PSL300 Final (copy)

4 Somatic senses

1. Touch

2. Temperature

3. Proception

   • Awareness of your body parts relative to each other

4. Nociception

   • Detection of tissue damage or threats, perceived as pain.

Somatosensory receptors

All on neuron cells

For sensations below your chin, the receptor cell bodies are in the dorsal root ganglia.

For sensations above the head, the receptor cell bodies are in the brain itself.

For both sensation locations, the part of the neurons that transduce the physical stimulus into an electrical signal are in the nerve endings. (Tips of skin, fibers, viscera)

Types of sensory receptors on skin

Free nerve endings

• Detect mechanical stimuli, temperature, chemicals.

• In the epidermis, the outermost layer of the skin.

Merkel receptors

• Mechanoreceptors that are nerve endings in close contact with specialized epithelial cells called Merkel cells.

• Fine texture and pressure.

• Tonic so fire as long as the stimulus is present.

• In the base of the epidermis

Encapsulated receptors

• Two parts, Meissner which is in hairless parts, specific to light, touch, and low frequency vibrations. Are phasic so respond to changes in stimulus.

• And Pacinian corpuscles which respond to pressure and high frequency vibrations. Also phasic.

• Deeper in the dermis.

Merkel discs

The Merkel receptors.

Saucer shaped receptors at the bottom of the epidermis.

Very sensitive to deformations on the skin → good at detecting fine details and texture.

Tonic, making them good at signaling continuous contact on the skin.

Are more receptors phasic or tonic

Most receptors are phasic.

After 3 ms, the membrane goes back to its steady state in the phasic receptor areas.

This is why you dont feel your clothes on your skin

Meissner corpuscles

A type of egg-shaped encapsulated receptor near the top of the dermis.

Found in hairless regions like your tongue and lips.

Responsible for detecting light touch and low frequency vibrations.

They are phasic, so they detect changes in shear/movement.

• Have loop endings that detect sideways shearing/when you move your hand sideways.

Pacinian corpuscles

An onion shaped encapsulated receptor deep in the dermis.

The nerve endings are arranged in a lot of layers, allowing them to detect very small displacements in skin.

Phasic, respond to vibrations or other fast-changing stimuli.

Receptor distribution

Palms, fingertips, and lips have a lot of densely packed receptors → have higher acuity ( ability to detect fine details and small differences)

Thermal receptors

A type of free-nerve ending.

Cold receptors respond maximally at ~30°C

Warm receptors at ~45°C

They are both phasic-tonic, allowing us to get used to water temperature.

Above 45 degrees, the pain receptors get activated but also the cold receptors for a second → leads to paradoxical cold where hot things feel cold for a second.

We have more cold receptors than warm, and few thermoreceptors in total

Nociceptors

A type of free nerve ending.

Some respond to chemicals released by damaged cells or serotonin released by platelets during injury.

Lots of nociceptors have ion channels in the transient receptor potential (TRP) channel family.

• Ex. TRPV1 channels, called vanilloid receptors, respond to damaging heat and chemicals. TRPM8 channels respond to cold and to menthol.

Somatosensory afferent fibers

Carry signals from the sensory receptors to the CNS

Two main types.

Small fibers

• Small fibers include the C and A delta fibers and come from free nerve endings.

  • C fibers are unmyelinated → no conducting sheath so produce slow action potentials at 2 m/s

  • The A delta fibers are thicker and myelinated → can conduct faster action potentials at 30 m/s.

  • They respond to different adequate stimuli

• Small fibers carry information about things like pain and temperature → enter spinal cord → synapse onto secondary order neurons at dorsal horn → axons cross the midline → ascend contralaterally in the spinothalamic tracts, located in lateral part of the spinal cord.

• evoke simple responses to specific stimuli like moving your hand when you feel something hot, shooing a bug away.

• can be handled in the spinal cord, without immediate input from the brain

Large fibers

• Large fibers include A Beta fibers and come from Merkel disks or encapsulated mechanoreceptors such as Meissner or Pacinian corpuscles

  • Myelinated and very fast signal conduction at 70 m/s

• Large fibers carry information from your mechanoreceptors → go up the spinal cord ipsilaterally (go up the same side that the entered) → at the spinal cord, they turn upwards → go through dorsal columns → at the medulla, synapse into secondary order neurons → axons cross the mid line contralaterally (go the the opposite side) → somatosensory cortex.

• provide feedback to the brain, especially to motor cortex, as it manipulates objects

• Their information has to travel a long way (up to the brain) quickly

Movement of signals

Signals from the spinal cord pass through the thalamus → thalamus directs signals to the appropriate region of the brain.

Signals below the chin are directed by ventroposterolateral (VPL) nucleus

Signals above the chin are directed by the ventroposteromedial nucleus (VPM)

Both pass to the primary sensory cortex called S1.

• In the parietal lobe.

• Somatotropic, so Neighboring areas of skin project to neighboring cells in cortex

• This makes S1 a map of contralateral body surfaces, but it is distorted cuz areas of high sensitivity and acuity (such

  as hands and lips) get more space.

Lateral inhibition of somatosensory fibers

lateral inhibition enhances spatial differences

If you step into a very hot bath, you feel the most discomfort not in your foot but at the line formed by the water surface around your leg, because that is the temperature edge

Pain

There are 2 types of pain that can be responded to

• Fast (carried by A delta fibers) and slow (carried by C fibers)

We have two types of pain because of the different responses that can be elicited.

• Quick withdrawal, a spinal reflex

• Prolonged immobilization that leads to healing.

Descending pathways through the thalamus can block nociceptive cells in the spinal cord in situations where you need to ignore pain to survive.

Pain that happens in your internal organs is called referred pain.

• Nociceptors from different locations converge on a single ascending tract → tract sends signals to the brain → the brain doesn’t know where the stimulus came from

• It assumes the problem is on a body surface cuz that is more common than organ pain.

When you get pain, the c fibers carry the pain to the secondary neurons → those secondary neurons are inhibited by a beta fibers through interneurons → activation of a beta fibers can dampen or block pain.

Pain and the body region

Drugs and pain

aspirin (Acetylsalicylic acid) inhibits prostaglandins and inflammation, and slows transmission of pain signals.

Opioids (such as morphine and codeine) decrease transmitter release from primary sensory neurons and postsynaptically inhibit secondary sensory neurons

The body makes natural painkillers such as endorphins, enkephalins, and dynorphins.

Smell

Sensed by olfactory receptors in the olfactory epithelium

The epithelium is on top of the nasal cavity and is pigmented

• The pigment is correlated with sensitivity → more vibrant = more sensitive.

Each olfactory neuron has a dendrite that goes into the olfactory epithelium → forms the nonmotile cilia (tiny hairs that do not move) → increases the surface area in the olfactory epithelium → higher chance of catching odorants.

Olfactory receptors

The olfactory receptors have specificity for each type of odorant

• We have 400 types of receptors = 400 types of odors

These receptors are also g protein coupled

• odorant binds → Golf is activated → cAMP concentration increases → receptor neurons depolarized → AP to the olfactory bulb

Have weird properties

• continually sipping in fluid and sending it along the nerves into the brain.

  • Called pinocytotic

• hey are short-lived, degenerating after a month or 2, to be replaced by new ones from below

• They send their axons into the brain through tiny holes in the cribriform (“sievelike”) plate (the bone at the base of the cranial cavity)

Olfactory bulb

extension of the cerebrum on the underside of the frontal lobes.

Once the action potential from the receptor is sent to the bulb, the axons forms the olfactory nerve, or cranial nerve I

• In the frontal and temporal lobe

Convergence from many receptors can also happen onto one bulb → increases sensitivity but decreases spatial accuracy.

The olfactory bulb can project onto the limbic system

• Used to be used for detecting danger and food but we don’t need that anymore so now smells just can bring up past emotions.

Pheremones

chemicals released by an animal into the environment which affect the physiology or behavior of other members of its species

Rodents have an olfactory structure in the nasal cavity called the vomeronasal organ (VNO), which is involved in their behavioral responses to sex pheromones

In humans, the VNO disappears during fetal development, but we do respond to airborne chemical signals.

Taste

Taste receptor cells are clustered into taste buds.

Each taste bud has around 100 receptors which are epithelial cells instead of neuronal cells → each taste bud has at least 5 receptor types

Types of taste receptors

Sweet receptor cells detect sugar (energy)

Umami receptor cells detect amino acid glutamate (indicating protein)

Bitter receptor cells detect poison

Salty and sour receptor cells detect Na+ and H+ — 2 important ions

The tongue may also have receptors for fatty acids

They don’t have specific locations, are all over the tongue.

Types of taste receptor cells

Type I cells may sense salt

Type II cells sense sweet, bitter and umami

• Type II cells release ATP, which acts on neurons and type IIIs

Type III cells sense sour

• Only type III cells form synapses with sensory neurons, activating them with serotonin

Cells for sweet, umami, and bitter have receptor molecules coupled to a G protein called gustducin → activates signal pathways → increases intracellular [Ca2+] → Triggering release of ATP.

Detection of salt and sour involves ion channels which are not linked with G proteins

Taste signal pathways

Receptor cells in the taste buds excite fibers of cranial nerves VII (facial nerve), IX (Glossopharyngeal nerve), and X (Vagus nerve) → synapse in medulla and thalamus en route to the cortex

TRP receptors in the walls of the mouth excite cranial nerve V, the trigeminal

• Info about temperature, texture, etc. not taste

Hypothalamus as the control center

Controls feeding, plasma osmolality, body temperature, and sexual and stress responses

• But the control over these has negative feedback that inhibits it.

• Some of the control systems are needed to stay steady to maintain homeostasis.

Can do this control neurally or hormonally

• Nuclei within the hypothalamus send neural signals to each other and to other parts of the brain

• Synthesizes hormones which it transports down axons to the posterior pituitary, where they are released into the blood.

• makes releasing hormones that travel through portal to the anterior pituitary, where they trigger the release into the blood of other hormones, made in the pituitary capillaries

Hypothalamus control of anterior pituitary

Anterior pituitary doesn’t act alone, it is tightly regulated by parvocellular neurosecretory neurons.

• Found in regions of arcuate nucleus, paraventricular nucleus, and preoptic nucleus.

These neurons send short axons to the median eminence → hormone released to primary capillary plexus supplied by superior hypophyseal artery → blood drains to hypophyseal portal veins → signals carried to secondary capillary plexus in the anterior pituitary → endocrine cells in surrounding respond by releasing their own hormones.

• Allows for precise localized control of hormone secretion.

Hypothalamus control of posterior pituitary

The posterior pituitary contains the axon terminals of the paraventricular nucleus and supraoptic nucleus.

• Axons pass through infundibulum → forms the hypothalamohypophyseal tract → ends in capillaries supplied by inferior hypophyseal artery.

The axons have herring bodies that store neurosecretory materials → released by stimuli → fire action potentials.

• Allows hypothalamus to act as sensor and immediate responder.

Hypothalamus control of eating

Controls how much caloric intake you have.

• Uses the ventromedial hypothalamus and lateral hypothalamus

• Both controlled by neurons of the arcuate nucleus

  • One of the neurons called arcuate NPY drives feeding

  • Another neuron called arcuate POMC inhibits feeding.

Damage to the hypothalamus can disrupt this feeding

• Damage to the ventromedial hypothalamus causes over eating

• Damage to the lateral hypothalamus causes under eating

Arcuate NPY function

When fasted, arcuate NPY neurons encourage feeding.

• Releases NPY, GABA, and sometimes AgRP

The arcuate NPY projects onto other hypothalamic areas.

• PVN (paraventricular nucleus), a satiety or anorexigenic center that usually sends signals to the sympathetic nervous system to cause sympathetic activity → high sympathetic activity inhibits feeding.

  • Arc-NPY sends signals to PVN → PVN inhibited → low excitation of the sympathetic nervous system → feeding not inhibited.

• LH (Lateral hypothalamus), a feeding center.

  • Arc-NPY sends signals to LH → LH excited → orexin released at synapses → PVN inhibited and feeding stimulated.

Arcuate POMC function

After a meal, arcuate POMC neurons inhibit feeding.

• POMC is cleaved to make α-melanocyte stimulating hormone (α-MSH)

Arcuate POMC also projects on other hypothalamic regions.

• α-MSH excites PVN → excite sympathetic nervous system → high sympathetic activity decreases feeding

• α-MSH excited VMH (ventromedial hypothalamus) → excited sympathetic nervous system → high sympathetic activity decreases feeding

• α-MSH inhibits dorsomedial hypothalamus (DMH) → sympathetic nervous system not inhibited → feeding inhibited

Arc-NPY inhibits Arc-POMC

Leptin

Helps the hypothalamus infer body weight.

• Leptin is released by fat cells → more fat = more leptin

Cells in your anorexigenic centers have receptors for leptin → mutations in leptin receptors can cause obesity.

Leptin directly inhibits Arc-NPY and LH → feeding not activated. At the same time, directly excited PVN → sympathetic activity increased → feeding inhibited.

Leptin also directly excited Arc-POMC, PVN, and VMH → increased sympathetic activity → feeding inhibited. At the same time, directly inhibits DMH → sympathetic activity not inhibited → feeding not activated.

Can’t tell your brain when to stop eating though because its too slow

fed vs fasted

Increases in blood glucose

• Eat → blood glucose increases → Arc-POMC excited, LH inhibited → further feeding inhibited

Sensors in the wall of the small intestine

• Detect stretch and sugar and protein → release of cholecystokinin (CCK), peptide YY (PYY), and glucagon-like peptide 1 (GLP-1) → go through blood → excite Arc-POMC, PVN, and VMH and inhibit DMH

• They also excite the vagus nerve, which excites VMH via the nucleus tractus solitarius, NTS

• These hormones act in a fed state to inhibit feeding

But when you’re fasted, Ghrelin is released by the stomach wall → Arc-NPY and LH excited, PVN inhibited.

• Release is stopped by stomach stretch

Circadian rhythm

Since the earth rotations cause changes in the environment (light during day, dark during night), we have evolved to have circadian rhythms (forage in the day, sleep at night).

These circadian rhythms are endrogenous

• Continue even when the environment is constant

Genes involved in circadian rhythms in flies

per (period) on the X chromosome has a 24 hour cycle:

• transcribed at night → per mRNA peaks at 10 pm → protein product PER peaks 6 hours later (4 am) → PER represses transcription of per

• Together, per and PER form a transcription-translation feedback loop, or TTFL

tim (timeless) behaves similarly:

• transcribed at night → TIM protein peaks later in the day → TIM + PER dimerize to form PER/TIM → represses transcription of both per and tim → at 4 am, per and tim mRNA expression low → no new PER/TIM made → PER/TIM levels drop → per and tim transcription no longer repressed → per and tim transcription restarts → cycle repeats.

if PER or TIM is absent → the TTFL is broken → no oscillation → no functional circadian rhythm.

how do PER/TIM work in flies

A gene called clk (clock) codes for CLK protein.

A gene called cyc (cycle) codes for CYC protein.

CYC and CLK form a dimer in the day called CLK-CYC → binds DNA and stimulates transcription of per and tim.

In the night, PER/TIM blocks CLK-CYC binding to DNA → represses transcription of per and tim.

Why is the cycle not shorter than 24 hours in flies

Normally, translation and transcription are super fast and efficient so you would expect cycle to be very short.

BUT, protein called DBT binds to PER → breaks it down → PER levels rise slower → cycle 24 hours

human circadian rhythm

In humans, PER forms a dimer with CRY instead of TIM.

Also, mammalian homologs of clk, cyc, and dbt are called clk, bmal1, and ck1ε.

CLK/BMAL1 dimer stimulates transcription of per and cry when not blocked by PER/CRY.

CK1ε slows the rise of PER protein levels

synchrony of cellular clock

Kept in sync by cues called zeitgeber.

The main one is light sensed by melanopsin retinal ganglion cells → project onto the master clock which is the suprachiasmatic nucleus (SCN) of the hypothalamus

melanopsin ganglion signals → SCN neurons → neurons fire → clock reset through breakdown of PER/CRY

• If the drop of PER/CRY happens after 4 am when the levels are already falling, the clock gets pushed forward (shorter than 24)

• If the drop happens when the levels are rising, the clock is set back (longer than 24)

The SCN neurons that receive the signals forward the signals to other neurons in the SCN → pass to other parts of the brain → neural and hormonal signals sent to the whole body

• Understand light vs dark.

• Called entrainment

In the dark, SCN neurons project onto pineal body behind diencephalon → secretes melatonin

sleepiness

Depends on the master clock

• In the daylight, SCN indirectly excites neurons in LH → orexin released → less tired.

  • Less orexin = more tired/narcolepsy.

• In the darkness, LH cells project throughout the brain → MCH (melanin-concentrating hormone) is released → sleep is induced.

• Orexin neurons and MCH neurons inhibit each other

Depends on sleep pressure

• When awake, ATP is broken down → adenosine is built up → makes you tired.

• When sleeping, ATP levels restored → adenosine falls → less tired.

• Caffeine blocks adenosine receptors but does not lower adenosine levels, so when the caffeine wears off, we “crash”.

Stages of sleep

First theres 3 stages of non-REM (NREM) sleep

• Dreamless with slower brain waves.

• Stage 3 is deep NREM.

After NREM, there is REM sleep.

• Have dreams, eyes move, high brain waves, muscle tone vanishes so you dont actually act out your dreams.

The first REM stage happens after 90 mins and as you continue to sleep, sleep becomes shallower and REM takes up more time.

Reflexes

Are innate, so genetically determined

• You lose a lot of them as you age

A sensory stimulus in the CNS results in a response to perform a certain task.

• has feedback loops to regulate things like force and position.

Can be monosynaptic

• Stimulus → receptor → signal sent to sensory neuron → synapse into the spinal cord with no input from the brain → send to efferent neuron → target cell → response

Can be polysynaptic

• Stimulus → receptor → sensory neuron → synapse to interneuron → synapse to spinal cord → efferent neuron → target cell → response

Stretch reflex

Stretch → Contract

Stimulus = Passive stretch of a muscle because of a load or contraction

Response = Active contraction of that muscle

Place load on hand → muscle spindles activated → motoneurons activated → contract the muscle that was stretched

Properties

• Needed for stabilizing posture

• Strongest in postural muscles

• Faster in forearm muscles than ankles.

• Spinal reflex

• Supressed during movement

Golgi tendon reflex

Stretch → Relax

Stimulus = Active tension in the muscle

Response = Relaxation of the muscle

Unlike stretch reflex, this is polysynaptic

• Golgi tendon organ (GTO) synapses onto interneurons → interneurons inhibit motoneurons of the muscle

Goal is to regulate amount of activity alongside the stretch reflex

• If there is an excessive load → golgi tendon organ fires → interneurons activated → motoneurons inhibited → muscle relaxes → load dropped

Properties

• Prevents movement

• Stabilizes posture

Flexion withdrawal reflex

Touch hot stove → flex hand

Stimulus = Noxious injury of limb

Response = Flex joints that are proximal to the stimulus, extend joints distal to stimulus

Also multisynaptic

• Nociceptors synapse onto interneurons

Pain receptors get activated in your forearm → proximal joint flexes, distal joint extends → arm is withdrawed.

Reciprocal inhibition

Activation of one motor nucleus inhibits an antagonistic motor nucleus.

• Ex. if the flexor motoneurons are activated, antagonist extensors are inhibited.

But when you also need the antagonistic motor nucleus, the circuit can be suppressed.

Patellar Tendon Reflex

Bang knee → kick

When patellar tendon is tapped → quad is stretched → quad contracts

At the same time, the hamstring contractions are being inhibited to allow for movement.

• If hamstring was not inhibited and also contracted, there would be no movement.

Cross extension reflex

Step on something sharp → flex leg → extend other leg.

nociceptors activated in one leg → flexor muscles same side as pain activated → leg withdraws. signal also travels contralaterally to the other side using commissural interneurons → extensor muscles activated → other leg stiffens for added support

Extensor thrust reflex

Stimulus = pressure on sole

Response = Activation of leg extensors

The mechanoreceptors project signal to intermediate zone interneurons → extensor motoneurons activated

Only active during stance.

This reflex is influenced by the corticospinal tract.

vestibulo-spinal reflex

Stimulus = downward deviation of head on one side → otolith afferents on

Response = downhill limbs extend

CPG

Central pattern generator.

Since reflexes can only help us perform simple movements, we need CPGs to program our posture and movement.

• Mostly needed for locomotion, motor control, and behavioral responses

They are located in the spinal cord and in brainstem, and activated in order of relevance.

Leg step cycle

Walking involves a cycle of flexing and extending the legs.

• Alternate between:

  • Swing phase = Toe off the ground, heel strikes the ground

  • Stance phase = Heel strikes ground, toe off ground

The cycle is programmed by the CPG in the intermediate zone of the lumbar spinal cord

• Each leg has two burst generators within its CPG

  • Flexor Burst Generator (FBG): drives flexor motor neurons → leg swings

  • Extensor Burst Generator (EBG): drives extensor motor neurons → leg extends

• FBG and EBG inhibit each other

Swing Phase

The swing phase is the flexion phase

• Driven by the flexor burst generator (FBG)

  • FBG is connected to the flexor motor neurons in the ventral horn → Activate FBG → Activate the flexor motor neurons → Leg flexes → Leg can swing.

• When the FBG is active, the EBG is inactive so you can be in the swing phase instead of the stance phase

The swing/flexion phase has a fixed duration regardless of speed.

• When FBG is active, it builds up inhibition on itself → eventually, when the inhibition is strong enough, the FBG is forced to stop firing action potentials → Flexor motor neurons now inactive → extensor burst generator not inhibited → Can switch to stance phase

Stance phase

The stance phase is the extension phase.

• Driven by the extensor burst generator.

  • EBG is connected to the extensor motor neurons in the ventral horn → Activate EBG → extensor motor neurons activated → Leg extends → leg is in stance

• EBG inhibits FBG

This is where speed of walking is adjusted

The stance phase is regulated by the mechanoreceptors on the back of the foot.

• They feed/send information to the nervous system to tell it that the foot has striked the ground and we are in the stance phase.

• Allows your brain to time the swing phase.

The stance phase is made of reflexes as well.

• Stretch reflex

• Golgi tendon reflex

• extensor thrust reflex.

Transition to swing phase

For the swing phase to start, there is criteria

• Leg is not bearing weight

• Hip is extended

• Opposite leg is in stance (bearing weight)

The two legs can coordinate this through crossed projections to the CPGs on opposite sides.

arm swings

Coordinated by CPGs in the cervical cord.

Flexion phase synchronous with contra-lateral flexion in leg

Phase-linking via propriospinal tracts (from one segment of cord to another)

Posture

Organized in reticular formation of pons and medulla

Depends on:

• Somatosensory system: Detects posture, pressure, and movement.

  • especially proprioception cuz that is awareness of your body parts in relation to each other.

• Vestibular system: Detects your head position and acceleration

• Visual system: slower system, but important vertical cues and motion cues

Red nucleus

contains Rubrospinal cells that activate localized synergies, especially in distal limbs and in the face (e.g. gripping and twisting movements of hands).

Unlike the reticulospinal and vestibulospinal tracts, the red nucleus is responsible for fine and specific limb control.

Synergy

group of muscles contracting together for a specific purpose

reticulospinal tract synergies are widespread to make support postures but rubrospinal synergies are more localized.

Motor cortex

Located in the precentral gyrus

Has somatotopic organization, meaning different parts are responsible for different body parts.

• but the areas of the cortex do not correlate to the size of the parts they control.

Most of the axons that are descending from the axon to the spinal cord first pass through interneurons → allows for communication with motor neurons.

But some neurons of the motor cortex can communicate directly with the motor neurons without the interneurons.

• distal limb muscles (fingers, hands)

• speech muscles

Path:
Motor cortex commands go through brainstem → crosses the midline → goes through lateral white matter → activates motoneurons either directly or through interneurons

Multiple Representation

You can go to many different zones in the motor cortex and elicit the same movement

• ex. finger flexion can be triggered from a bunch of different points in the finger zone.

These zones also have synergies.

• A combination of different movements to make one thing like holding a pen.

Motor field

Set of motor nuclei that synapse onto one corticospinal axon (The axon that connects motor cortex to the spinal cord)

• Happens across multiple spinal segments

• Made of lots of synapses, and most are silent as in don’t contribute to activity.

Motor field has plasticity

• Since its made of multiple motor nuclei, corticospinal axon has access to multiple parts of the body → can unsilence synapses to control a certain part of the body when it needs to.

Somatosensory Inputs

Input can only come from pathways with direct access to the motor cortex.

• cutaneous (skin) input comes from somatosensory association areas → helps motor cortex know about posture + motion

• Proprioceptive (joint) input direct from thalamus (and from somatic association cortex)

Premotor

The premotor areas are those that project onto the motor cortex but are also have routes to the motor nuclei

• They go and put motor cortical synergies into the sequence needed for a specific movement.

The premotor cortex processes sensory inputs for cueing movement phases

• especially visual and auditory,

• the dorsal visual stream goes to the dorsal half on the cortex to tell it where the object is (spatial recognition)

• the ventral visual stream goes to the ventral half to tell the cortex what something is

• There is also broca’s area for sequencing language elements for speech or writing-typing

Sensorimotor Cues

Can be lots of different environmental cues

• Sensory association areas recognize the cues and forward the signal to the frontal lobe

Premotor cortex selects appropriate response synergies in motor cortex

Visuomotor Response

A coordinated sets of activities and cues that want to initiate the synergies the premotor cortex selects.

Preparation of motor cortex

Premotor neurons set up the motor cortex by facilitating appropriate synergies → send a warning cue then a go cue

• The premotor neurons not active during performance because they are preparing the motor cortex

Supplementary Motor Area

Located on the medial wall of hemisphere

Needed for a somatotopic representation of body, but less detail than motor cortex

Controls bilateral coordination of limbs when different motions done on each side

Processes internal ‘volitional’ signals that drive movements

• voluntary signals

Neurons of the ANS

divided into its preganglionic and postganglionic components

• The preganglionic neuron cell bodies of both the parasympathetic and sympathetic portions are in either the brainstem or spinal cord.

• The preganglionic neurons project axons onto the postganglionic neurons.

• The postganglionic neurons are in the autonomic ganglia between the CNS and target tissue

• Autonomic ganglia allows for communication between the two ganglionic neuron types.

• The post ganglionic neuron axons project onto target tissues.

This arrangement allows for one preganglionic neuron to synapse onto multiple postganglionic neurons

• Called divergence

Preganglionic neuron in BS or SC → Postganglionic neuron in Autonomic ganglia → Target tissue

Communication between preganglionic and post ganglionic neurons of ANS

Preganglionic neuron in BS or SC → Secretes acetylcholine → binds to nicotinic receptors on the postganglionic neurons in the autonomic ganglia → postganglionic neurons in the sympathetic system secrete norepinephrine onto adrenergic receptors on the target tissue. Postganglionic neurons in the parasympathetic system secrete Ach onto muscarinic receptors on the target tissue.

Sympathetic autonomic communication

The preganglionic neurons are located in the thoracolumbar spinal cord.

• Their nerve fibers/efferents/axons begin in the intermedio-lateral thoracic cord and synapse onto the autonomic ganglia parallel spinal cord.

• Very short because they have to stay around the spinal cord

The autonomic ganglia are arranged in a sympathetic chain parallel to the spinal cord.

The preganglionic neurons secrete acetylcholine to the nicotinic receptors of the postganglionic neurons in the autonomic ganglia.

• The postganglionic neurons are long as they have to go from the spinal cord to the target tissues.

The postganglionic neurons secrete norepinephrine to the adrenergic receptors of the target tissue.

Sympathetic activities

• Fight-or-flight response

• Prepare for emergency, stress, and exercise

• Increase heart rate and blood pressure

• Mobilize energy stores

• Pupillary dilation

• Diffuse effect due to its widespread and interconnected innervations

• Decrease gastrointestinal and urinary functions

• Releases epinephrine

Adrenal medulla

Activation of the sympathetic system signals release of epinephrine from the adrenal medulla.

• Preganglionic neurons in SC → Postganglionic neurons in adrenal medulla → have no axons to project onto target cells → instead secrete epinephrine

• These axon-less cells are called chromaffin.

Prolonged response since hormonal.

Parasympathetic autonomic communication

The preganglionic neurons are located in the sacral spinal cord or the brain stem.

• Their nerve fibers/efferents/axons start in the multiple cranial motor nuclei and the intermedio-lateral part of the sacral cord and synapse onto the autonomic ganglia embedded in the target tissue.

• Are very long because they have to go from the brainstem or spinal cord all the way to the target tissue.

The preganglionic neurons secrete acetylcholine to the nicotinic receptors of the postganglionic neurons in the autonomic ganglia.

• The postganglionic neuron has short nerve fibers as they are already at the target tissue.

The postganglionic neuron releases acetylcholine to the muscarinic receptors of the target tissue

Parasympathetic activity

• Quiet, relaxed states

• Active in “rest and digest”

• Increase gastrointestinal activities

• Decrease heart rate and blood pressure

Duel innervation

Organs in the body have both sympathetic and parasympathetic activity → the two branches have opposing effects.

• Both are active at rest but parasympathetic dominates

Primary function is to regulate organs to maintain homeostasis.

• Sympathetic: cardiac output increased, skin vasoconstriction, sweating, piloerection, blood diverted from gut and skin to muscle

• Parasympathetic: digestion promoted, cardiac output reduced, slow breathing, urination

• Complementary, not antagonistic.

Targets of autonomic neurons

smooth muscles, cardiac muscles, glands.

The synapse between the post ganglionic autonomic neurons with its target cells = neuroeffector junction

• Not neuron to neuron

• The postganglionic neurons don’t have an axon terminal, they have Varicosities

• These are axon swellings that contain the neurotransmitters.

• Released in response to an action potential.

Sympathetic pathway:

Action potential to varicosity → voltage gated ca channels open → ca influx triggers NE release → NE binds to an adrenergic receptor on the target tissue → target tissue response. NE can reuptake or recycle → metabolized by MAO

Autonomic reflexes

produced by the autonomic efferent networks but can be modulated

Act as a negative feedback loop

Want to maintain homeostasis

1. Pupillary Light Reflex

2. Baroreflex

Pupillary Light Reflex

in pretectal area of midbrain

Uses ON and OFF afferents to luminance and darkness detectors.

Too bright → On afferents detect luminance → parasympathetic reflex activated via 3rd cranial nerve → ciliary ganglion → circular iris muscles → constrict pupil

Too dark → off afferent detect darkness→ sympathetic reflex via thoracic cord → sympathetic chain to radial muscles → dilate

Baroreflex

When BP or HR too high:

NTS receives input from the baroreceptors → NTS sends information to the caudal VLM → caudal half inhibits the rostral half that is responsible for blood pressure→ reduces blood pressure or heart rate

Low BP:

Want to turn on the rostral VLM thru less activation of the caudal half.

Autonomic Control Centers

The ANS works with endocrine and behavioural system to maintain

homeostasis

• The autonomic reflexes are integrated in the brain (thalamus, hypothalamus, and brainstem) → these centers regulate heart rate, blood pressure, etc to maintain homeostasis.

the Brainstem Autonomic Centers (hypothalamus, pons, medulla) use the feedback of the sensory system to regulate other functions.

• The brainstem itself contains control centers Cardiovascular center, and respiratory pattern generator in lateral medulla/pons

• Relays the information it receives to muscles and glands.

• Also uses the PAG, the center for autonomic behavioural programs

PAG

The PAG found in midbrain and functions as the coordinator of

autonomic behaviours

• Has columns for behaviour patterns.

• Ex. fight: PAG projects to cardiovascular center to increase BP and also the respiratory center to increase breathing rate and causes release of serotonin to activate motor neurons and also inhibits pain

Works with the hypothalamus and acts through the hypothalamus and the reticular formation.

Reticular Activating Systems

Works through a diffuse modulatory system that causes a global shift in the CNS so everything everywhere on

• Cholinergic: determines level of attention, and sleep-wake cycle; mainly ascending (ACh)

• Serotonergic: for stressful situations; influences mood, sleep-wake cycle (Serotonin)

• Adrenergic: for stressful situations, vigilance (Norepinephrine NE)

• Dopaminergic: reward center (Dopamine)

• Histaminergic: sleep wake control, supports the waking state (Histamine)

Skeletal muscles

Only muscle type that is under conscious voluntary control.

• Needs to be activated by the somatic nervous system.

Activation of the skeletal muscles by the central nervous system needs to happen through motor neurons.

• The motor neuron and its fibers together are called a motor unit.

The motor neurons and the skeletal muscles synapse and communicate with each other at the Neuro-Muscular Junction (NMJ)

The contractile filaments of the skeletal muscles are called sarcomeres

• Made of actin and myosin

• Organized in an overlapping arrangement called striated.

Skeletal muscles have the best sarcoplasmic reticulum of all muscle types

• An intracellular organelle that stores calcium

Skeletal muscle fibers

Made of myofibrils.

• Thin filaments made of actin

  • Has a binding site for myosin

  • Myosin binding site is covered by tropomyosin when there is no calcium/muscle is relaxed.

  • When there is calcium or muscle is contracting, the Ca binds to a troponin complex → movement of tropomyosin → myosin binding site exposed → myosin can bind → muscle can contract

• Thick filaments made of myosin → has lots of crossbridge → can connect actin and do muscular contractions.

  • Myosin head has the actin binding site and an ATP binding site for energy

Goes from tendon to tendon

its plasma membrane is called the sarcolemma

• Invagination of the sarcolemma into the muscle fiber is called the T tubule system → allows for spread of AP into the muscle fiber

During a muscle contraction, the sarcomere shortens but the filament lengths dont change.

Muscle fiber types

Slow twitch oxidative fibers

• Contract slowly

• Have lots of mitochondria

• Depend on oxidative metabolism → Small force but low fatigue

• Innervated by small diameter motor neurons

Fast twitch glycolytic fibers

• Fast twitch time

• Lots of tension

• Low mitochondria → depend on glycolytic metabolism → Fatigue fast due to lactic acid accumulation

• Innervated by large diameter motor neurons.

Fast twitch oxidative glycolytic fibers

• In between the two

Motor unit

All the fibers in one unit contract together.

• The smoothness and movement of the contractions depends on the number and timing of motor units active.

Small motor units are more easily excited than big ones → contractions begin with the small units

All the fibers in one unit are the same → there are 3 types of fibers → there are 3 types of units

• Slow twitch

• Fast twitch

• In between

Neuro-Muscular Junction (NMJ) properties

Its axon terminals are called terminal bouton and opposite the terminals are the membrane called the motor end plate

• Terminal bouton receives the action potential while the motor end plate causes depolarization in the muscle itself.

Communication happens here

In the peripheral tissues and muscles, there is no BBB so there is no protection from toxins.

• Nicotinic receptor blockers: Makes it hard to generate an action potential in the muscle fibers.

  • A poison dart form is called curare.

  • Can be used as a muscle relaxant.

  • Blocks reflexes

• Exocytosis blocker: No ACh release

  • Botox does this

• Ach-esterase inhibition: ACh not broken down → depolarization continues → paralysis

Skeletal Muscle contraction

Starts with excitation contraction coupling of skeletal muscle

• Command sent to motor neurons → action potential started → goes to terminal bouton of NMJ → voltage gated Ca channels open → Ca influx → ACh release is triggered → binds to nicotinic recepotrs at the motor end plate of NMJ → Na and K Channels opened → depolarization of skeletal muscle → action potential started in skeletal muscle → AP travels deep into the muscle through T tubules → DHP receptor changes conformation → Change causes RyR in the sarcoplasmic reticulum to open → Ca release into cytoplasm → Ca binds to troponin → tropomyosin moves from myosin binding site of actin.

Moves on to generation of force

• When there is high energy, myosin has a high affinity for actin.

• Myosin binds to actin’s binding site → starts a power stroke where it pulls the thin filaments to the center of the muscle → force is generated → ADP is released from myosin → ATP binds to myosin → Myosin hydrolyzes ATP → its head rotates → actin now bound weakly → if no calcium bound anymore, tropomyosin moves back to cover the myosin binding site → contraction ends.

Muscle twitch

A single contraction-relaxation cycle.

3 phases

• Latent period

  • Excitation contraction coupling

• Period of contraction

  • High intracellular Ca

  • Cross bridge cycle

• Period of relaxation

  • Low intracellular Ca

  • tension goes down to 0

Summation of force

More action potentials → increased tension through summation

• Successive twitches fuse together and the contractile force increases

Eventually, the contractions fuse into one contraction called tetanus

When your muscles fatigue, the tension will rapidly drop

Smooth muscle

Found in the internal organs and blood vessels.

Controlled by the ANS, not voluntary control.

Actin and myosin not organized parallel, diamond shaped instead.

• Actin and myosin are longer than in the skeletal muscle → allows them to have a longer range of contraction → Can operate on a range of lengths

Also contracts more slowly

Classified by either location or communication with neighbouring cells.

• Single unit or multi unit

Single unit smooth muscle

Found in the intestinal tract and blood vessels

Have spontaneous activity

Contracts when stretched

Can exert tension even without stimulation

• Some processes need tension to work even with no stimulation.

Multi unit smooth muscles

Found in airways or arteries

Each fiber acts individually

Heavily innervated and contracts with stimulation only.

Excitation contraction coupling of smooth muscle

Ca is from both the sarcoplasmic reticulum and the ECF → slower contraction.

Slower relaxation time cuz of slower removal of calcium.

Opening of calcium channels → Influx of Ca → More calcium release is triggered → Ca binds to calmodulin → calmodulin activates MLK (a kinase) → phosphorylates myosin → cross bridge cycling can occur

To stop the cycle, phosphatases are also needed on top of the calcium ATPases.

• Removes phosphate from myosin

Cardiac muscles

Has contractile and conductile cells.

• Conductile cells are responsible for conducting the excitation between atria and ventricles

Certain heart cells can to automaticity

• Pacemaker cells

Striated and has a SR like the skeletal muscles

Its gap junctions allow excitation to spread, allowing a synchronous heart beat.

Modulated by ANS

Cardiac muscle AP

During an AP in cardiac muscles, Ca channels and Na channels open

• Ca channels open slower and stay open longer → Ca can enter from ECF

The AP lasts as long as contraction and relaxation

C

Cardiac muscle contraction

Recruitment of more cells or frequency doesn’t increase force, but muscle length does.

More blood volume → More contraction force because of more overlap of myosin and actin

Excitation contraction coupling of cardiac muscle

Ca released from ECF and SR

Done by contractile proteins

To relax, Ca needs to be removed by Ca pump

Unlike the rest, there is a Na/Ca membrane exchange that removes Ca from the cytosol.

Digitalis increases force of contractions by inhibiting Na/K ATPase → increased intracellular Na → Na/Ca membrane exchange has decreased Na influx and decreased Ca efflux → Increased intracellular Ca → Increased contraction strength.