Download Neuronal function

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+
Negative Proteins
[-70 mv]
Inside__________________________________________
Cl-
Na+
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