B&B Neuro Flashcards
Functions of the hypothalamus
- Homeostatic mechanisms controlling hunger, thirst, sexual desire, sleep-wake cycles, etc
- Endocrine control via the pituitary
- Autonomic control
- Limbic mechanisms
mnemonic: HEAL
contains axons & terminals of neurons whose cell bodies are located in the hypothalamus (supraoptic and paraventricular nuclei are the hypothalamic nuclei that have termination here)
-secretion of oxytocin & vasopressin into circulation
posterior pituitary
region where hypothalamic neurons release regulating factors carried by portal vessels to the anterior pituitary
-these can either stimulate release of hormones or inhibit release of hormones from the glandular (anterior) pituitary
median eminence
4 major regions of hypothalamus
- preoptic area
- anterior (supraoptic) region
- middle (tuberal) region
- posterior (mammillary) region
contains lateral and medial preoptic nuclei
preoptic area
- contains supraoptic & paraventricular nuclei (these contain oxytocin & vasopressin) which project to the posterior pituitary
- contains suprachiasmic nucleus (SCN) or “master clock”
anterior (supraoptic) region of the hypothalamus
nuclei from which descending autonomic fibers originate
paraventricular nuclei
contains the arcuate nucleus, ventromedial nucleus and dorsomedial nucleus
middle (tuberal) region of the hypothalamus
projects to the median eminence to control anterior pituitary
arcuate nucleus
includes the medial mammillary nucleus, intermediate mammillary nucleus, lateral mammillary nucleus & posterior hypothalamic nucleus
posterior (mammillary) region of the hypothalamus
lesion to this area of the hypothalamus causes insomnia
anterior region
lesion to this area of the hypothalamus destroys histaminergic neurons in the TMN, as well as orexin-containing neurons, causing hypersomnia
posterior region
hormones of the anterior pituitary (6)
- ACTH
- Growth hormone
- prolactin
- thyroid-stimulating hormone
- luteinizing hormone
- follicle-stimulating hormone
* note: release is controlled by the hypothalamus via hypophysial portal system
hormones of the posterior pituitary (2)
- oxytocin
2. vasopressin (ADH)
stimulates appetite and lesion to this area of hypothalamus causes weight loss
“tells when to eat”
lateral nucleus of hypothalamus
“lesion lateral loss”
inhibits appetite and lesion to this area of the hypothalamus causes weight gain
“tells when to stop eating”
medial hypothalamus
hormone that increases appetite
Ghrelin
regulates thirst
-activated by hypovolemia or elevated body temp
osmoreceptors of the anterior hypothalamus
Detects increased body temp and activates heat dissipating mechanisms
-lesion causes hyperthermia
anterior hypothalamus
“cool facade” or dog pANTs to cool off
conservation of heat
-lesion causes poikilothermia
posterior hypothalamus
“hot posterior”
feedback loop for cortisol
hypothalamus releases CRH which stimulates release of ACTH by the anterior pituitary. ACTH stimulates adrenals to produce cortisol. Cortisol inhibits release of CRH.
*chronic steroid administration can cause atrophy of adrenals and abrupt discontinuation of steroids can cause life-threatening deficiency of cortisol
Functions of the limbic system
- Homeostatic functions: autonomic & neuroendocrine
- Olfaction
- Memory
- Emotions and drives
mnemonic: HOME
Major structures of the limbic system (9)
- Limbic cortex
- Hippocampal formation
- Amygdala
- Olfactory cortex
- Diencephalon
- basal ganglia
- basal forebrain
- septal nuclei
- brainstem
nuclear complex that lies in the anteromedial temporal lobe & controls emotions and drives
amygdala
contains cholinergic neurons that provide major cholinergic innervation for entire cerebral cortex
nucleus basalis (of Meynert)
contains cholinergic neurons that project to the hippocampal formation and play important role in memory function
medial septal nucleus
mediates changes in HR, peristalsis, gastric secretion, piloerection, sweating, & other changes seen in strong emotion
reciprocal connections between amygdala, hypothalamus & brainstem
nuclei of amygdala (3)
- corticomedial
- basolateral
- central
connects olfaction with hypothalamus relating appetite states
corticomedial nucleus of amygdala
involved in direct and indirect connections of amygdala to cortical areas, basal forebrain & olfactory areas
basolateral nucleus
involved in rational thinking (weighing consequences based on contingency and the triggers of emotional states)
amygdala
prefrontal cortex
striatal & thalamic connections
- expression and comprehension of affective aspects of speech
- negative emotions
- perception of facial expressions
right hemisphere
- positive emotions
- language
left hemisphere
contains medium spiny neurons that modulate in the influence of dopamine
-receives projections from the VTA
nucleus accumbens
*drugs of abuse prolong the action of dopamine in the nucleus accumbens or potentiate the activation of neurons of the VTA & nucleus accumbens
Functions of the association cortex (6)
- higher-order sensory processing
- motor planning
- language processing and production
- visual-spatial orientation
- determining socially appropriate human behavior
- abstract thought
Unimodal association cortices (4)
- somatosensory association cortex
- Visual association cortex
- Auditory association cortex
- Motor association cortex
Regions of the association cortex (4)
- dominant hemisphere
- nondominant hemisphere
- frontal lobes
- visual association cortex
skilled complex motor tasks for both limbs (praxis)
- language
- mathematical calculation
- analytical skills of trained musicians & sequence
- follow written directions
dominant hemisphere
- nonverbal functions
- complex visual-spatial skills
- emotional significance to language (prosody) and events
- mathematical estimation
- music perception (complex music in trained musicians & musical ability in untrained)
- attention to both sides of the body
- big picture: “overall gestalt” -> finding one’s way
nondominant hemisphere
- contralateral neglect syndrome with lesion
- perceptual awareness (inferior lobe governs attention)
- lesion causes one to get lost moving from one room to another in own home
parietal association cortex
- planning, control and execution of actions
- personality
- lesion causes:
- impaired restraint
- disordered thought
- perseveration (repetition of behavior)
- inability to plan appropriate action
frontal association cortex
mismatch of verbal or cognitive symbols with sensory stimuli
difficulty naming
agnosia
inability to recognize and identify faces
prosopagnosia
recognition and identification of stimuli that are attended to, particularly complex stimuli
- right lesion: agnosia for faces & objects
- left lesion: difficulty with language-related material
temporal association cortex
recognition of voluntary behavior
parietofrontal mirror system
recognition of affective behavior
limbic mirror system
roles of mirror neurons
- recognition and understanding of what others are doing, as well as why they are doing it
- intention of interaction
empathetic activation of motor circuits provide a link between observed actions and observer’s store knowledge of the nature, motives and consequences of his own corresponding actions
*Note: in autism there is a lack of activation of the motor system when the child observes someone performing an action -> do not understand the intentions of others
Direct matching hypothesis
mirror neurons
area that lies in the opercular and triangular portions of the inferior frontal gyrus in the dominant hemisphere & produces words and sentences
Broca’s area
syntax and comprehension depend upon this area
frontal structures
defect in language processing caused by dysfunction of the dominant hemisphere
- affects both spoken and written language
- note: most common cause is cerebral infarct
aphasia
Caused by infarct of left middle cerebral artery (superior division)
-decreased fluency (phrase length
Broca’s aphasia “expressive aphasia”
Caused by infarct of left MCA inferior division
- impaired comprehension (cannot follow commands)
- normal fluency to spontaneous speech but is empty, meaningless and full of paraphasic errors
- neologisms
- impaired naming
- impaired repetition
- reading and writing fluent but meaningless
- contralateral visual field cut
- apraxia
- anosognosia
- angry or paranoid behavior
Wernicke’s aphasia “receptive aphasia”
unaware of deficit
Impaired awareness
anosognosia
Caused by left MCA inferior & superior infarcts
- weakness on right side of face and paralysis of right limbs
- impaired fluency, comprehension & repetition
- damage to anterior language region, basal ganglia & insula, and auditory cortex
Global aphasia
normal fluency and comprehension but impaired repetition
- paraphasic errors common
- naming impaired
Conduction aphasia
inability to carry out an action in response to verbal command, in absence of any comprehension deficit, motor weakness or incoordination
apraxia
disturbance of speech articulatory apparatus without language disturbance
- foreign accent syndrome
- effortful, poorly articulated speech with normal written language
- may be mute
aphemia
causes of agraphia without aphasia
lesions of parietal lobe in language-dominant hemisphere
lesions of corpus callosum (disconnect between language and motor)
cause of alexia without agraphia
lesion of dominant occipital cortex extending to corpus callosum, preventing processing of visual info from right hemifield
-can’t name colors
cause of alexia with agraphia
lesion of the dominant inferior parietal lobule in the region of the angular gyrus
synaptic terminals are strengthened by correlated activity during development and will be retained or sprout new branches
-weakened by uncorrelated activity
Hebb’s postulate
the time when experience and neural activity that reflects that experience have maximal effect on the acquisition or skilled execution of a particular behavior
-once this time is over, the core features of the behavior are unaffected by subsequent experience
Critical Period
cortical blindness
- loss of acuity, diminished stereopsis & problems with fusion that arise from early deficiencies in visual experience
- most often the result of strabismus
amblyopia
crossed eyes
esotropia
wall eyes
exotropia
two eyes cannot be aligned
strabismus
two regions of the brain that can generate adult stem cells
*Note: stem cells can differentiate to glial cells, neurons and additional stem cells
- olfactory bulb
2. hippocampus
inability to establish new memories
*lesion to hippocampus can cause it
anterograde amnesia
difficulty retrieving memories prior to neuropathology
*lesion to temporal lobe may cause this
retrograde amnesia
element of LTP & memory storage that ensures only events of high significance are placed in memory
cooperativity
element of LTP & memory storage: paired input of weak stimulus with strong stimulus is required to cause superpolarization to expel magnesium
(AMPA + NMDA)
associativity
element of LTP & memory storage: if the synapse is not activated by a stimulus, the NMDA receptors lose response to glutamate
synapse specificity
functions of sleep
- restoration of brain glycogen
- conservation of energy
- consolidation of synaptic connections producing memories
histaminergic nuclei modulate the neurons of the raphe and locus ceruleus
Tuberomammillary nucleus (TMN)
lateral hypothalamus secretes orexin to activate the TMN & promote waking
neurons in thalamus are synchronized with those in the cortex “disconnecting” the cortex from the outside world
-maximal during slow wave sleep
Bursting (oscillatory) state
*note these neurons are tonically active when awake
- chronic condition affecting mostly men
- frequent REM sleep attacks during the day
- cataplexy (temporary loss of muscle tone)
- may be caused by orexin-2 receptor gene
narcolepsy
tx: modafinil, amphetamines, methylphenidate
detection of synchronized activity of ensembles of pyramidal cortical neurons
field potentials (of EEG)
phases of a seizure
- interictal period
- synchronized activity within seizure focus
- seizure spread
- secondary generalization
(2-4 = ictal phase)
Acute confusional state with hallucinations and agitation characterized by fluctuating behavior
delirium
failure of recent memory and other intellectual functions, usually with insidious onset and gradual progression
dementia
delayed dementia from head trauma
dementia pugilistica
multi-infarct dementia characterized by step-wise decline in cognitive function
vascular dementia
characterized by personality change and disinhibition Variants include: -primary progressive aphasia -progressive nonfluent aphasia -progressive apraxia -semantic dementia
frontotemporal dementia (FTD)
headache with elevated ICP with no mass lesion
most common in adolescent females
pseudotumor cerebri
can be caused by subarachnoid hemorrhage or orthostatic headache or neoplasms
mass effect
vaculitis that affects the temporal arteries and other vessels supplying the eye
temporal arteritis
sudden burst of aggressive behavior (sham rage) is elicited by a lesion this region of the midbrain tegmentum; stimulation causes pleasant sensation
septum
location of the primary auditory cortex
superior band of Sylvian fissure in the temporal lobe
Wernicke’s cortex is adjacent to this
encoding, storage and retrieval of learned information
memory
storage and retrieval of material that is available to consciousness
Ex: phone number, words to a song, past event
declarative memory
procedural memory
The acquisition and storage of neural associations and motor skills that are unconscious and not dependent on medial temporal portions of the brain
Ex: knowing how to sing a song
nondeclarative memory
ability to hold and manipulate information in the mind for seconds to minutes while it is used to achieve a particular goal
-closely related to attention
working memory = short-term memory
What would a medial temporal lobe lesion cause?
Impaired retrograde episodic memory. It encodes and consolidates declarative memories.
Semantic memory would be spared.
What would a lesion to the hippocampus cause?
profound anterograde amnesia for declarative memory
major long-term repository for many aspects of declarative memory
cerebral cortex
LTP sequence
Glutamate released from presynaptic neuron binds to NMDA and AMPA receptors. AMPA receptors open and generate action potential that expels the Mg2+ blocking the NMDA channel. NMDA channel is now permeable to calcium ions. Calcium ions trigger downstream signaling pathways that increase the response of the postsynaptic cell to glutamate & increase release of glutamate from the presynaptic neuron.
Note: Memantine for Alzheimer’s disease is a noncompetitive antagonist for the NMDA receptor. It sits on the Mg2+ site.
causes relative paralysis during REM sleep
increased GABAergic neuron activity in the pontine reticular formation projecting to inhibitory neurons that synapse with the LMN in the spinal cord
main functions of acetylcholine in the CNS
attention, memory & learning
