Week 5

Important concepts

1. GABAergic inhibition

• GABA: Neurotransmitter gamma-Aminobutyric acid
• Inhibition: Decrease in activity
• Enzymatic step: Transformation of a molecule through another molecule.
• Cytosol: Internal cell fluid.

2. Inhibitory synaptic conductances

• Shunting: Directing flow.

3. Benzodiazepines

• Compound: Assembly of proteins.
• Antagonist: Receptor blocker.

4. GABAergic projections

• Thalamus: Connective brain centra.

5. Neocortical inhibition

• Volume transmission: Diffusion through extracellular fluid.

Resources

Plain text

• 5.1.txt
• 5.2.txt
• 5.3.txt
• 5.4.txt
• 5.5.txt

PDF

• (2 MB) 5_1_GABAergic_inhibition.pdf
• (1 MB) 5_2_Inhibitory_synaptic_conductances.pdf
• (2 MB) 5_3_Benzodiazepines.pdf
• (6 MB) 5_4_GABAergic_Projections.pdf
• (2 MB) 5_5_Neocortical_Inhibition.pdf

Videos

• 5.1
• 5.2
• 5.3
• 5.4
• 5.5

Questions

Question 5.1.1

Which of the following statements about the neurotransmitter GABA is correct?

• GABA is synthesized in a single enzymatic step, in which the GAD enzyme produces GABA from acetylcholine
• GABA is packaged into synaptic vesicles through the VGAT transporter
• The concentration of GABA inside a synaptic vesicle is about 100 nM
• GABA is the main inhibitory neurotransmitter in the spinal cord, but not in the brain

Question 5.1.2

Which of the following statements is not correct:

• GABAergic neurons make synapses at specific dendritic locations
• GABA acts upon postsynaptic neurons to prevent them from firing action potentials
• GABAergic inhibition counteracts glutamatergic excitation in neuronal networks of the brain
• Most neurons in the brain are GABAergic in order to maintain the balance between excitation and inhibiton

Question 5.1.3

There are two major classes of GABA receptors, GABA-A receptors and GABA-B receptors. How do these two classes of GABA receptors inhibit neuronal activity?

• GABA-A receptors selectively conduct K+, and GABA-B receptors activate selective Cl- conductances via G-proteins
• GABA-A and GABA-B receptors both conduct Cl- and K+
• GABA-A receptors selectively conduct Na+, and GABA-B receptors selectively conduct Cl-
• GABA-A receptors selectively conduct Cl-, and GABA-B receptors activate selective K+ conducances via G-proteins

Question 5.1.4

Which of the following statements about Cl- concentration is not correct:

• The concentration of Cl- in the cytosol of a mature neuron is about 50 mM
• The concentration of Cl- in the extracellular space is about 120 mM
• The KCC2 transporter is important for maintaining chloride concentrations within the neuron low
• In early development, chloride concentration is high (~30 mM) in the cytosol of a neuron

Question 5.1.5

GABA-A mediated postsynaptic conductances:

• have approximately the same time course as GABA-B mediated postsynaptic conductances
• are faster in onset and shorter in duration than GABA-B mediated postsynaptic conductances
• are faster in onset and longer in duration than GABA-B mediated postsynaptic conductances
• are slower in onset and longer in duration than GABA-B mediated postsynaptic conductances

Question 5.2.1

The reversal potential of the GABA-A receptor Cl- conductance is typically about:

• 0 mV
• -35 mV
• -55 mV
• -75 mV

Question 5.2.2

Which of the following statements about the time course of inhibitory conductances mediated by GABA-A receptors is correct?

• GABA-A inhibition is fast, and short lasting compared AMPA-mediated excitation
• GABA-A inhibition is fast, but it’s much slower than AMPA-mediated excitation
• GABA-A inhibition has almost the same duration as AMPA-mediated excitation
• GABAergic inhibition is a slow process, but it's much faster than AMPA-mediated excitation

Question 5.2.3

Which of the following statements regarding IPSPs and/or IPSCs is not correct?

• The time course of the synaptic current is the same as the time course of the synaptic conductance
• IPSPs have longer durations that IPSCs
• If the membrane potential is at the chloride reversal potential, then there is no GABA-A-mediated synaptic conductance
• An IPSC typically lasts ~10 ms

Question 5.2.4

Which of the following statements regarding hyperpolarising inhibition is correct?

• GABA-A synaptic input causes hyperpolarising inhibition when the membrane potential is depolarised relative to the Cl- reversal potential
• GABA-A synaptic input causes hyperpolarising inhibition when the membrane potential is hyperpolarized relative to the Cl- reversal potential
• GABA-A synaptic input causes hyperpolarising inhibition when the membrane potential is at the Cl- reversal potential
• GABA-B synaptic input causes hyperpolarising inhibition when the membrane potential is hyperpolarised relative to the K+ reversal potential

Question 5.2.5

Which of the following statements regarding shunting inhibition is correct?

• GABA-A synaptic input causes shunting inhibition due to increased input resistance of the soma
• GABA-A synaptic input causes shunting inhibition due to increased membrane time constant
• GABA-A synaptic input causes shunting inhibition due to increased axial resistance
• GABA-A synaptic input causes shunting inhibition due to decreased membrane resistance

Question 5.3.1

Which of the following compounds is not a GABA receptor blocker?

• picrotoxin
• bicuculline
• gabazine
• CNQX

Question 5.3.2

Which of the following statements about the action of benzodiazepines is correct?

• Benzodiazepines act upon all GABA-A receptors
• Benzodiazepines act upon all GABA-B receptors
• Benzodiazepines act upon specific subtypes of GABA-A receptors
• Benzodiazepines act upon specific subtypes of GABA-B receptors

Question 5.3.3

Which of the following statements about the mechanism of action of benzodiazepines is not correct?

• Benzodiazepines do not activate GABA-A receptors by themselves, but they only potentiate GABA-evoked currents
• Benzodiazepines increase the affinity of GABA to GABA-A receptor
• Benzodiazepines are GABA-A receptor antagonists
• Benzodiazepines act on GABA-A receptors containing the a1, a2, a3 or a5 subunits, but not the a4 and a6 subunits

Question 5.3.4

How do benzodiazepines affect mouse behaviour?

• Benzodiazepines induce a sedative effect (sleep) and an anxiolytic effect (anti-anxiety) by acting on the same types of GABA-A receptors
• Benzodiazepines induce an anxiolytic effect, which is largely mediated by GABA-B receptors
• Benzodiazepines induce a sedative effect (sleep), which is largely mediated by GABA-A-a1 receptors
• Benzodiazepines induce an anxiogenic effect (increased anxiety), which is mediated by GABA-A-a2 receptors

Question 5.3.5

Why might someone be prescribed benzodiazepenes by their doctor?

• To reduce anxiety
• To promote sleep or sedation
• As an anticonvulsant to prevent epileptic seizures
• All of the above are valid

Question 5.4.1

What neuronal circuit mediates feedback inhibition in the thalamus?

• Inhibitory thalamic projection neurons inhibit excitatory nucleus reticularis (NRT) neurons
• Cortical glutamatergic excitation drives neurons in NRT, which innervate the principal thalamic nuclei
• Glutamatergic thalamic projection neurons excite GABAergic NRT neurons which inhibit the thalamic projection neurons
• Striatal GABAergic neurons reciprocally innervate the main thalamic nuclei

Question 5.4.2

Why might feedback inhibition be useful to the brain ?

• Feedback inhibition prevents run-away excitation
• Feedback inhibition can help select the most important strong excitatory inputs, while filtering out smaller signals
• Feedback inhibition can help sharpen spatiotemporal receptive fields
• All of the above

Question 5.4.3

Where do GABAergic striatal projection neurons innervate?

• Cerebellum
• Substantia nigra (SNr)
• Olfactory bulb
• Barrel cortex

Question 5.4.4

Which statement about dopamine is not correct?

• Dopaminergic innervation of striatum is prominent
• Symptoms of Parkinson's disease likely result importantly from degeneration of dopamine neurons
• Dopamine acts on D1 and D2 receptors expressed on different cell-types in the striatum
• Dopamine acts on ionotropic dopamine receptors in the striatum

Question 5.4.5

What are the output neurons of the cerebellar cortex and which neurotransmitter do they release?

• Pyramidal neurons / Glutamate
• Pyramidal neurons / GABA
• Purkinje cells / Glutamate
• Purkinje cells / GABA

Question 5.5.1

Which statement about neocortical GABAergic neurons is incorrect?

• Neocortical GABAergic neurons prominently inhibit sub-cortical nuclei
• Some subtypes of neocortical GABAergic neurons inhibit other neocortical GABAergic neurons
• Neocortical GABAergic neurons represent about 10-20% of the total number of cortical neurons
• Most neocortical GABAergic neurons are local interneurons and don't have long-range axonal projections

Question 5.5.2

Which one below is not a neocortical GABAergic neuron?

• Parvalbumin-expressing (PV)
• Somatostatin-expressing (Sst)
• Vasoactive intestinal peptide-expressing (VIP)
• Purkinje cells

Question 5.5.3

Parvalbumin-expressing (PV) basket cells innervate which part of postsynaptic target neurons?

• Distal dendrites
• Soma and proximal dendrites
• Gap junctions
• Axon initial segment

Question 5.5.4

Where do neocortical somatostatin-expressing GABAergic neurons (Sst) prominently innervate excitatory pyramidal neurons?

• Distal dendrites
• Basal dendrites
• Nodes of Ranvier
• Soma

Question 5.5.5

Which neocortical GABAergic neuron sub-type is thought to signal mainly by volume transmisson?

• Somatostatin-expressing GABAergic neurons (Sst)
• Parvalbumin-expressing GABAergic neurons (PV)
• Neurogliaform GABAergic neurons
• Vasoactive intestinal peptide-expressing GABAergic neurons (VIP)

Updated on 2020-08-21.