Part III 	A..  Neurons: Basic Mechanisms
		1.  Resting Potentials: Making information possible  
			A) Ions and membrane permeability
			B) Na/K+ pump

		2.  Action Potential:  Informational units
			A) Ion gates:  Thresholds, refractory periods, stimulus codes
			B) Myelin: saltatory conduction for fast signals

		3. Synapses:  Communication between neurons
			A)electrical synapses
			B) chemical synapses

		4.  Post-synaptic potentials
			A) EPSP & IPSP
			B) Neuronal decisions via summation
			C) Ionic vs metabolic synapses

		5.  Presynaptic potentials
			A) Autoreceptors and pre-synaptic inhibition

		6. Neurotransmitters
			A) Receptors
			B) Distribution in brain
			C) Drug actions
Read Kalat chapter 2  and 3 

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Important neuron parts:
	Dendrites
	Soma or Cell Body (contains axon hillock)
	Axon	Synaptic Bouton (vesicles)

Glia (glial cells) are the other chief type of brain cell.  Name from Greek "glue"
	-process metabolic wastes
	-provides structure, early growth guidance,  scar tissue after damage
	-provides blood brain barrier

NEURONAL RESTING POTENTIALS
Ion contents
Cl-     Na+    K+
Outside___________________________________________
K+   Cl-   Na+   Negative Proteins    [-70 mv] 
Inside__________________________________________

Concentration differences of IONS produces Potential (voltage difference across membrane] = -70 mv  (-30 to -90)
	1. Selective membrane permeability 
	2.  Electrical gradients resulting from selective permeability
	- Similar charges repulse each other: acts to segregate Cl- and K+

Na+/K+ pump:   ACTIVE mechanism of neuron,
-Carrier molecule picks up 3 Na+ inside ions and takes out;   2 K+ outside ions, brings in

ACTION POTENTIAL:   unit of  neuron information.
Traveling Wave:   propagated along the axon
What Happens:
1. Threshold to open Na gate = approximately  -60 mv	
2.  Na gate swings shut after 0.5 msec open:  ALL OR NONE
	Na Gate can't be re-opened for 1.0 msec more:  Absolute Refractory Period
3.  K gate opens at peak
	-Overshoots at pit: Relative refractory period of several msec    (ends by dissipation & Na/K pump)
NOTE STEREOTYPED ALL OR NONE UNIT

Implies that information can be coded only in two ways.
1. Temporal code: soft loud & relative refractory period: Quantitative
2. Labeled line:  soft, loud;  also red, green;  sweet sour: Qualitative

MYELIN  and Saltatory Conduction
Myelin = Fatty Glial cells (Brain oligodendrocytes,    peripheral Schwann cells
	Multiple Sclerosis:  Death of Schwann cells & glia 

SYNAPSES:  Communication between neurons
1.GAP JUNCTIONS:   ELECTRICAL
-special low resistance membrane at junction  
2.  CHEMICAL		
	-at Synaptic Cleft, Presynaptic Vesicles  release  Neurotransmitter
1.  Action potential open CALCIUM ion gates at bouton
2.  CA++ enters cell;    Causes release of Neurotransmitter into Cleft
3.  Entire vesicle bursts:  QUANTA of Neurotransmitter
4.  Postsynaptic Signals:  2 Kinds:  IONIC  and METABOLIC
	A. . Ionic:  1.  Directly opens ion gates on postsynaptic membrane
		EPSP = Depolarization
		IPSP  =  Hyperpolarization
	B. Metabolic:  receptors trigger internal second messenger systems that later alter ion gates

EXCITATION  VS  INHIBITION
-Many synapses are inhibitory
- Humans especially use inhibition:
	Rabbit, Cat = 30% inhibitory synapses in Cortex
	Rhesus Monkey = 45%
	Humans = 75%
A stimulus can result in final excitation (positive sensation) via chain of inhibition

-BENEFIT of synapses:  DECISION making
	1.  SPATIAL SUMMATION  
	2.  TEMPORAL SUMMATION:

Additional  influence on decisions by Pre-Synaptic modulation
A.  AUTORECEPTORS  -  neuron talks to itself
B.  PRE-SYNAPTIC INHIBITION & POTENTIATION: depend on RELATIVE height of action potential

NEUROTRANSMITTERS
-Dozens of neurotransmitters;   
RECEPTOR is the real determinant of neurotransmitter effect
	Receptor is LOCK, neurotransmitter is only the KEY

-DRUGS: act primarily on neurotransmitters or on receptors -
AGONISTS - turn neurotransmitter systems on
	Presynaptic: act on release, etc, prior to the receptor
	Postsynaptic:  activate receptor
	
ANTAGONISTS -suppress neurotransmitter systems 
	Pre-synaptic:  Suppress release or increase breakdown
	Post-synaptic: Block receptors

All real drugs exert a combination of effects
-Ex:  Ecstasy = MDMA + metadimethylamphetamine
	Has Amphetamine-like DA & NE pre-synaptic agonist action
	LSD-like serotonin post-synaptic agonist/ pre-synaptic depletion

LONG-TERM EFFECTS
1. Receptor-Down Regulation-  Tolerance = postsynaptic downregulation = possible withdrawal
	-antidepression Dopamine Agonists (tricylic & MAO I)
		A)  suppresses postsynaptic receptors (suppress system)
		B)  autoreceptor downregulation  (increases system)
2. Sensitization = some neural systems show reverse effect
	-Dopamine after prolonged Amph, Cocaine = HYPERACTIVE = Addiction CRAVING
3.  Neurotoxicity:  some drugs are toxic to neurons at high doses (amphetamine