February 16, 2010

Sleep and Daily Rhythms

Sleep is a state of mind; during sleep, brain discontinues processing continual sensory information from the 5 basic senses.

Functions? All ideas are currently hypothesis- not thesis.

Hypothesis- educated guess- test construct for gathering information.

Western approach--> reductionist concept, where hypothesis "test" at most two variables to determining key factors.

Idigeonous Science--> global view- observation of how parts work together as opposed to a reduction theory, a continuum, successful hypothesis that leads to theory.

Theory- a statement based on observation and data collected under experimental conditions (controlled environment)

Theories are tested through perdictive experiments and may involve multiple variables. Therefore, if all variables are defined becomes fact.

Indigenous Theories often based on different time scale. Therefore, it is different to test or compare with western theory. As spiritualism is sometimes evoked to account for changes with time. (sleep is an altered state of consciousness)

Sleep is also a complex bhvr. - occurs in mammals and birds -> birds "evolved" from reptiles. But mammals and birds did not evolve from hypothesized ancestors. Sooooo.... Why do birds and mammals share a complex bhvr.?

Study of sleep is important to understanding main function
-evidence suggests that the frontal lobe is "inhibited" at all sleep levels

Approaches to studying sleep-
A) Circadian Cycles and Rhythms
B) EEG and wave patterns
C) Sleep Cycles and autonomic nervous systems (hormones)

A) Circadian Rythms occur in most endoderms daily fluctuation of activity ruled by hormonal influences

The suprachiasmatic nucleus (SCN) contains neurons that keep the clock running

SCN neurons can grow in petri dish (culture) will display rhythmatic activity.
12 hours on/12 hours off (some cultures have days longer than 24 hours) ~the rhythm generators, motor that run the clock.~

But, SCN does not determine period of activity.

Day- Diurnal
Night- Nocturnal

How does the SCN tell time?

3 genes A/B) per, tim (timeless) C) gene clock (circadian locomotor output cycle kaput)

per and tim-> proteins-> inhibit the production of clock protein

But.... per/tim proteins are degraded, eaten by enzymes, at a certain rate (concentration of proteins and enzymes present) When per/tim decrease this allows for expression of clock gene to occure- clock proteins increase. When clock increases it promotes (binds to genes of per/tim to increase proteins.

increase of per/tim then inhibit of clock which stops production of per/tim. (All this cycles back up to where per/tim degraded by enzymes)

SCN keeps time -> SCN regulates/regulated by melatonin ->produced by pineal gland (body) gland-> anything that secretes a hormone.

Melatonin-> synthesized from seratonin which is made from the amino acid tryptophan which is also called indolemine

Melatonin is low during the day and highest in early hours when it's most difficult time to be awake. M is regulated by light. An increase in light equals a decrease in M, a decrease in light equal and increase in M. M (melatonin) is a sleep inducing hormone.


M is a hormone that regulates cells, usually through changing gene transcription.

Hormone help establish if animal is nocturnal or diurnal.

cortisol- wake up
growth - sleep phase

Jet lag -> time or light shift. SCN will adapt with in 48 hours (reticulo hypothalamic) daily rhythm can take up to a week.

Another hormone related to daylight: SAD (seasonal affective disorder) which is a lack of light.

EEG Sleep

A)Discovered pattern of activity that lead to stages of sleep
B) stages of sleep corresponds to different autonomic levels (parasymp= slow, symp=faster)
C) REM occurs in predictable pattern (rapid eye movement moves side to side, not up and down)

NREM--> 4 stages of non REM
1)Theta (θ) rhythms
2) sleep spindles --> K complex
3) δ (delta) rhythms initiate
4) Repetitious δ

Rem--> 1 stage---->β activities (wakeful)

REM-> increase in sympathetic nervous system. Muscle paralysis in REM (fingers/paws), Blocking descending motor pathway recticulo spinotract.

Cycles of sleep--->
A) Require 4 stages of NREM to achieve REM
B)True REM= 90 mins includig sleep cycle
C) After REM, no longer need stages 3-4
Final stage, no 4th

Sleep pattern change across life span
A) Babies need lots of sleep (first 13 days critical for development)
B)Puberty decrease in stage 3-4 NREM and REM. Increasing desire for sleep because without 4 we can't get to REM.
C) Over 40 years, decrease in need for sleep, easier to get REM (See fig. 11.11)

All this just to maintain our blood volume! Wow!

Zona inserta- an area in the midbrain that may participate in the initiation of drinking behavior.

Amylin --> area postrema --> NTS--> Hypothalamus

insulin --> puts sugar into cells
glucogen (not to be confused with glycogen) --> release glucose for the liver

Hypothalamus- appetite center was thought to be here. Leision Ventromedial Hypothalamus in a rat resulted into a fat rat (hyperphagia).

*inject neuropeptide Y (NPY) = hog wild (time independent)

*AGRP- agouti related protein -> eat * δ= MSH decrease in appetite

*CART (cocaine amphetamine related trascript peptide) decreases appetite

MC4

Fat->hormone (leptin)->brain

Leptin is a reinforcing hormone that causes us to eat.

If Insuline doesn't work
A) Insulin resistance (glucose doesn't go into cells)
B) Insulin replacement B-cells burnout (high glucose in blood stream. Therein sugar binds to protein.
C) Death

DNA---->RNA---->Protein---//-diabetes----->no environment



Type I diabetes in kids, Type II diabetes in adults.

Self-Image of Anorexic patients
1)most things have been tried by themselves
2)multiple known pathways to stimulate appetite
3)identify cortical problem in mPFC-self (reward pathway converge here)

February 9, 2010

Hypothalamus- autonomic nervous system. Controls parasympathetic (gut control, decreases heart rate) and sympathetic (epinephrine, raises blood pressure and heart rate).

Hormone-> any chemical released into the extracellular environment which is usually the blood plasma = hormones then act on selective cells to alter homeostasis. Selective cells express receptors for the hormones.

Homeostasis= physiological equilibrium. Or, as defined by our professor: efficient reaction to the env. to maintain cellular function (life!)

Hormones released by the hypothalamus, plus the neural connections, provide motivation for a variety of bhv.
A) Temp= set point = balance ----------->
B) Fluid Balance
C) Energy Balance- appetite

Temp --> set point => HOT- hyperthermia or COLD- hypothermia both used in homeostasis.

endoderms=> internal temp regulation (e.g. sweating, panting, licking nose, spreading of wings/ears, all an evaporation process.

Vasodilation- the increase of blood flow to peripheral tissue. Blood flow is the primary mechanism for temp set point. To regulation temp through metabolism, the hypothalamus uses TRH (Thyroid Releasing Hormone)

TRH->Thyroid->T3 +T4+hyroxine-> cells increase metablolism

Brown fat is an uncoupling protein.

Fever=>disease increase Temp=> increase the fluid in the interstital space.

Interstital space= extracellular environment increases immune response.

Hyperthermia = death

Hypothermia = loss of conciousness -> death

Fluid balance pertains mostly to water

Intracellular 67%
Extracellular 33%

A)Interstitial fluid ----- 25%
B)Blood --------------- 7%
C) Cerebral Spin. Fluid - 1%

hormones usually travel in blood stream, but ultimately most go to interstitial fluid -> cells

Within the Hypothalamus fluid balance is regulated by osmosis (diffusion of molecules through a semipermeable membrane from a place of higher concentration to a place of lower concentration, also called diffusion). In this example, the water cannot pass through the lining of this tube, but can pass through the Na+ and K+ channels easier.

Kidneys work by moving Na+ and H2O to make urine. Sooo..... where Na+ goes, H2O follows.

Kidneys regulate or retain H2O based on hormones from hypothalamus, Neuropeptide vasopressin (ADH)

ADH- anti-diuretic hormone. Diuretic increases urine volume. Why release ADH in terms of blood volume? Capillaries shrink to increase blood pressure.

ADH causes the kidney to release Renin= a protein that is an enzyme that acts as a circulating hormone angiotensinogen (At) -> to make At I another At converting enzyme (ACE). Both AtI and At I. (ACE inhibitors are the best of blood pressure meds)

At II is going to
1) increase blood pressure by reducing capillary volume
2) initiate feedback loops (i.e. reflex arc)
a)brain-subfornical organ (SFO): situated on the ventral surface of the fornix, at the foramen of Monro, is one of the circumventricular organs of the brain.
b) adrenal gland- Aldosterone-> retains Na+

In relation to thirst:
Hypothalamus-> bloodstream (ADH)-> Kidney-> Feedback (brain)-> hypothalamus indicating "You need a drink"

SFO is a circumventricular organ (CVO)- a location where blood/brain barrier contains a window of various thickness different CVO's have different permeability to hormones.

AtII H2O Balance CVO monitor whats in our blood
1) Hypothalamus 1) hormones
2) Motor Output 2) chemicals (sugar, H2O, etc.)

CVO= area portrema with in the medulla (on the floor of the VI ventrical) ->Blood -> CSF
Area postrema connects to the nucleus tractus solitarius (NTS).

See fig 9-10 for Neural Connectivity of the Hypothalamus

January 21, 2010

The more axons used the lesser time in the reaction period. Handy to know right? That's why it's more easier for you to spell something or txt your buddy without much thought because there's more axon's for that being used than when you are trying to remember AP and where to find the basal ganglia.

Somatosensory cortex: caudal (in front of) to the central sulcus.

Homunculus (lit. "little person") indicates which parts of the motor cortex are used for certain parts of the body.

Plasticity --> change The brain is very plastic in the sense that parts of the brain, if not used (like in amputation), can be taken over by the neighboring section of the brain and be used by that specific body part. Consider the experimentation on the chimp where the scientist sewed together his fingers one at a time to prove this thesis. The neighboring areas of the brain used by the index finger would slowly start merging with the middle finger area and when one area was prodded, both fingers were affected. This process was continued until the whole area was taken over by the felxing of the hand. The plasticity surely shows in the reversal of this experimentation where the chimpanzee was able to use his index finger area only for his index finger and not both index and middle finger. Plasticity is a relatively new concept brought more into the light by Dr. Ramachandran who discovered the intricacies of 'blindsight' and helps amputated patients move past their phantom pains.

Lat. Spinothalamic Pathway- Fibers that carry pain and temperature information from the substantia gelatinosa to the thalamus. Pain and temperature information carried by Aδ and C fibers and carried mostly with in the Lateral Spinothalamic pathway. --> information enters spinal column through Dorsal horn of the synapse in layer II and III of the dorsal horn (grey matter) [crosses in the medulla] --> These 2° (secondary) order neurons cross with in the spinal comumn and proceed rostraly up the cord to the ventral posterior (VP) and intralaminar nuclei of the thalamus --> 3° (thirdly) neuron project to the somatosensory cortex and anterior cingulate cortex= emotional response.

Something you should know: White matter is faster than the grey matter. That's why pain information crosses over into the white matter and the temperature travels up through the grey matter.

Aδ and C fibers in dorsal ganglion cells-Pain

capsacin= chemical in hot peppers. Why is it soooo hot?! Because it keeps the channels open in an AP, there is no refraction period. It activates receptors in dorsal root ganglion (DRG) cells. Substance P => NT

Substance P: a neuropeptide: an undecapeptide that functions as a NT and as a neuromodulator. Substance P and its closely related neuropeptide neurokinin A (NKA) are produced from a polyprotein precursor after differential splicing of the preprotachykinin A gene. It is released from the terminals of specific sensory nerves, it is found in the brain and spinal cord, and is associated with inflammatory processes and pain.

opioids = morphine, blocks the 2° neuron (in red) from getting pain signal.

Decending pathway modulating incoming info. by opioids. Periaqueductal Grey (PAG), aqueductal-> around the fluid. Grey-> lots of cells/Mμ receptors