n2 e2

Exam 2

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Central visual pathways:

Retinotopic maps:

~Light representing the RIGHT visual field drives neurons in:

The left hemisphere of the brain.

~Which retina(s)?

The nasal retina of the right eye and the temporal retina of the left eye.

~Which lateral geniculate nucleus/nuclei (LGN)? Does the lateral geniculate nucleus receive inputs from both eyes?

The left LGN. The LGN receives inputs from both eyes but processes them separately in different layers.

~Which primary visual cortex?

The left primary visual cortex (V1).

~Does the primary visual cortex receive inputs from both eyes?

Yes, but they remain segregated in ocular dominance columns.

~What is the ideal stimulus for a cell in V1?

A bar of light with a specific orientation.

~How is V1 organized? What features of the visual world do neurons in V1 respond to? How is this different from retinal ganglion cells/LGN?

V1 is organized in a columnar structure that responds to orientation, spatial frequency, and binocular disparity, unlike retinal ganglion cells/LGN, which respond to spots of light.

 ~What are the differences between the where and what pathways?

The "where" (dorsal) pathway processes motion and spatial location, while the "what" (ventral) pathway processes object identity and recognition.

~Which includes the area in the parietal lobe? Temporal lobe?

The dorsal (where) pathway is in the parietal lobe; the ventral (what) pathway is in the temporal lobe.

~To which pathway do each of the following areas belong: MT, V4, IT, FFA?

MT (motion) → dorsal; V4 (color/form) → ventral; IT (object recognition) → ventral; FFA (face recognition) → ventral.

~Neurons in MT are driven by what visual feature?

Motion.

~Damage or inactivation of MT leads to what condition?

Akinetopsia (motion blindness).

~Neurons in V4 are driven by what visual feature?

Color and complex shape features.

~Damage or inactivation of V4 leads to what condition?

Cerebral achromatopsia (loss of color vision).

~Neurons in IT are driven by what visual feature?

Complex object features, including faces.

~Damage or inactivation of FFA leads to what condition?

Prosopagnosia (face blindness).

General movement:

~Which functions of movement are carried out by each level of control?

The spinal cord controls reflexes, the brainstem manages posture, and the motor cortex/cerebellum fine-tunes voluntary movements.

Lower motor neurons:

~Organization of spinal cord (diagram it out with emphasis on proximal and distal muscles):

dorsal and ventral horns, medial and lateral parts of ventral horns, cervical and lumbar enlargements?

The ventral horn contains motor neurons, with medial regions controlling axial muscles and lateral regions controlling limb muscles.

Motor unit

~What is it?

A motor neuron and the muscle fibers it innervates.

~What is evoked by stimulation of ventral horn motor neurons?

Muscle contraction.

~Fast-Fatigable vs. Fast Fatigue-Resistant vs. Slow

FF: powerful but tires quickly; FR: intermediate; Slow: weak but fatigue-resistant.

~How does the force needed for a movement determine which order motor units are recruited?

Slow → FR → FF, depending on force needed.

Local circuit neurons

~short-distance vs. long distance

Short-distance control distal muscles, long-distance control axial muscles.

~reflex: resistance to passive stretch

The stretch reflex maintains muscle tone.

~reflex: flexion – crossed extension

Withdrawal of one limb while extending the opposite limb.

~Central pattern generators – what do they accomplish by recruiting flexion – crossed extension reflexes

Control rhythmic movements like walking by coordinating flexion-crossed extension reflexes.

~Cranial nuclei/nerves – what do they control? Where are the lower motor neurons?

Motor and sensory functions of the head and neck.

Brainstem nuclei.

Upper motor neurons:

Organization

~Axial and proximal limb muscles

Controlled by medial descending pathways.

~Distal limb muscles

Controlled by lateral descending pathways.

~Head and neck

Controlled by cranial nerve motor pathways.

Primary motor cortex

~What is evoked by stimulation of M1?

  Muscle movement.

Premotor cortex

~What is the role of the premotor cortex?

Planning and selection of movements.

~What causes mirror neurons to become active?

When performing or observing an action.

Cerebellum:

~What are the characteristics of cerebellar ataxia? (e.g. balance, walking, pointing, reaching, moving eyes to visual target)

Poor balance, uncoordinated movements, and difficulty targeting objects.

~What information comes into the cerebellum?

Proprioceptive, vestibular, and motor command information.

~What does the cerebellum do with the information – how is it processed?

Compares expected vs. actual movement and adjusts motor output.

~What information comes out of the cerebellum? 

Deep cerebellar nuclei send motor corrections to the brain and spinal cord.

~How does the cerebellum function like a servomechanism? 

It detects errors and corrects movement in real time.

~Given all of the above, what role does the cerebellum play in controlling movement and why does cerebellar ataxia present with the symptoms you described (e.g. balance, walking, pointing, reaching, moving eyes to visual target)?

Coordination and error correction; ataxia results from disrupted feedback.

Diagram the basic inputs and outputs of a deep cerebellar nucleus cell. Include:

~Efferent copy of motor command

Internal copy of motor commands.

~Feedback from proprioceptive/vestibular systems

Provides real-time movement data.

~Purkinje cell – excitatory or inhibitory

Inhibitory; regulates deep cerebellar nuclei.

~Output of deep cerebellar n. Cell

Adjusts movement via motor cortex/brainstem.

Basal Ganglia:

 Basal ganglia function

 ~Direct path (structures and nature of effect, i.e. excite/inhibit) – diagram these out)

Structure: Cortex → Striatum (caudate/putamen) → Globus Pallidus internal (GPi) → Thalamus → Motor Cortex.

Effect: Activation of this pathway disinhibits the thalamus, increasing motor cortex activity and promoting movement. The striatum inhibits GPi, reducing its inhibitory output on the thalamus, which leads to movement facilitation.

~Indirect path (structures and nature of effect, i.e. excite/inhibit) – focus on output of indirect path – what effect does it have on movement?

Structure: Cortex → Striatum → Globus Pallidus external (GPe) → Subthalamic Nucleus (STN) → GPi → Thalamus → Motor Cortex.

Effect: This pathway increases inhibition of the thalamus, reducing motor cortex activity and suppressing movement. The STN excites GPi, which strongly inhibits the thalamus, leading to movement suppression.

~How do inhibition and disinhibition control initiation of movement in the direct path?

The basal ganglia control movement through inhibition and disinhibition mechanisms. At rest, the GPi tonically inhibits the thalamus, preventing unwanted movement. When the direct pathway is activated, the striatum inhibits GPi, reducing its inhibition of the thalamus (disinhibition), thereby allowing movement to proceed.

~Dopamine – effects on direct and indirect paths

Dopamine from the substantia nigra pars compacta (SNc) modulates movement by differentially affecting the direct and indirect pathways.

~(which pathway has D1 receptors – what is the effect of DA at D1?)

Found in the direct pathway (striatum → GPi).

Dopamine excites D1 receptors, increasing striatal inhibition of GPi, which disinhibits the thalamus and facilitates movement

~(which pathway has D2 receptors – what is the effect of DA at D2?)

Found in the indirect pathway (striatum → GPe).

Dopamine inhibits D2 receptors, reducing striatal inhibition of GPe. This results in less excitation of GPi by the STN, leading to less inhibition of the thalamus and more movement.

~Loops – what are the different structures, but similar function between body movement loop and oculomotor loop

Both loops involve the cortex, striatum, globus pallidus, thalamus, and associated regions.

The body movement loop regulates voluntary motor control, whereas the oculomotor loop controls eye movement by integrating signals from the frontal eye fields, superior colliculus, and basal ganglia. Both loops use similar inhibitory and disinhibitory mechanisms to regulate movement.

Disorders

~Huntington’s disease – cause, symptoms, treatments

Genetic mutation causing loss of inhibitory neurons.

Chorea (involuntary movements), cognitive decline.

Dopamine antagonists, symptom management.

~Parkinson’s disease – cause, symptoms, treatments

Loss of dopaminergic neurons in substantia nigra.

Bradykinesia, rigidity, tremor.

L-DOPA, deep brain stimulation.

~Why are impulse control disorders a side-effect of Parkinson’s treatment?

Dopamine agonists can overstimulate reward pathways.

Taste

~For each basic taste listed, how is the taste neuron activated (direct/ion channel or indirect/G-protein coupled receptor)?

~Sweet

G-protein coupled receptors.

~Bitter

G-protein coupled receptors.

~Umami

G-protein coupled receptors.

~Salt

Direct sodium ion channel.

~Sour

Hydrogen(Proton)-sensitive ion channels.

~What is a labeled line?

A dedicated neural pathway for each taste.

Motivated behavior

Main differences between neurotransmitters and hormones:

Neurotransmitters act locally and quickly; hormones travel through the bloodstream and last longer.

~Where are they produced:

NT: Produced in neurons, specifically in the presynaptic terminal.

Hormones: Produced in endocrine glands (e.g., pituitary, adrenal glands, pancreas).

~Where are they released:

NT: Released into synapses between neurons.

Hormones: Released into the bloodstream to travel throughout the body.

~What target do they affect:

NT: Affect nearby neurons, muscles, or glands through specific receptors.

Hormones: Affect distant organs and tissues with the appropriate receptors.

~How long do their effects last:

NT: Act rapidly (milliseconds to seconds) and have short-term effects.

Hormones: Act more slowly (minutes to hours) and have longer-lasting effects.

~Why are neurons near the ventricular system able to respond to physiological factors (blood glucose, hydration level, peptides released from gut, hormones released from glands, etc)?

They lack a blood-brain barrier.

~Where is ghrelin released from?

Stomach.

~When are ghrelin levels low? High?

High at meals and dies down after… slowly starts rising until meal again

~If ghrelin is administered into an animal (into gut or brain), what behavior is observed?

Increases hunger and food intake.

~Where is leptin released from?

Fat cells.

~When are leptin levels low? High?

After meals = high… low before meals

~If leptin is administered into an animal (into gut or brain), what behavior is observed?

Decreases hunger.

~Where is GLP-1 released from?

Decreases hunger.

~When is it released?

After meals.

~What is the effect of GLP-1 receptor agonists on body weight?

Reduces appetite and weight.

Diagram a model of the arcuate nucleus of the hypothalamus – include:

~AgRP/NPY neuron – what kind of receptors does it have?

Ghrelin (activates), leptin (inhibits).

~How does it affect the activity of POMC neurons?

Inhibitory.

~How does it affect the activity of downstream second-order neurons that control eating?

Increases appetite.

~POMC neuron – what kind of receptors does it have?

Leptin (activates).

~How does it affect the activity of AgRP/NPY neurons?

Inhibitory.

~How does it affect the activity of downstream second-order neurons that control eating?

Decreases appetite.