Exam 3 Flashcards
two hypotheses for functions of default network
- sentinel: always be aware of our surroundings
2. internal mentation: thinking, remembering, and envisioning future events
two types of attention
exogenous (bottom-up) & endogenous (top-down)
attention enhances responses of neurons in what cortex
many areas, but especially parietal, where it was shown that response is enhanced if the target presentation is followed by a saccade to the target. V4 also showed the same thing
pulvinar nucleus
in thalamus, provides input to V4 and IT. may aid ability to focus attention on objects in contralateral field
frontal eye field
organized by motor fields, which controls saccades to a specific place
lateral intraparietal cortex
constructs a priority map based off of bottom up and top down inputs
what do lesions to LIP (lateral intraparietal cortex) lead to
neglect syndrome
what’s the attention network called and what are some things it contains
frontoparietal attention network
lPFC, FEF, LIP, V4, V1, V2, pulvinar and superior colliculus
behavioral goals = established in frontal and parietal areas, priority map create in LIP and FEF, and modulation of visual areas enhances perception of selected objects
neural correlates of consciousness
minimal neuronal events sufficient for a specific conscious percept
where are effects of binocular rivalry seen
inferotemporal cortex (IT)
what does an eeg measure
voltage generated by currents that flow. during excitation of dendrites of pyramidal neurons in cerebral cortex
meg vs eeg vs fmri
meg is better at localizing sources of neural activity, especially deep ones. Both eeg and meg can record faster fluctuations of neural activity
kinds and ranges of oscillations
- delta (<4) deep sleep
- theta (4-7)
- alpha (8-13) quiet waking
- beta (15-30)
- gamma (30-90) attention
2 methods of generating synchrony
- pacemaker cell
2. mutual excitation and inhibition
what structure acts as a pacemaker
thalamus
how does a two neuron oscillator work
constant active input to an e cell, which synapses onto an I cell, which synapses back onto the e cell
atonia
loss of ability to move skeletal muscle
waves during REM vs non REM sleep
REM: very fast, like in an awake brain, uses more oxygen than when awake and concentrating, sympathetic NS
non-REM: slow waves, parasympathetic NS
how many stages of sleep
4, more REM as night progresses, cycle is about 90 minutes long
two theories of sleep
- restoration
2. adaptation for conserving energy or staying out of harms way
why do we dream
- activation-synthesis hypothesis: pontine neurons activate random stuff and cortex tries to synthesize it
- consolidation of memories
how long do humans free run for
at first, about 25 hours, but eventually can get to 30-36 hours
can the body have more than one biological clock
yes, sleeping/waking and temperature can be uncoupled from one another at their own pace
name for biological clock
suprachiasmatic nuclei. however, doesn’t really regulate sleep which appears to regulate itself based on
james-lange theory of emotion
we experience emotion in response to physiological changes in our body
cannon-bard theory of emotion
emotions can occur without physiological changes
unconscious emotion
we can have physiological responses to stimuli without even being conscious of them
broca’s limbic lobe
group of cortical areas bordering corpus callosum
papez circuit aka limbic system
cingulate cortex determines emotional experience, which feeds to hippocampus, which feeds through fornix to HT, which governs emotional expression. HT goes through anterior nuclei of thalamus back to cingulate cortex. cingulate cortex also interacts both ways with neocortex, which is responsible for emotional coloring
basic theories of emotion
anger, disgust, fear, happiness, sadness, and surprise are unique and innate across cultures
dimensional theories of emotions
emotions can be broken down into different dimensions
psychological constructionist theories of emotions
emotions are constructed from psychological components like language, attention, and internal and external sensations
where is amygdala
in temporal lobe just below that one sulcus. medial
groups within the amygdala
basolateral nuclei (where info comes in), corticomedial nuclei, and central nucleus
amygdala is very connected to what
hypothalamus
what does amygdala control
fear and aggression, visual recognition of some emotions, and learned fear
where does amygdala get inputs and outputs from in learned fear
inputs: somatosensory and sensory cortices to BL nuclei
outputs: from central nucleus to HT (autonomic response), brain stem (behavioral response), and cerebral cortex (emotional experience)
neurobiology of aggression
cerebral cortex lesions cause sham rage. posterior HT may be particularly influential in this, and is probably normally inhibited by telencephalon. HT then influences ventral segmental area and periaqueductal gray matter
serotonin deficiency hypothesis
lack of serotonin causes aggression
HPA axis
HT releases CRH, AP releases ACTH, adrenal gland releases cortisol. hippocampal activation also suppresses CRH release
amygdala controls what
HT, periaqueductal gray matter (avoidance behavior), and other systems (increased vigilance)
gluticorticoid receptors
hippocampus contains them, help regulate negative feedback
benzodiazepines
make GABA much more effective
HPA theory of anxiety/depression
in depressed patients, feedback of hippocampus to HPA is disrupted. glutocorticoid receptors are regulated by early sensory experience
what brain region is associated with depression
anterior cingulate cortex
antidepressant drugs
- tricyclic compounds which do a bunch of stuff but also block reuptake of NE and ser
- SSRIs
- NE and 5-HT selective reuptake inhibitors
- MAO inhibitors, reduce enzymatic degradation of ser and NE
dopamine hypothesis
too much dopamine in SZ
glutamate hypothesis
inhibition of NMDA receptors in SZ
three steps of homeostasis behavior
- humoral response (HT neurons respond to signals by controlling pituitary hormones)
- visceromotor response (HT neurons adjust balance of sympa and para outputs of ANS)
- somatic motor response (lateral HT incites behavioral response)
two forms energy is stored in
glycogen (found in liver and muscle) and triglycerides (adipose tissue)
anabolism
assembly of macromolecules from simple precursors
catabolism
breaking down complex macromolecules
lipostatic hypothesis
brain monitors amount of body fat and acts to defend this energy store from changes
leptin
released by fat cells and acts directly on HT neurons to decrease appetite
legions of lateral HT cause
anorexia
lesions of ventromedial HT cause
obesity
total fed pathway
fat cells release leptin, activates arcuate nucleus, releases alphaMSH and CART, which activates paraventricular nucleus, which regulates TSH & ACTH to increase metabolism
other projections
arcuate nucleus projects directly to spinal cord and lateral HT to inhibit feeding behaviors, paraventricular nucleus also projects to brain stem and spinal cords
anoretic peptide
diminish appetite
orexigenic peptides
increase appetite
AgRP and alphaMSH are
antagonistic NTs, bind to MC4 receptor
three phases of eating
- cephalic (sight and smell trigger hunger)
- gastric (chewing and swallowing)
- substrate (nutrients absorbed)
ghrelin
released into bloodstream when stomach is empty
vagus nerve
extends from stomach wall to brain and activates nucleus of the solitary tract in medulla to inhibit eating
cholecystokinin
released in response to stimulation of intestines by fatty foods, acts on vagal axons
insulin
triggers cell uptake of glucose. rises after start of each of the three phases
does dopamine control liking food or wanting it
wanting it: dopamine is more involved in reward prediction
serotonin response to food
rise in anticipation and spike during a meal, then decrease, especially with carbs. elevated baseline serotonin decreases appetite
volumetric thirst
thirst triggered by decrease in blood volume. vasopressin (ADH) is released bc of reduced blood flow to kidneys and mechanoreceptors in heart. also stimulates ANS to constrict arterioles and motivate behavior
osmometric thirst
thirst triggered by hypertonicity of blood. sensed by vascular organ of lamina terminalis (OVLT) which directly excites the cells that secretes ADH
diabetes insipidus
no ADH secreting neurons, so lots of thirst and urination
where are neurons for temperature homeostasis
anterior HT. fall in temperature stimulates TSH release
periventricular zone of hypothalamus
where deviations from optimal range are detected
prandial state
blood is filled with nutrients after a meal
what organ is affected by rabies
hippocampus
two major pathways that connect amygdala to hypothalamus
ventral amygdalofugal pathway and stria terminalis
two major pathways that connect the hypothalamus to the brain stem
medial forebrain bundle (projects to ventral segmental area in midbrain and stimulates predatory aggression) & dorsal longitudinal fasciculus (projects to periaqueductal gray matter for affective aggression)
adenosine in sleep
caffeine is an antagonist of the adenosine receptor, so adenosine promotes sleep. how? it inhibits stuff like ACh, NE, and serotonin which promote wakefulness
nitric oxide
triggers release of adenosine
muramyl dipeptide
cause fever and stimulate immune cells usually, but in sleep-deprived goats it facilitated sleep
interleukin-1
a cytokine, which is a small signaling peptide involved in immune system. promotes sleep
melatonin
derivative of tryptophan, only released at night
melanopsin
photopigment in light sensitive ganglion cells that feed directly to suprachiasmatic nucleus
clock gene
transcribed to mRNA, then protein, the protein decreases gene expression, but eventually more gene expression starts. this cycle takes about 24 hours
default mode network includes what regions
posterior cingulate cortex, mPFC, precuneus, angular gyrus
attention and voluntary movement associated with which direction
lateral
