4b nervous system pt 1

How is the nervous system hierarchically divided?

• Nervous system → central nervous system and peripheral nervous system

• Central nervous system: brain and spinal cord

• Peripheral nervous system → autonomic and somatic divisions

• Autonomic division → sympathetic and parasympathetic branches

• Slide 3.

Contrast the central and peripheral nervous systems.

• Central nervous system: brain and spinal cord; central processing and coordination

• Peripheral nervous system: nerves outside the brain and spinal cord; carries sensory input toward the central nervous system and motor output toward the body

• Slide 3.

Contrast the autonomic and somatic divisions

• Autonomic: self-regulated activity of internal organs and glands

• Somatic: voluntary control of skeletal muscles

• Both belong to the peripheral nervous system

• Slide 3.

Compare sympathetic and parasympathetic activity.

• Sympathetic: arousing, fight-or-flight response; mobilizes energy and elevates bodily activity

• Stress pathway can produce cortisol plus the catecholamines epinephrine and norepinephrine

• Parasympathetic: calming, rest-and-digest response; conserves energy and supports digestion

apart of autonomic nervous sys

• Slide 4.

Trace a somatic motor command and identify the key neurotransmitter.

• Motor command descends from the brain through the spinal cord to skeletal muscle

• At the neuromuscular junction, acetylcholine signals the muscle to contract

• Direction: brain → spinal cord → body action

• Slide 5.

How do black widow venom and botulism produce opposite effects at the neuromuscular junction?

• Black widow venom causes excessive acetylcholine release → excessive muscle activation and spasms

• Botulinum toxin suppresses acetylcholine release → reduced or blocked contraction

• Botox uses this effect locally to prevent targeted muscles from contracting

• Slide 5.

Trace somatosensory information and match each stimulus to its receptor.

• Signals ascend from body → spinal cord → brain

• Pressure: mechanoreceptors

• Body position without vision: proprioceptors

• Temperature: thermoreceptors

• Pain: nociceptors

• Slide 6.

Contrast A-delta and C pain fibres, and explain the danger of hereditary sensory autonomic neuropathy.

• A-delta fibres carry fast, sharp, well-localized pain

• C fibres carry slow, dull, throbbing or burning pain

• Hereditary sensory autonomic neuropathy can prevent pain detection, so injury may continue without the person recognizing bodily damage

• Slide 6.

Why does the level of a spinal cord injury matter?

• The spinal cord carries information between brain and body

• Injury interrupts pathways at and below the damaged level

• Higher injuries generally disrupt more of the body because more ascending sensory and descending motor traffic is cut off

• Slide 8.

Compare scoliosis and spina bifida.

• Scoliosis: abnormal spinal curvature that may affect nearby nerves

• Spina bifida: incomplete closure of the embryonic neural tube

• Adequate prenatal folate lowers the risk of neural-tube defects such as spina bifida • Slide 9.

What can reflex testing reveal, and how does the Babinski response change with age?

• A reflex arc can produce a rapid response through sensory neuron → spinal-cord interneuron → motor neuron, without waiting for conscious brain processing

• Typical or abnormal reflexes help assess neurological function

• Toe fanning after stroking the sole is typical in infants; inward toe curling is expected later, so an adult Babinski sign can indicate neurological damage • Slide 10.

What are glial cells, and why are they essential to neural signalling?

• Glia are non-neuronal support cells of the nervous system

• They support, protect and maintain neurons

• Myelinating glia insulate axons, allowing efficient electrical transmission

• Damage to glia can therefore impair neural communication even if the neuron itself initially survives • Slide 13.

Distinguish Schwann cells from oligodendrocytes.

• Schwann cells myelinate axons in the peripheral nervous system and each cell wraps one axon segment

• Oligodendrocytes myelinate axons in the central nervous system and one cell can wrap segments of multiple axons

• Multiple-axon myelination is space-efficient in the brain • Slide 13.

types of gilia cells

Why can a tumour originating in glia have broad cognitive or behavioural effects?

• Glial tumours can grow and spread through brain tissue • They may compress, infiltrate or disrupt neurons and their support systems • Resulting symptoms depend on the neural networks compromised, so cognition and behaviour can change even though the tumour began in glia • Slides 12 and 14.

Compare sensory neurons, motor neurons and interneurons.

• Sensory neurons are specialized for a modality and carry environmental or bodily information inward

• Motor neurons relay movement commands from brain or spinal cord to muscles

• Interneurons connect neurons within the central nervous system and support integration and cognition • Slide 15.

Why are interneurons especially important for cognition?

• They are the most abundant neuron type

• They combine different streams of information and form processing networks

• Their integration supports functions such as memory, understanding a lecture, reasoning and coordinated responses • Slide 15.

Map the major parts of a neuron to their functions.

• Dendrites receive signals

• Soma integrates inputs and maintains the cell (cell body)

• Nucleus contains genetic material

• Axon hillock is the action-potential trigger zone

• Axon carries the electrical signal

• Myelin insulates the axon

• Nodes of Ranvier regenerate the signal

• Terminal buttons release neurotransmitter • Slide 16.

How does neuronal morphology support function? Use a Purkinje cell as an example.

• Neurons vary in shape according to the information they must receive and transmit • A Purkinje cell in the cerebellum has an enormous, highly branched dendritic tree • This morphology lets it integrate input from up to about 100,000 synapses • Slide 17.

Where are electrical and chemical transmission used in the flow of information between neurons?

• Within a neuron, an electrical action potential travels from the axon hillock down the axon to the terminals

• Between neurons, chemical neurotransmitters cross the synaptic cleft

• The receiving neuron converts that chemical message into a change in membrane potential • Slides 18 and 23–24.

How does a neuron move from resting potential to an action potential?

• Resting membrane potential is about −70 mV

• The neuron receives excitatory and inhibitory inputs

• If their summed effect brings the axon hillock to threshold, an action potential begins

• If threshold is not reached, no action potential occurs • Slide 19.

What does the all-or-none principle mean, and how can stimulus intensity still be represented?

• Once threshold is reached, each action potential has essentially the same size and strength • A stronger input does not create a larger action potential • Stimulus intensity can instead be represented by how frequently neurons fire and how many neurons are recruited • Slide 19.

What happens during depolarization?

• Voltage-gated sodium channels open

• Sodium ions move into the axon

• The inside becomes less negative and then positive relative to the outside

• This rising phase produces the action-potential peak • Slide 20.

What happens during repolarization and hyperpolarization?

• Repolarization: sodium channels inactivate and potassium leaves the neuron, driving the membrane potential back downward

• Hyperpolarization: potassium channels close slowly, so the membrane becomes briefly more negative than resting potential

• Ion distributions are then restored and the neuron returns to about −70 mV • Slides 20–21.

Give the complete sequence of electrical transmission.

• Receive excitatory and inhibitory inputs

• Reach threshold and initiate an action potential

• Depolarize

• Repolarize

• Hyperpolarize

• Return to resting potential

• The rapid sequence occurs over only a few milliseconds • Slide 21.

Explain saltatory conduction and predict the effect of multiple sclerosis.

• Myelin insulates the axon, so the action potential is regenerated mainly at Nodes of Ranvier and appears to jump node to node

• This saltatory conduction makes signalling fast and efficient

• In multiple sclerosis, central myelin is damaged, so signals slow, weaken or fail • Slide 22.

Identify the structures and sides of a synapse.

• Presynaptic side: axon terminal containing vesicles filled with neurotransmitter • Synaptic cleft: small gap between cells • Postsynaptic side: usually a dendrite with receptor proteins • Neurotransmitters act like keys that affect only receptors with a compatible lock • Slide 24.

What are the first three steps of chemical transmission?

• Action potential reaches the presynaptic terminal • Calcium ions enter the terminal and trigger vesicles to move to and fuse with the membrane • Vesicles release neurotransmitter into the synaptic cleft • Slide 25.

What happens after neurotransmitter enters the cleft, and how do EPSPs differ from IPSPs?

• Neurotransmitter diffuses across the cleft and binds the appropriate postsynaptic receptor • Binding changes the postsynaptic membrane potential • An EPSP moves the neuron closer to threshold • An IPSP moves it farther from threshold • Slide 26.

How is a neurotransmitter signal terminated?

• After producing its effect, the neurotransmitter detaches from the receptor • Reuptake transports it back into the presynaptic cell • Deactivation breaks it down chemically • Blocking reuptake can prolong neurotransmitter action, a mechanism used by some antidepressants • Slide 27.

Give the complete seven-step sequence of chemical transmission.

• Action potential arrives at terminal • Calcium causes vesicles to fuse with the membrane • Neurotransmitter is released into the cleft • It crosses to the postsynaptic cell • It binds a matching receptor and changes membrane potential • It detaches • Reuptake or deactivation resolves the signal • Slides 25–28.

If neurons use the same basic action potential, what gives different neurons different functions?

• Connectivity determines which cells provide input and which cells receive output • Neurotransmitter type determines the chemical message sent • Receptor type determines how the receiving cell responds • Function therefore depends on the circuit and chemistry, not on a larger or smaller action potential • Slide 29.

Compare glutamate and GABA.

• Glutamate is the primary excitatory neurotransmitter and is important for learning and memory • GABA is the primary inhibitory neurotransmitter and restrains neural activity • Their balance helps prevent neural activity from becoming too weak or excessive • Alcohol enhances GABA-related inhibition, contributing to impaired coordination • Slide 30.

What functions are associated with dopamine, and what disorder illustrates the importance of dopamine pathways?

• Dopamine contributes to reward processing, movement and working memory • Loss of dopamine-producing cells in movement pathways is associated with Parkinson’s disease • More dopamine is not automatically better; function depends on having an appropriate level in the relevant pathway • Slide 30.

Match serotonin, norepinephrine and acetylcholine to their major functions.

• Serotonin: mood • Norepinephrine: arousal, alertness and conscious readiness • Acetylcholine: memory and attention, plus skeletal-muscle activation at the neuromuscular junction • Acetylcholine dysfunction is relevant to memory problems in Alzheimer’s disease • Slides 5 and 30.

Distinguish a neurotransmitter agonist from an antagonist.

• Agonist increases a neurotransmitter’s effect by mimicking it or enhancing its action • Antagonist reduces a neurotransmitter’s effect by blocking receptors or otherwise opposing transmission • The correct drug strategy depends on which transmitter and pathway are underactive or overactive • Slide 31.

How do psychopharmacology and the Yerkes–Dodson curve guide drug treatment?

• Psychopharmacology studies how changing brain chemistry can improve functioning • Treatment requires choosing which neurotransmitter to target and whether to raise or lower its effect • Yerkes–Dodson predicts an inverted-U relation: performance is poorer at very low or very high arousal and best at an intermediate level • The goal is an optimal level, not simply more stimulation • Slide 31.