differentiate exam 3 biopsych

Monocular Cells in V1

• Receive input from one eye only

• Reflect segregated LGN input

• No depth perception processing

• Dominant early in processing stream

Binocular Cells in V1

• Integrate input from both eyes

• Enable stereopsis (depth perception)

• Sensitive to disparity between eyes

• Critical for 3D perception

Effect of monocular deprivation during the critical period

• Competitive imbalance → open eye takes over cortex

• Shrinkage of deprived-eye ocular dominance columns

• Leads to amblyopia (functional blindness)

Effect of binocular deprivation during the critical period

• No competition → both eyes equally weak

• Overall reduced responsiveness but less asymmetry

• Visual system underdeveloped, not dominated

Dorsal streams

• Parietal lobe

• Motion, spatial location, visually guided action

• Linked to sensorimotor integration

Ventral streams

• Temporal lobe

• Object identity, faces, color

• Linked to recognition and memory

Face-selective neurons (temporal lobe)

• Encode identity and invariant features

• Damage → prosopagnosia

facial expression cells (amygdala)

• Encode emotional salience (fear, threat)

• Rapid, subcortical processing

Orientation Selective Cells in V1

• Respond maximally to specific edge orientation

• Built from LGN center-surround inputs

• Foundation for feature detection → object perception

Visual agnosia

• Cannot identify objects despite intact vision

• Damage to ventral stream

prosopagnosia

• Selective face-recognition deficit

• Damage to fusiform face area

Lateral geniculate nucleus of the thalamus

visual relay (retina → V1)

Medial geniculate nucleus of the thalamus

auditory relay (ear → auditory cortex)

how they act on what specific receptors or on what step of NT signaling? (Alcohol)

↑ GABA (enhances inhibition), ↓ NMDA glutamate (reduces excitation)

how they act on what specific receptors or on what step of NT signaling? (Marijuana/ cannabinoids)

CB1 receptor agonist → ↓ neurotransmitter release (retrograde signaling)

how they act on what specific receptors or on what step of NT signaling? (Benzodiazepines/barbiturates)

Enhance GABA-A receptor activity → increased inhibition

how they act on what specific receptors or on what step of NT signaling? (Amphetamine)

↑ release of dopamine and norepinephrine

how they act on what specific receptors or on what step of NT signaling? (Cocaine)

Blocks reuptake of dopamine (also NE, serotonin)

how they act on what specific receptors or on what step of NT signaling? (Nicotine)

Agonist at nicotinic ACh receptors → ↑ DA release

how they act on what specific receptors or on what step of NT signaling? (LSD/Psilocybin/MDMA)

Act on serotonin receptors (5-HT); MDMA ↑ serotonin release

how they act on what specific receptors or on what step of NT signaling? (Ketamine)

NMDA receptor antagonist → ↓ glutamate signaling

Depressants

increase inhibition (GABA)

stimulants

increase DA/NE

hallucinogens

alter serotonin/glutamate signaling

opiates

activate opioid receptors → ↓ pain, ↑ DA indirectly

Structural effects on drugs on the brain

Neuron loss, dendritic pruning, brain volume changes

functional effects on drugs on the brain

Changes in signaling (receptors, NT levels) without cell death

Presynaptic autoreceptors

Detect NT release and reduce further release.

Postsynaptic receptors

Receive NT and produce cellular response.

How is this negative feedback?

NT binds autoreceptors → inhibits further release.

Effect on the amount of NT release in response to: Agonist binding of autoreceptors

↓ NT release

Effect on the amount of NT release in response to: Antagonist binding of autoreceptors

↑ NT release

Effect on the amount of NT release in response to: Ionotropic receptors

fast, direct effects

Effect on the amount of NT release in response to: Metabotropic receptors

slower, modulatory effects

Effect on the amount of NT release in response to: Excitatory neurotransmitters

↑ firing

Effect on the amount of NT release in response to: Inhibitory neurotransmitters

↓ firing

Acetylcholinesterase

Breaks down acetylcholine in synapse.

Monoamine oxidase

Breaks down monoamines (DA, NE, serotonin).

Positive symptoms and DA pathways involved

↑ dopamine → mesolimbic pathway

• Hallucinations (usually auditory)

• Delusions (false, fixed beliefs)

• Disorganized speech (incoherent, loose associations)

• Disorganized behavior (erratic, unpredictable actions)

• Agitation / psychosis

Negative symptoms and DA pathways involved

↓ dopamine → mesocortical pathway

• Flat affect (reduced emotional expression)

• Avolition (lack of motivation)

• Alogia (reduced speech)

• Anhedonia (loss of pleasure)

• Social withdrawal

• Reduced goal-directed behavior

Types of drugs that block either kind of symptoms (Thorazine typical)

Blocks D2 receptors → reduces positive symptoms.

Types of drugs that block either kind of symptoms (Clozapine atypical)

Blocks D2 + serotonin receptors → treats both positive and negative symptoms.

Size of ventricles and sulci (schizophrenic brain)

enlarged

Size of ventricles and sulci (normal brain)

Normal size

Amount of frontal lobe blood flow (schizophrenic)

relatively normal or slightly elevated at rest, but fails to increase (or increases less) during tasks → hypofrontality

Amount of frontal lobe blood flow (normal brain)

moderate at rest → increases with task

Amount of grey matter loss in adolescence (schizophrenic brain)

greater during adolescence

Amount of grey matter loss in adolescence (normal brain)

minimal

Dopamine hypothesis (schizophrenia)

Symptoms are due to dopamine imbalance (↑ mesolimbic, ↓ mesocortical)

Glutamate hypothesis (schizophrenia)

NMDA receptor dysfunction contributes to both positive and negative symptoms

Cocaine/amphetamine effect on neurotransmitters

Increase dopamine

Cocaine/amphetamine support which hypothesis?

Dopamine hypothesis

PCP/ketamine effect on receptors

Block NMDA (glutamate) receptors

PCP/ketamine support which hypothesis?

Glutamate hypothesis

PCP/ketamine symptoms

Can cause both positive and negative symptoms of schizophrenia

Disorders of movement

Parkinson’s (↓ dopamine in nigrostriatal pathway → bradykinesia, rigidity, tremor) and Huntington’s (degeneration of striatum → hyperkinetic movements like chorea)

Disorders of thought/emotion

Schizophrenia (dopamine/glutamate dysfunction → positive + negative symptoms) and depression (monoamine imbalance → low mood, anhedonia, cognitive changes)

Basal ganglia (normal function)

Uses direct (facilitates movement) and indirect (inhibits movement) pathways to balance motor output; dopamine from substantia nigra modulates both to allow smooth, controlled movement

Basal ganglia in Parkinson’s

Loss of dopamine neurons in substantia nigra → ↓ activation of direct pathway + ↑ activity of indirect pathway → excessive inhibition of thalamus → reduced cortical motor output → slowed movement

Basal ganglia in Huntington’s

Degeneration of inhibitory neurons in striatum (indirect pathway) → reduced inhibition of thalamus → excessive cortical activation → uncontrolled, hyperkinetic movements

Motor symptoms of Parkinson’s

Bradykinesia (slow movement), rigidity (muscle stiffness), resting tremor, postural instability due to reduced motor cortex activation

Psychological symptoms of Parkinson’s

Depression (dopamine loss in reward pathways), cognitive decline (prefrontal cortex involvement)

Surgical treatments for Parkinson’s (deep brain stimulation)

Electrical stimulation (often of subthalamic nucleus or globus pallidus) reduces abnormal inhibitory output from basal ganglia, improving movement

non-surgical (drug) treatments for Parkinson’s (L-DOPA treatment)

Dopamine precursor that crosses BBB and is converted to dopamine in brain → restores dopamine levels

non-surgical (drug) treatments for Parkinson’s (Dopamine agonists)

Directly stimulate dopamine receptors → mimic dopamine effects in basal ganglia circuits

Parkinson’s (motor deficits)

slow, reduced movement (bradykinesia, rigidity) due to excessive inhibition of motor output

Huntington’s (motor deficits)

excessive, uncontrolled movement (chorea) due to reduced inhibition of motor output

Genetic component (Parkinson’s)

usually sporadic (not strongly genetic, though some cases are)

Genetic component (Huntington’s)

autosomal dominant mutation (HTT gene), fully penetrant

Neurotransmitter & brain area affected (Parkinson’s)

↓ dopamine from substantia nigra → impaired nigrostriatal pathway → reduced movement; typically later onset

Neurotransmitter & brain area affected (Huntington’s)

Loss of GABAergic inhibitory neurons in striatum (caudate/putamen) → excessive thalamic activation → hyperkinesia; earlier onset

Subcortical dementia

Movement + slower cognition (huntington/parkinson)

Cortical dementia

Memory, language deficits (alzheimer’s)

Early onset Alzheimer’s (genetics & age)

Strong genetic component; typically occurs before age 65

Late onset Alzheimer’s (genetics & age)

Weak/indirect genetic risk; typically occurs after age 65

Genes causing early onset Alzheimer’s

APP, PSEN1, PSEN2

Gene associated with late onset Alzheimer’s

APOE (ε4 allele) → increases risk but does not directly cause disease

Soluble Aβ peptides

• Small, diffusible

• More toxic to synapses

Insoluble Aβ peptides

• Aggregated

• Forms plaques

Amyloid plaques

• Extracellular

• Made of Aβ

neurofibrillary tangles

• Intracellular

• Made of tau

Effect of THC on young brains

• Disrupts development

• ↓ memory, learning, executive function

Effect of THC on old brains

• ↓ inflammation

• May slow neurodegeneration (some evidence)

Melanopsin containing RGCs for vision

• Minimal role in image-forming vision

• Not for detailed sight (rods/cones do that)

Melanopsin containing retinal ganglion cells for vision

• Detect light → send to SCN

• Control circadian rhythms & pupil reflex

Function of molecular clock in the SCN

• Master clock → sets body’s circadian rhythm

• Synchronizes sleep, hormones, temperature

Function of molecular clock in other cells

• Local clocks → regulate cell-specific timing

• Follow SCN but can run independently

Stages of sleep

NREM 1 → NREM 2 → NREM 3 (slow-wave) → REM

Asynchronous cortical activity (awake)

• Low amplitude, high frequency

• Neurons fire independently

Synchronous cortical activity (asleep)

• High amplitude, low frequency

• Neurons fire together (slow waves)

REM sleep

• Rapid eye movements

• High brain activity (awake-like)

• Muscle paralysis

• Dreaming

Non-REM sleep

• Slow-wave activity

• Physical restoration

• Lower brain activity

Insomnia

Difficulty falling or staying asleep

Narcolepsy

• Sudden sleep attacks

• Direct entry into REM sleep

Endocrine system

• Hormones in bloodstream

• Slow onset, long-lasting, widespread effects

Nervous system

• Neurotransmitters at synapses

• Fast onset, short-lasting, targeted effects

Duct glands

Secrete through ducts to surfaces (skin, organs)

Ductless glands

Secrete hormones into bloodstream

Neurotransmitter chemical signals

• Local (synapse)

• Rapid, precise

Hormone chemical signals

• Circulate in blood

• Slower, broader effects