Part vi motivation

A. Sleep & arousal
`	1.  Sleep patterns
	2. Brain mechanisms: 
		a. Brainstem identification
		b. Onset of slow wave sleep: 
			1. RAS 
			2. Raphe
		c. Rem
			1. FTG cells & other triggers
B. Specific motivations
	1. Forebrain limbic system
C. Hunger
	1. LH and VMH in distributed circuit
D. Sex
	1. Early modification of the brain by hormones
	2. Adult neural mechanisms: preoptic and anterior hypothalamus. 
E. Aggression
	1. Septal rage & amygdala taming
	2. Interaction via hypothalamus
F.  Reward
	1.  Role of dopamine systems 
		a)  common neural currency for natural and artificial incentives

Reading : : kalat chapt 9 (sleep only, not rhythms)  10  (hunger; not temperature or thirst)
		11 (all) , 12 (reinforcement, fear & aggression; not  stress
-----------------------------------------------------
Sleep & waking
Electroencephalograph measure (EEG) = averaged electrical activity of all cells (epsps & ipsps)

-awake EEG: 	desynchronized & random
		
Sleep: 5 stages
-first 4 stages = progressive slow waves (about 2 hz), large amplitude sine waves
	mild muscle tone (crouching cat asleep)
	usually dreamless

-rem 5th stage:  "awake" EEG (paradoxical)
		eyes scan (rem= rapid eye movement)
		muscle atonia
		fast twitches of muscles in fingers, paws, ears, face muscles
		dreams

Brain mechanisms of sleep
A.   Basic sleep/arousal states are generated in brainstem
This is shown by the following evidence.
1.  Bremer's  cerveau isole & EEG  (midcollicular transection)
	produced permanent sleeping forebrain EEG
	therefore, arousal must generated in brainstem:
2. Arousal from reticular activating system: 
-   Morruzi & Magoun: found that activating electrode in upper pons of anesthetized cat woke the cat up 
-   therefore an activational mechanism exists within the pons
3-  slightly lower transection (mid-pons: pretrigeminal transection) produced constantly aroused EEG forebrain
Thus an arousal mechanism in exists lower midbrain & upper pons: reticular (activating) system

B. Sleep is also actively generated as a positive state
1.  Raphe nucleus triggers sleep onset
-lesions of raphe alone lead to loss of sleep (slow wave)
- electrical stimulation of raphe at low frequencies induces sleep
		raphe = serotonin source
- serotonin microinjection into raphe can also elicit sleep
Thus: slow wave sleep onset depends on activation of serotonergic raphe system

C. REM sleep
-onset is marked by PGO (pontine-geniculate-occipital) spikes: electrical activity from brainstem to visual cortex (a possible basis for dreams)
1. Neural generation of PGO spikes:
	a. FTG (field tegmentalis gigantocellularis)
	b. Other anterior reticular formation cells
	c. Most controversial: specific structures like dorsal raphe ((and locus coeruleus: not in kalat iv)

Topic b.   Specific motives require the  forebrain limbic system
-	hypothalamus
	amygdala
	septum
	and associated projection systems	

Topic c.  Hunger & hypothalamus
Historically, attention focused on the hypothalamus
-lateral hypothalamic lesions lead to aphagia for months
	therefore LH originally thought to be hunger center
-but this is an oversimplification.  The LH is actually:
	1.- A multifunctional system, which does many things related to feeding
		a. Monitor body energy stores (liver, vagus, blood)
		b. Control use of stores (metabolic reflexes vagus)
		c. Complex coding of food incentives: sight of food
		d. Taste processing & pleasure
	lesions destroy all these functions, and therefore produce aphagia
	2. A -a complex anatomical system, which has several distributed parts
		a. LH electrode lesion destroys 2 principal systems:
			-lh cells
			- nigrostriatal dopamine pathways
		either destruction produces aphagia
Conversely, ventromedial hypothalamus lesions produce hyperphagia, and the individual becomes obese
	-again, the lesion syndrome is due to a system effect.  The VMH is
	1. Multifunctional
		a.  Controls metabolic functions such as regulating insulin secretion,  
			influencing body weight and appetite
		b. Psychological:  lesions increase the perceived palatability of food, and makes food pleasantness more 				important as a factor controlling feeding
	2. A complex anatomical system with distributed parts
		a. Example:  hyperphagia also caused by dorsal pons lesion.  The ability to mimic effects by more than 				one lesion reflects the distributed nature of the appetite system in which the VMH is embedded.

Topic d.  Sex
Many sex differences can be found in brain structure (spinal, hypothalamus, cortex, etc.)
But male & female brains begin as identical: mammalian basic prototype or default brain sex appears to be female
- without early " masculinizing" hormonal events all brains develop in a female pattern regardless of genotype

-early hormone effects: estrogen & testosterone
	- all fetuses have estrogen (from mother)
	- male fetuses also have testosterone
Paradoxically, "masculinization" of brain cells to male pattern is done by estrogen!
How?  3 facts must be understood:
1.-  Blood-borne estrogen is normally kept out of brain by alpha-feto-
2. Male testosterone is not bound by the protein, and so can enter brain cells
3. Chemical reaction (aromatization) within certain neurons converts testosterone to estrogen
		
In primates, and especially humans, " hormonal determinism" is diluted by other factors.  However, early effects of hormones have been detected several human studies of sexualization.

Brain mechanisms of adult sexual behavior
Although elements of sexual behavior are controlled by the spinal cord (lordosis, erection, pelvic thrusting, etc),
Integrated sexual seeking, copulation, etc. Appears to depend most directly on the hypothalamus
A. Male behavior & pre_optic area
	-pre-optic area lesions abolish male sexual behavior
	- pre-optic stimulation conversely elicits male sexual behavior
B. Female behavior & anterior hypothalamic area
	-lesions: anterior hypothalamic lesions disrupt lordosis by either sex
	- stimulation of anterior hypothalamus elicits proceptive seeking, courtship, lordosis

Topic e:  brain mechanisms of aggression
Two brain sites of special interest: "amygdala  and septum
1.amygdala
-stimulation of amygdala (basolateral nucleus) elicits aggression in animals and humans.  
 amygdala activation acts via a descending tract to lh
-lesions of amygdala produce a 'taming'; but this doesn't mean the amygdala is the brain's "seat of aggression"
	instead, reflects a change  in many motivational systems

2. Septum (septal nuclei)
-septal lesions produce the phenomenon of 'septal rage'
-rage is blocked if a lesion is also made in the amygdala
-thus in a sense, intact septum "inhibits" aggressive activity mediated by the amygdala

Topic f:  reward
- a single neural system seems to mediate many different rewards
	dopamine pathways from the midbrain to the forebrain (especially nucleus accumbens) pass through the hypothalamus.  The system may have opioid triggers and targets.
	- electrical  stimulation of this system is rewarding in hypothalamus rewarding
	- natural rewards (food, sex, etc.) Activate this system
	- rewarding drugs (heroin, cocaine, etc.) Also activate this system
	- suppression of this neural system makes all rewards ineffective
Thus activity in the ascending dopamine system appears to be a 'common neural currency' of rewarding events.