick a water reward spout?
Injection of TTX into the C2 barrel column
Injection of CNQX and APV into the C2 barrel column
Optogenetic stimulation of neurons in the C2 barrel column
All the above
Question 7.2.5
What pattern of neuronal activity is found in the C2 barrel column of mouse primary somatosensory cortex (S1) during a detection task in which a 1 ms impulse is applied to the C2 whisker, and the mouse is trained to lick a water reward spout?
An early sensory response that reliably encodes sensory stimulus
A late depolarization that encodes the subjective sensory percept
Both of the above
None of the above
Question 7.3.1
Which of the following statements about reward-based learning is not correct?
In reward-based learning we learn that in a specific stimulus context we should perform a specific motor output that will then lead to a reward
In reward-based learning an animal needs to learn to transform sensory inputs into useful motor outputs
Reward-based learning likely strengthens the synaptic circuits linking a specific sensory input with the motor circuits driving the rewarded motor output
All learning relies upon reward signals
Question 7.3.2
Which statement about the activity of midbrain dopaminergic neurons is not true?
Dopamine neurons transiently increase their firing when an unexpected reward is delivered
Dopamine neurons transiently increase their firing when a cue is presented that predicts future reward
Dopamine neurons transiently decrease firing rate when an expected reward is delivered
Dopamine is thought to signal reward prediction error and is therefore a useful learning signal
Question 7.3.3
Where do the midbrain dopaminergic neurons of the substantia nigra pars compacta (SNc) prominently innervate?
Hippocampus
Amygdala
Striatum
Olfactory bulb
Question 7.3.4
Which of the following statements about striatal projection neurons is correct?
D1R-expressing projection neurons directly inhibit the substantia nigra reticulata (SNr) (direct pathway), resulting in disinhibition of brainstem motor nuclei ('go' signal)
D1R-expressing striatal projection neurons directly inhibit the substantia nigra reticulata (SNr) (direct pathway), resulting in inhibition of brainstem motor nuclei ('no go' signal)
D2R-expressing striatal projection neurons directly inhibit the external globus pallidus (GPe), which in turn innervates the SNr (indirect pathway), resulting in disinhibition of brainstem motor nuclei ('go' signal)
D2R-expressing striatal projection neurons directly inhibit the substantia nigra reticulata (SNr) (direct pathway), resulting in disinhibition of brainstem motor nuclei ('go' signal)
Question 7.3.5
Which of the following statements about the action of dopamine is not correct?
Dopamine appears to potentiate cortical input onto the direct pathway striatal projection neurons through the activation of D1 receptors (strengthens direct pathway)
Dopamine appears to depress cortical input onto the indirect pathway striatal projection neurons through the activation of D2 receptors (weakens indirect pathway)
Dopamine acts on D1 receptors to promote the insertion of both AMPA and NMDA receptors onto the postsynaptic membranes of direct striatal projection neurons
Dopamine acts on D2 receptors to promote calcium entry into indirect striatal projection neurons
Question 7.4.1
According to the study of Gustavsson et al. (2011), how many people suffered from brain disorders in Europe in 2010?
Less than 3 million
50 million
100 million
More than 150 million
Question 7.4.2
What are the early clinical symptoms of Parkinson's disease?
Tonic seizures with high fever
Forgetting conversations or appointments, routinely misplacing possessions
Bradykinesia, tremor, rigidity, difficulty in walking
Double vision or blurring vision, fatigue, problems with bowel and bladder function
Question 7.4.3
What is thought to cause these symptoms of Parkinson's disease?
Degeneration of glutamatergic neurons in sensorimotor cortex
Degeneration of dopaminergic neurons in substantia nigra pars compacta
Degeneration of astrocytes in hippocampus CA1 region
Degeneration of Purkinje cells in cerebellar cortex
Question 7.4.4
L-DOPA is an effective first treatment for the symptoms of Parkinson's disease. However, for some patients L-DOPA gradually becomes less effective and is associated with serious side-effects. As a further treatment for the symptoms of Parkinson's disease, deep brain stimulation might be considered. Which statement is true about deep brain stimulation?
Deep brain stimulation is an experimental therapy, with mixed results, and not in general available as a treatment, but only as part of clinical trials
Implantation of electrodes in human brains is unethical and not allowed in Europe
More than 100,000 people across the world have already been implanted with deep brain stimulation electrodes with overall good results
Many millions of Parkinson's patients have already been implanted with deep brain stimulation electrodes and this is now a standard therapy
Question 7.4.5
Which region of the human brain is typically targeted by deep brain stimulation to alleviate symptoms of Parkinson's disease?