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201 Cards in this Set
- Front
- Back
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Perilymph
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Low K+
In scala vestibuli and scala tympani |
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Endolymph
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High K+
In organ or corti |
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Vestibular Hair Cells
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Arranged on crista with stereocilia poking into cupula.
Have resting basal activity. |
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Kinocilium
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Tubule based - longest length "hair" encoding directionality
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Deflection Towards Kinocilium
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Activation - Depolarization
Tip link pulls open ion channel and K+ flows inward. NT release on CN VIII. |
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Deflect Away from Kinocilium
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Inactivation - Hyperpolarization
close channel, less K+ flow than at rest |
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Adaptation
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Ion channel moved down stereocilium relieving tension on tip link allowing channel to close
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Turn Head - Vestibular Response
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Endolymph pushes cupula in one direction causing hair cell deflection
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Vestibular Pathway
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Hair cells stimulate CN VIII to vestibular nucleus to cerebellum (balance and orientation) and MLF (eye and head movement)
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How do you find location of sound?
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Horizontal
Interaural time difference for low frequencies and interaural level difference for high frequencies. For middle frequencies use both. Vertically Pinna |
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Utricle
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Parallel to the ground while standing and deflects while lying down. Does not adapt.
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Saccule
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Perpendicular to the ground and deflected while standing and parallel while lying down.
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Which muscles contract in the ear with sound?
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Tensor tympani contracts and is attached to malleus. Stapedius connected to stapes also contracts before voicing to prevent self-deafening.
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Eustachian Tube
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Connection from middle ear to pharynx. Straight in children and angled in adults. Angle promotes drainage. May be cause for frequent ear infections in children.
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Frequency map on cochlea
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At base, higher frequency.
At helicotrema, low frequency. |
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Pathway of Sound
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Vibrations come into outer eat and make tympanic membrane vibrate transferring sound from malleus to incus to stapes pushing on the oval window. Up the scala vestibuli, down scala tympani to round window.
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Reissner's Membrane
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Separates scala vestibuli from scala media.
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Basilar Membrane
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Separates scala media from scala tympani.
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Tectorial Membrane
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Weighted membrane in organ of corti in which stereocilia of hair cells are embedded.
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Auditory hair cell deflection caused by?
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Endolymph shearing forces.
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Auditory Pathway
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Hair cells to CN VIII to cochlear nucleus to superior olive to inferior colliculus to MGN to auditory cortex (in the sylvian fissure)
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Antibiotic Auditory Effects
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Destroy hair cells both in vestibular and auditory systems causing hearing loss and vertigo. Affects high frequency and outer hair cells first.
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Conductive Hearing Loss
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Inability for external sound to cause vibrations. Caused by outer ear and middle ear problems. Ear wax, tympanic membrane rupture, otitis media (inflammation), otosclerosis (loss of ossicle movement).
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Noise Trauma
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Destroy IHCs and OHCs at high frequency
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Cochlear Implants
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Directly stimulate the auditory nerve fibers inside the cochlear with electrical impulses. Does not make sound louder like a hearing aid.
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Tinnitus
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Ringing in the ear that my be caused by inappropriate activation of hair cells due to efferent input dysfunction.
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Meniere's Disease
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Inability to drain cochlear ducts or lymphatic areas. Causes dizziness and hearing loss.
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Macula
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Center of vision. Fovea causes shallow depression. Has cones - high acuity.
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Retinal Layers
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RGCs are the 2nd layer that make axons making the top layer. RGC axons come together to form the optic nerve that punches out the back of the eye.
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Blind Spot
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Blind spot is caused by the optic nerve punching out the back of the eye (no photoreceptors there). The optic nerve is pushed medially towards the nose but the blind spot is lateral. Don't perceive the blind spot when both eyes are open because its filled in by the other eye.
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Central and Peripheral vision
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Central vision is 20/20 - contains cones that do color and detail. Peripheral vision declines as you move from the center down to 20/800. Has rods which are very sensitive but can only discriminate light and motion.
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Cones
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Center - color and detail
Blue, red, and green opsins |
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Rods
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Periphery - light and motion
See best at low light, maximal sensitivity at starlight. Absent in the fovea. |
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Dark Current
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In the dark, photoreceptor is relatively depolarized (-40mV) and there is high cGMP which keeps Na Channels open.
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Light Reaction
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Light induces retinal change from cis to trans and is released from opsin. Cascade causes drop in cGMP and Na channels close causing hyperpolarization.
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Retinal Isomerase (RPE)
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RPE converts retinal back to cis in order to restart cycle. Defect in RPE causes Leber's congenital amaurosis - blindness in infants.
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Light Adaptation
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Modulated by Calcium channels. Prolonged exposure to light leads to drop in calcium levels, channels closed, calcium pumped out. Decreases hyperpolarization.
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On and Off Center RGCs
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On Center: when light hit objects starts firing.
Off center: fires when no light is on object. |
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Visual Pathway
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RGCs bundle into optic nerve and can go through optic chiasm (nasal RGCs) or straight back (temporal RGCs) in optic tract. Most go to LGN which projects optic radiations.
Other RGCs go to Edinger Westphal nucleus which controls parasympathetic pupillary constriction. Others go to hypothalamus SCN to control circadian rhythm. Others to superior colliculi to adjust head. |
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LGN
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LGN secondary neurons project axons called optic radiations back to the occipital lobe.
Ipsilateral eye: 2 (M), 3 and 5 (P) Contralateral eye: 1 (M), 4 and 6 (P) |
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Magnocellular and Parvocellular Neurons in the LGN
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Magnocellular neurons get information from many rods (layers 1-2 - max sensitivity low acuity) and parvocellular neurons (3-6) receive input from cones usually 1:1 (low sensitivity, high acuity)
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Optic Radiations
Superior Inferior |
Superior (parietal) radiations see contralateral inferior world
Inferior (temporal, Meyer's Loop) radiations see contralateral superior world |
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Primary Visual Cortex
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Superior occipital lobe sees lower world and inferior occipital lobe sees upper world.
Brodmann's area 17 |
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Ocular Dominance
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Alternating columns of left and right eye but blend to allow for depth perception
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Hypercolumn
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Contours in specific orientation are all the same in a vertical column
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Optic Nerve Lesion
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Blinds ipsilateral eye
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Optic Chiasm Lesion
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Bitemporal hemianopia (usually caused by pituitary tumor)
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Magnocellular and Parvocellular Neurons in the LGN
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Magnocellular neurons get information from many rods (layers 1-2 - max sensitivity low acuity) and parvocellular neurons (3-6) receive input from cones usually 1:1 (low sensitivity, high acuity)
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Optic Tract Lesion
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Contralateral homonymous hemianopia - lose contralateral hemifield
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Optic Radiations
Superior Inferior |
Superior (parietal) radiations see contralateral inferior world
Inferior (temporal, Meyer's Loop) radiations see contralateral superior world |
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Optic Radiation Lesion
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Quadrantanopia
Inverted contralateral |
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Primary Visual Cortex
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Superior occipital lobe sees lower world and inferior occipital lobe sees upper world.
Brodmann's area 17 |
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Occipital Cortex Lesion
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Homonymous Hemianopia or Quadrantanopia with macular sparing
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Ocular Dominance
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Alternating columns of left and right eye but blend to allow for depth perception
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Hypercolumn
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Contours in specific orientation are all the same in a vertical column
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Optic Nerve Lesion
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Blinds ipsilateral eye
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Optic Chiasm Lesion
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Bitemporal hemianopia (usually caused by pituitary tumor)
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Optic Tract Lesion
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Contralateral homonymous hemianopia - lose contralateral hemifield
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Optic Radiation Lesion
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Quadrantanopia
Inverted contralateral |
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Occipital Cortex Lesion
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Homonymous Hemianopia or Quadrantanopia with macular sparing
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Group I (Aa) Fibers
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Proprioception from muscle spindles and GTOs. Largest, highly myelinated, fastest conducting.
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Group II (AB) Fibers
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Touch and vibration from mechanoreceptors in the skin.
Cutaneous low threshold - project to III/IV |
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Group III (AD) Fibers
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Pain and temperature (nociception). Project to lamina I-II.
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Group IV (C) Fibers
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Unmyelinated small diameter carrying pain and temperature. Project to Lamina I - II.
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Ruffini Endings
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Slowly Adapting receptors in dermis and joint casule responding to skin stretch and joint movement.
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Merkel Cells
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Slowly adapting in epidermis - superficial touch receptors.
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Meissner's Corpuscles
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Rapidly adapting in epidermis - responding to pressure and touch. Many in sensitive areas.
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Pacnian Corpuscles
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Rapidly adapting in dermis and joint.
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Receptive Field
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Region on skin that is registered directly by a certain sensory receptor. Bigger in deeper receptors and is also a function of innervation density (highly sensitive, high density of receptors, small receptive fields)
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Lateral Inhibition
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Central receptor stimulated most by stimulus. Inhibitory interneuron inhibits neighboring lateral neurons from firing which sharpens and narrows the stimulus.
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Dorsal Column Medial Lemniscal Pathway
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DRG primary sensory neuron bifurcates with one process terminating in dorsal horn and other traveling up dorsal column to cuneate and gracile nucleus. 2nd order neurons cross the midline and collec tin ML which goes up to the VPL. 3rd order neurons from VPL project to the primary somatosensory corex (postcentral gyrus).
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Spinothalamic Pathway
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DRG primary sensory neuron terminates in dorsal horn and 2nd order neurons cross midline and collect in spinothalamic tract which runs up to the VPL. 3rd order VPL neurons run to the postcentral gyrus (primary somatosensory cortex).
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Somatosensory Cortex Brodmann's Areas 3,1,2
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3a: proprioception and pain
3b: SA and RA mechanoreceptor touch and vibraiton 1: 3b input - SA and RA touch 2: 3b proprioceptive and 3a pain. |
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Columnar Organization
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Vertical columns contain same receptive field. SA and RA are arranged in alternating columns.
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Training effects on Cortical Representation
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Decreases the size of receptive fields. Increases activity in area.
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Right Horizontal Gaze
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Use right CN VI for lateral rectus which sends info through MLF to left CN III to use medial rectus.
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Abducens Nerve Injury
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If a right CN VI injury, try to look right. Left eye medial rectus moves, but right lateral rectus and stays centered.
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Abducens Nucleus Injury
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Neither eye can move - gaze palsy. CN VI can't get signal and can't transmit to CN III
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MLF Injury
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CN VI talks to lateral rectus to move but can't get signal to CN III. Right eye lateral rectus moves, left eye stays centered.
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Head moves left- Vestibular Input
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Left CN VIII talks to Right CN VI which talks to Left CN III all through the MLF.
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Cold water in the right ear
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Causes right gaze and left beating nystagmus
Stimulate left VIII, right VI, left III creating right gaze. Left beating is a corrective movement. |
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Parapontine Reticular Formation Neurons
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Burst neurons that start firing when movement is initiated.
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Nucleus Prepositus Hypoglossi Neurons
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Gaze holding neurons that have tonic neuron firing as long as you hold the gaze. Neural integrator.
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Omnipause Neurons
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"Parking Brake". Fire when there is no movement, stops firing when there is movement.
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Allodynia
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Pain due to non-painful stimulus. Caused by activation of non-nociceptive afferents.
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Cutaneous Afferents
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Low threshold information carried by AB and AD fibers and nociceptive information carried by AD and C fibers. Encoding by specificity, projects to small region of spinal cord making it easy to localize. Somatotopic organization in brain and spinal cord.
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Visceral Afferents
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Low threshold and nociceptive information carried in AD and C fibers. Encoding through intensity. Poor ability to localize stimuli as fibers project to I-II, V, X through 5-10 segments.
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Activation and Sensitization
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Pinch and SP causes activation. However, SP + Pinch gives same amplitude so there is no sensitization.
Bradykinin causes activation. Add prostaglandin. Now each time bradykinin activates there is bigger amplitude. This is sensitization. Activation does not always lead to sensitization. Sensitization can occur without activation. |
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Dorsal Horn Lamina
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Lamina I-II and V nociceptive
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Nociception
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AD and C fibers carry pain and temperature to lamina I, II, V, VI
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Low threshold neurons
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Encode non-noxious stimuli. Project to lamina III - IV through AB fibers.
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Wide Dynamic Range Neurons
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Respond to low threshold and noxious stimuli and project to lamina I, II, IV, V, VI
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Nociceptive Stimulus Neurons
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Only respond to noxious stimuli which project to lamina I-II, V-VI through AD and C fibers.
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Peripheral Sensitization
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Caused by increased excitability of primary afferent causing primary hyperalgesia. Decreased threshold, increased suprathreshold, and spontaneous pain.
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Central Sensitization
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Activity dependent increase in synaptic efficiency in the spinal cord. Leads to secondary hyperalgesia. Decreased threshold, increased suprathreshold, spontaneous pain, expansion of receptive field beyond site of injury. Lose subliminal fringe.
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Visceral Pain Presentation
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Diffuse localization, referred sensation/pain, greater emotional and autonomic response, sensitization of somatic tissue, whole body and non-specific motor responses (doubling over)
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Visceral Dual Innervation
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Splanchnic nerves - cell bodies in thoracolumbar DRG - travel in same nerves as sympathetics. Go through CG, IMG, SMG to innervate viscera.
Sacral afferents - cell bodies in nodose ganglion and sacral DRG travel with parasympathetics. |
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Referred Pain vs. Secondary Hyperalgesia
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Pain felt away from site of injury that is not evoked.
Caused by convergence of visceral and somatic primary afferents onto same dorsal horn neurons. Secondary hyperalgesia is also pain felt away from site of injury but must be evoked. |
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Adequate Stimulus
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Stimulus that causes visceral pain - hollow organ or solid organ capsule distension, ischemia, inflammation, muscle spasm, traction on mesentary
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Lateral Spinothalamic Pathway
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Carries sensory components of pain - location, duration, quality, intensity. Travels in large fast fibers. Somatotopically organized.
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Medial Spinothalamic Pathway
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Carries affective emotional component of pain through thin slow fibers. No somatotopic organization. Projects to limbic system, hypothalamus, thalamus, reticular, PAG.
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Descending Pain Pathways
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Low threshold stimulus can close gate while noxious stimulus opens the gate. There is some cortical and interneuron modulation of pain.
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ON vs OFF Cells
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ON cells facilitate nociceptive neurons - turn on pain response.
OFF cells inhibit nociceptive processing, stop firing during pain response. |
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Brief high frequency tetanic stimulus causes:
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Long Term Potentiation - increased synaptic efficacy - memory
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LTP Expression
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Presynaptic: increase release probability, increase number or release sites per spine, increase vesicles released
Postsynaptic: increase receptor sensitivity, increase receptor number, increase pre-postsynaptic contacts |
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NMDAR KO Deficits
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No LTP - deficit in memory and impaired performance in water maze task (hippocampal task)
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Hippocampus Removal Deficits
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Lose declarative memory for facts and events. Retain procedural memory - can improve skills but don't remember doing it. Can remember to get to house from a certain point, but can't tell you step by step. will use response strategy.
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Procedural Memory
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In cerebellum and striatum - skills, habits
Lesion procedural memory - use place strategy. |
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Emotional Memory
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In amygdala - fear response
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Limbic System Circuit
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Cingulate - hippocampus - fornix - hypothalamus - AN of thalamus - cingulate
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Remove amygdala
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Lose fear response, but can explain fear association (declarative).
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Autonomic NS Pathway
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CNS preganglionic neuron projects to autonomic ganglia (outside BBB) where it synapses. Postganglionic neuron projects to the target organs. Parasympathetic and sympathetics follow same pathways but synapse in different ganglia.
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Sympathetic Pathway
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Preganglionic neuron to paravertebral ganglia where it can either synapse and go to heart/lung or go up to superior cervica ganglion (head) or down chain to SMG, IMG, celiac to innervate gut. Sensory autonomics project to lateral horn.
Fight or flight response - generalized. Long postganglionic fibers. |
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Parasympathetic Pathway
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CNS preganglionic fiber (CN nuclei) projec tot synapse at parasympathetic ganglia near or in target organ. Short postganglionic fibers.
Vagus: preganglionic from dorsal motor nucleus to synapse in intestinal wall on postganglionic. Restorative rest and digest. |
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Basal activity of ANS
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Both parasympathetic and sympathetic have basal resting activity. can be modulated up or down. Fine tuning. Not all or none.
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Neurotransmitters of ANS
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Preganglionics of both sympathetics and parasympathetics use Ach.
Postganglionics of sympathetic release NE (exception: Ach on mAChR in sweat glands). Postganglionics of parasympathetic release Ach on nAchR and mAchR. |
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Slow Potential Components
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Na Channel: AP
nAchR: Fast EPSP (increase Na and K conductance) mAchR: slow EPSP (increase K conductance) and slow IPSP (decrease K conductance) peptideric: LS-EPSP (decrease K conductance) |
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Which two potential components share a receptor? A channel?
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mAChR (slow EPSP and slow IPSP) share same receptor
K+ channel decreasing K conductance used by both slow IPSP (maChR) and peptideric (LS-EPSP). Two receptors coupled to same channel. |
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Light Reflex
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Reciprocal: sympathetic and parasympathetics innervate different opposing muscles.
Light on retina RGCs to edinger westphal - parasympathetic light reflex - ciliary ganglion - constrictor muscle - pupil constriction (miosis) Bilateral innervation - consensual light reflex Sympathetics - preganglionic to superior cervical through ciliary innervates dilator - pupil dilation (mydriasis) |
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Horner's Syndrome
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Sympathetics disrupted - pupil constricted and decreased sweating and flushing ipsilaterally
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Bladder Reflex
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Sympathetic: as bladder fills, innervation relaxes detrusor and contracts internal sphincter. Stretch activated channels (TRP) allow Ca influx - vesicles released - vesicle membranes add to surface area and ATP stimulates afferent fibers sensing stretch.
Parasympathetic: voidnig - preganglionics to inferior hypogastric postganglionics constract detrusor and relax internal sphincter. |
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Blood Pressure Reflex
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Dual - sympathetic and parasympathetics innervate same target but one is excitatory and the other is inhibitory.
BP sensory send info to NST which afects sympathetic and parasympathetic activity. |
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Parasympathetic Effects on BP with pathway
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NST affects parasympathetics through vagal motor nucleus releasing Ach on mAChr in heart causing hyperpolarization (decrease HR and BP)
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Sympathetic Effects on BP with pathway
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Thoracolumbar spinal cord - release Ne on heart and vessels causing increased HR, TPR, contractility, and BP
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How can you cause excessive sleepiness? Excessive wakefulness?
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Excessive sleepiness: lesion posterior hypothalamus (midbrain)
Excessive wakefulness: lesion VLPO (anterior hypothalamus) |
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VLPO Region
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Sleep promoting region - contains sleep active cells and depresses wake active cells.
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How many stages of sleep?
How long are cycles? |
5 stages of sleep, 90 min for each cycle.
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What are proportions of deep sleep (stage 3/4) and REM during earlier and later into the night?
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Earlier in the night there is a bigger proportion of deep sleep, but that decreases as REM sleep increases.
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Sleep Stage 1
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Hypnogogic - drowsy sleep
Theta Waves (4-7 Hz) Sudden twitches, lose some muscle tone and awareness |
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Sleep Stage 2
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sleep spindles (12-16 Hz)
50% of total sleep Lose conscious awareness, muscle activity |
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Sleep Stage 3/4
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Deep slow wave sleep - delta waves (0.5-4 Hz)
Night terrors, sleep walking |
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REM Sleep
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Most like awake EEG- 25% of total sleep. Most memorable dreaming with muscle atonia. Most relaxed, hardest to wake up from.
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Which causes decreased performance? Deprivation of deep sleep or REM?
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REM
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Midbrain Reticular Formation (MRF)
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Responsible for wakefulness. If you lesion this area you cannot stay awake. Regulates thalamic gate through intralaminar nuc of thalamus.
Does not need external stimuli to stay awake. |
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PPT and LDT neurons
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Pedunculopontine and lateral dorsal tegmental cholinergic neurons fire both when awake and in REM sleep.
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Locus Coeruleus Neurons
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LC noradrenergic neurons fire when awake.
Used particularly when under stress. |
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VTA neurons
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Ventral tegmental area dopaminergic neurons fire when you want something, stop when you et it. Particularly used in pleasure/reward situations.
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REM Sleep
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Most like awake EEG- 25% of total sleep. Most memorable dreaming with muscle atonia. Most relaxed, hardest to wake up from.
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Raphe Neurons
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Raphe serotonergic neurons fire when awake. Used particularly in relaxed and satiated state.
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Which causes decreased performance? Deprivation of deep sleep or REM?
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REM
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Thalamus Arousal System
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Thalamocortical activation during wakefulness and REM sleep.
Intralaminar nucleus fires at 40 Hz - source of EEG rhythm. |
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Midbrain Reticular Formation (MRF)
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Responsible for wakefulness. If you lesion this area you cannot stay awake. Regulates thalamic gate through intralaminar nuc of thalamus.
Does not need external stimuli to stay awake. |
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Hypothalamus Arousal System
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Posterior hypothalamus: discharge when awake.
Histaminergic neurons in TMN (tuberomamillary nucleus): wake activating Orexinergic Neurons: excitatory to PPT, LDT, DR, LC, VTA, TMN - highest at end of day maintaining wakefulness as sleep drive increases. |
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PPT and LDT neurons
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Pedunculopontine and lateral dorsal tegmental cholinergic neurons fire both when awake and in REM sleep.
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Narcolepsy - what neurons degenerate?
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Orexinergic neurons
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Locus Coeruleus Neurons
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LC noradrenergic neurons fire when awake.
Used particularly when under stress. |
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VTA neurons
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Ventral tegmental area dopaminergic neurons fire when you want something, stop when you et it. Particularly used in pleasure/reward situations.
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Raphe Neurons
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Raphe serotonergic neurons fire when awake. Used particularly in relaxed and satiated state.
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Thalamus Arousal System
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Thalamocortical activation during wakefulness and REM sleep.
Intralaminar nucleus fires at 40 Hz - source of EEG rhythm. |
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Hypothalamus Arousal System
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Posterior hypothalamus: discharge when awake.
Histaminergic neurons in TMN (tuberomamillary nucleus): wake activating Orexinergic Neurons: excitatory to PPT, LDT, DR, LC, VTA, TMN - highest at end of day maintaining wakefulness as sleep drive increases. |
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Narcolepsy - what neurons degenerate?
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Orexinergic neurons
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Alcohol Mechanism
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Binds to GABA receptors increasing affinity for GABA - potentiate effects of inhibition
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Opiate Mechanism
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Binds to opioid receptor to decrease NT release from other neurons.
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Cocaine Mechanism
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Binds to Dopamine reuptake receptors blocking them increasing dopamine effects.
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Marijuana Mechanism
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binds to CB1 causing disinhibition and increased arousal.
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Olfactory Pathway
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OSNs to glomeruli (with OSNs that have the same OR) where they synapse on mitral and tufted cells that project to the olfactory cortex and limbic system.
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Olfactory Transduction Cascade
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Odor binds to odor receptor on single apical dendrite of OSN. OR is a GPCR working through AC to make cAMP that binds to cyclic nucleotide gated channel allowing Na and Ca influx causing depolarization. Ca also opens Cl channels causing Cl efflux.
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Olfactory Adaptation
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calcium binds to calmodulin decreasing cyclic nucleotide gated channel to cAMP
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Olfactory Code
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Pattern coding - individual receptor can bind more than odor and individual odor can bind more than one receptor.
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Accessory Olfactory System
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If VNO deleted - can't tell if male or female. Projecst to hypothalamus
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What makes olfactory pathway so unique?
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Does NOT have obligate thalamic relay to get to cortex. Projects straight to cortex from 2nd order mitral and tufted cells.
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Taste Buds
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Modified epithelial cells (NOT neurons) that synapse with nerve fibers. On tongue, soft palate, epiglottis.
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Taste Bud Cell Types
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Type I: enzymes that clear NTs
Type II: GPCR - sweet, bitter, umami with atypical synaptic contacts using atp that comes out of gap junctions onto CN nerve fibers Type III: sour sensitive cell subtype with typical synapse that releases vesicles |
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Taste information Coding
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Labelled line coding: distinct populations of sweet, bitter, umami, salty, and sour cells in taste buds. If you activate a sweet cell, no matter how, it will always elicit sweet.
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T1Rs and T2Rs
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T1R3 + T1R1: umami
T1R2 + T1R3: sweet T2R: bitter Both are GPCRs that activate PLCB2 to cleave PIP2 to IP3 and DAG. IP3 opens IP3R channels allowing release of intracellular calcium stores which binds to TRP channels allowing Na influx - depolarization - release ATP onto CN nerve fibers (7,9,10) |
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Miraculin Protein
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Changes taste to sweet
Neutral pH: closed and can't activate sweet receptor Acidic pH: open and binds to sweet recepto activating it |
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Why does saccharin taste bitter to some people?
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T2R (bitter) variant that is sensitive to saccharin - activates both sweet and bitter.
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Why do you get sweet illusion from lactisole inhibitor or artichokes?
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All cause inhibition. When wash away with water, all slam shut removing inhibition, activate at same time - sweet perception.
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Gustatory Pathway
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CN 7,9,10 innervates taste cells to NST to VPM to gustatory cortex (insula)
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Hypothalamus Function
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Maintain homeostasis - BP, electrolytes, body temperature, metabolism, emergency response
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Hypothalamus Neurons and Response
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Neurons senstiive to temperature, osmolality, glucose, Na, and Hormones. Compare sensory info with set point and respond accordingly - autonomic, endocrine, behavioral.
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Borders of Hypothalamus
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In diencephalon
Anterior: anterior commissure - lamina terminalis - optic chiasm Posterior: posterior commissure to mamillary bodies Superior: hypothalamus sulcus |
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What divides medial and lateral divisions of the hypothalamus?
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Columns of the fornix
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Circumventricular area of Hypothalamus
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Lines 3rd ventricle - access to circulatory/CSF cues
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Rostral to caudal divisions of hypothalamus
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Preoptic area + anterior hypothalamus (PVN, SCN, SON), tuberal (VMN, arcuate, DM), posterior (mamillary)
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Blood Brain Barrier
Where is it weak? |
Made by TJs between endothelial cells, basement membrane, astrocytic foot processes. Prevents infiltration of pathogens and immune cells but also prevents drug access. Weak at median eminence of hypothalamus - monitor endocrine signals.
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Hypothalamus blood supply
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Preoptic and anterior get branches of ACA and the rest get branches of PCA, ICA, AComm
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Pituitary blood supply
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Anterior pituitary: superior hypophyseal artery
Posterior pituitary: inferior hypophyseal artery |
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Median Eminence
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fenestrated capillaries - releasing factors here can act on anterior pituitary
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Hypothalamic Pathways
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Fornix: hippocampus to hypothalamus
Stria terminalis: amygdala and hypothalamus MFB and DLF are bidirectional between hypothalamus and brainstem and spinal cord DLF NST afferents from vagus and efferents to motor nucleus of the vagus Unidirectional mammillothalamic tract (mammillary bodies to AN of thalamus), retinohypothalamis tract (RGCs to SCN), HPA axis (hypothalamis to pituitary) |
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HPA Axis
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Parvocellular neurons from PVN of hypothalamus to median eminence release releasing factors to act on anterior pituitary.
PVN and SON hypothalamus axons project into posterior pituitary and release vasopressin and oxytocin into the blood stream. |
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Vasopressin
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Anti-diuretic - increase BP
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Oxytocin
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uterine contractions, promote lactation
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CNS effects of vasopressin and oxytocin
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Effects from local release
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Hypothalamus Releasing Factors with associates areas
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Preoptic: GnRH
PVN: CRH, TRH Arcuate: GHRH, dopamine Periventricular nucleus: somatostatin |
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Thermoregulation
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Temperature set point. Warm and cold cells in hypothalamus - some directly sensitive to temp and some indirectly through neural input.
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Hypothalamus warm and cold cells
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Warm cells - sweating, vasodilation
Cold cells - heat retention, vasoconstriction, pilorerection, behaviors |
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Hypothalamic Metabolism Regulation
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Leptin and insulin long term indicators of energy state and short term satiety (glucose, ghrelin, vagal input, CCK, GLP-1)
Nuclei: PVN, arcuate, LHA, VMN |
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Circadian Rhythms
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RGCs (melanopsin positive) project to SCN which is the pacemaker
These RGCs project to rods and cones and LGN but dont play a role in image formation |
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What happens when you...
Ablate melanopsin postive RGCs? Lesion SCN? |
Ablate melanopsin positive RGCs - loss of photo entrainment - shifting of day but still stays 25-26 hrs
Lesion SCN - lose pacemaker - totally random - no day or night (activity) |
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Parietal Assocation Area
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Assocation of visual and touch/proprioception
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Parietal Lesions
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Astereognosis (inability to recognize objects by touch alone) or body neglect syndromes (ignore contralateral side of body/visual field)
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Prefrontal Assocation area
Lesions |
Short term working memory
Lesions (principal sulcus) - can't do delayed alternative test Neurons fire after visual cue is gone making map of contralateral visual space |
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Limbic System
Anterior temporal (hippocampus) lesion Orbitofrontal cortex lesion |
Cingulate gyrus, orbitofrontal, anterior temporal cortex (hippocampus)
anterior temporal cortical lesion including hippocampus will lose long term memory (declarative learning - facts and events) Lesion orbitofrontal cortex - decreased aggressiveness (lobotomy) |
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Broca's Area
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Premotor area - control speech muscles to make fluent speech
Lesion: expressive aphasia - slow halting speech. retain comprehension. |
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Arcuate Fasciculus
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Connects wernicke's and broca's. Word salad with retained comprehension.
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Wernicke's Area
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Superior temporal and inferior parietal junction - language comprehension.
Direct's brocas area to make comprehensible speech. Lesion: receptive aphasia - word salad - impaired comprehension |
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Angular Gyrus
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Integrates visual input to language centers
Lesion:Alexia - can't read, fine to understand spoken language |
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Left brain
Right brain |
Left brain - right hand, right visual field - spoken response. Analytical and language.
Right brain - left hand, left visual field - pick up. Manipulo-spatia. |
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Transfer across commissure
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stereognosis - split brain - deficit
consolidated memory is not transferred (memory traces need to be made bilaterally) |
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Aprosodia
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Defect in ability to understand and/or express emotional content of language
Broca's: speak clearly with flat affect Wernicke's: express inappropriate emotional content and can't understand in others Disconnection aprosodia: understand other's emotional content but can't control your own These are all made on right side of brain in corresponding area to left language centers. |
