neurophysiology Flashcards
how do you call the canyon and mountain like structures of the brain ?
gyri
sulci
what is grey and what is white matter in the brain ?
Grey matter –unmyelinated nerve cells bodies (cerebral cortex)
White matter –myelinated axons
what kind of desease is schizophrenia and what about altzheimers and parkinsons ?
neurodevelopmental( schizo)
neurodegenerative( altz, parkinsons)
The anatomy of the CNS – key concepts? Cerebral cortex
Lobes= Frontal , Pariental, occipital,temporal
also brodmann’s areas are more specific= 1,2,3,4,5,…
The anatomy of the CNS – key concepts?
Subcortical nuclei
Telengephalon
*Basal ganglia
*Amygdala
Diencephalon
*Hippocampus
*Thalamus
*Hypothalamus
*Pituitary
*Pineal gland
how does The cerebral cortex work as a center for integrating sensory
information and a decision-making region
1.Primary sensory area
2.Corresponding association area
(integration)
3.Perception
Motor cortex
Primary motor cortex
Motor association cortex (premotor cortex)
The lateralization principle is real?
yes but it is just that some roles are more pronounced in some areas of the brain in relation to others.
where is th Processing of spoken and visual language done in the brain ?
wernike’s and broca’s areas
W- you speak but it doesn’t make sense because you dont understand
B- Telegram speaking,Aphasia but you understand
Example of emotions in the brain
Fear of a lion –sensory input – thalamus processing it – cortex higher lvl of processing info ( event registered now) ( compare the real lion to the lion in the textbook) – Lympic system gets as scared- hypothalamus start a lot of physiological reactions and prepares you to start running away
Thalamus connects to lympic directly to make the process faster ( responding with emotions )
That’s how phobias work
two types of leearning ?
- Nonassociative learning
- Associative learning
what is non associative learning ?
A change in behavior after repeated exposure to a stimulus
Habituation
Decreased response to a stimulus
Sensitization
Increased response to a stimulus
Associative learning
- Classical conditioning
*Instrumental conditioning
Classical conditioning
Associating two stimuli (Pavlov’s dogs)
Instrumental conditioning
Associating a behavior and a response
The function of the Na+ / K+ - pump?
Sodium / Potassium pumpNa+ / K+ -ATPase-pump
Na+ / K+ ”exchange” pump
*
Active ion transporter, actively moves ions through the plasma membrane:
-
potassium (K+) inside the cell
- sodium (Na+) outside the cell
*
Produces an uneven distribution of Na+ and K+ ions in intracellular vs. extracellular fluids.
The Na+ / K+ -pump moves Na+ and K+ ions against their concentration gradients.
It produces and maintains transmembrane gradients for Na+ and K+ ions.
how does short memory become long-term memory?
Consolidation
( Working memory –a special form of short-term memory)
The factors that determine the resting membrane potential?
Resting membrane potential
At rest (no stimulation) most cells have a
negative (inside) membrane potential:
Nerve cells: -70 mV, muscle cells: -90 mV
the differences in ion concentration of the intracellular and extracellular fluids and
the relative permeabilities of the plasma membrane to different ion species.
Equilibrium potential for K+ ions (Ek) is around -100 mV
But:
RMP in neurons is -70 mV
The Nernst equation predicts the
equilibrium potential (E) for a given ion
Involvement of other ions to the RMP:
The Goldman equation
-
The RMP depends on the relative permeability of the membrane to several ions
-
However, at rest, the permeability of the membrane for Na+ ions is low, and it is high for K+ ions (PK»_space; PNa)
-
Na+ ions influence the RMP to a small degree
*RMP = difference in electrical potential across the plasma membrane at rest.
*The resting membrane potential of a cell is mostly determined by the flux of K+ ions across the membrane (which is more permeable to K+ than to other ions at rest), through non-gated (leak) K+ channels. Na+ ions affect the resting membrane potential to a small extent.
*K+ ions move passively across the plasma membrane down their concentration gradient (intracellular to extracellular) taking their charge with them.
*Intracellular side of the membrane becomes more negative, extracellular positive.
*An electrical gradient is generated, opposite to the chemical gradient.
*Positive charges on extracellular side of the membrane repel K+ ions.
*At electrochemical equilibrium there is an exact balance between 2 opposing forces: 1) concentration gradient, 2) electrical gradient.
*The equilibrium potential is the electrical potential generated across the membrane at electrochemical equilibrium. It can be predicted by the Nernst equation.
*The RMP can be predicted by the Goldman equation
The mechanisms involved in the production of action potentials?
*
Initial stimulus: a graded depolarization large enough to change resting potential (- 70 mV) to threshold level of voltage-gated Na+ channels (- 60 to - 55 mV)
*
Rising phase: the neuronal membrane becomes temporarily permeable to Na+ due to opening of more and more voltage-gated Na+ channels. The membrane potential depolarizes and approaches, but does not reach, ENa
*
Falling phase: Decrease in Na+ permeability (inactivation of Na+ channels) and delayed opening of voltage-gated K+ channels cause repolarization of the membrane toward EK and resting levels.
*
During the undershoot phase (afterhyperpolarization, AHP) the K+ permeability is greater than it is at rest.
*
All channels close. The membrane potential returns to resting levels.
*
All-or-none principle: If a stimulus is large enough to produce membrane depolarization to threshold, an action potential is triggered. If the membrane potential does not reach threshold, action potentials are not triggered.
*
With stronger stimulus intensities, the number of action potentials (firing frequency) increases, not their amplitude or duration.
-
Action potentials are initiated in the axon initial segment (AIS).
-
Action potentials are conducted along the axon.
-
Both AIS and axon contain voltage-gated Na+ channels and voltage-gated K+ channels.
The structure and function of myelin in the axon?
Layers of lipid membrane formed by glial cells (oligodendrocytes in the central nervous system, Schwann cells in the peripheral nervous system).
- It isolates the axon and prevents the passage of current through the axonal membrane.
Conduction velocity of action potentials:
- unmyelinated axons:
0.5 to 2.0 m/sec
- myelinated axons
3 to 120 m/sec
The different nerve fiber types and their conduction velocities?
motor axons fast
Sensory axons fast and slower
Autonomic preganglionic slow
in general Aa faster that Ab faster than Ac faster than Ad faster than C
Structure and function of electrical and chemical synapses?
electrical =
through gap junctions
Direct physical contact between cells
*
Passive ion current flow
*
Flow of substances (e.g., ATP)
*
Bi-directional synaptic transmission
*
Fast (minimal delay)
*
Synchronization of electrical activity among neurons
chemical=
the message starts before the axon hillock
and
initial segment
▪
Synaptic transmission occurs through chemical synapses between presynaptic and postsynaptic neurons.
▪
Neurons integrate incoming information on dendrites and soma.
▪
Neurons initiate and conduct action potentials along the axon
Ca+
The pre- and postsynaptic mechanisms of signal transmission in the chemical synapse?
pre- synaptic
Action potentials are conducted along the axon.
-
Both AIS and axon contain voltage-gated Na+ channels and voltage-gated K+ channels
+Saltatory action potential conduction along a myelinated axon through the nodes of ranvier
After nerve stimulation, the vesicles with the neurpthransmiter fuse together with the presynaptic membrane:
release of neurotransmitters = Exocytosis
Ca+ facilitates
post -synaptic
transmiter binds to the receptors and their channels open - then the current causes a post synaptic excitatory or inhibitory potential
The different groups and main role of neurotransmitters?
1.Small molecules
oAcetylcholine: Control of movement, cognition, autonomic control
oBiogenic amines (or monoamines):
-Catecholamines:
dopamine: affect, reward, control of movement
noradrenaline(norepinephrine): affect, alertness/wakefulness, ANS
adrenaline(epinephrine): visceral functions, stress, fear
-Indoleamines: serotonin (5-HT): mood, modulation of pain, gut regulation
- Imidazoleamine: histamine: arousal, attention
oAmino acids:
-GABAand Glycine(mostly inhibitory)
-Glutamateand Aspartate(mostly excitatory)
2.Neuropeptides
-
Opioids (enkephalin, dynorphin, endorphin): Control of pain
-
Somatostatin: Endocrine functions
-
Substance P: Perception of pain, inflammation, mood
3.Others/ ” non-classical ” (non-vesicular release
-
Neuroactive gases: nitric oxide (NO), carbon monoxide (CO)
-
Endocannabinoids (anandamide)
Neurotransmitters are chemical messengers that your body can’t function without. Their job is to carry chemical signals (“messages”) from one neuron (nerve cell) to the next target cell. The next target cell can be another nerve cell, a muscle cell or a gland.
The main classes of neurotransmitter receptors?
Slow synaptic transmission
*
Ionotropic receptors = Ligand-gated channels
-
Fast synaptic transmission
A neurotransmitter usually has several receptors
A neurotransmitter has both ionotropic and metabotropic receptors or only metabotropic receptors
The different types of postsynaptic potentials and how they are generated?
FAST TRANSMITIONS
EPSP =
Excitatory Postsynaptic Potential
Activation of excitatory (glutamate) synapse
Glutamate is released from the presynaptic axon terminal
Glutamate binds to ionotropic receptors (AMPA and NMDA)
Na+ ions enter the cell and cause depolarization (EPSP)
IPSP =
Inhibitory Postsynaptic Potential
Activation of inhibitory (e.g., GABA) synapse
GABA is released from the presynaptic axon terminal
GABA binds to ionotropic receptors (GABAA)
Cl- ions enter the cell and cause hyperpolarization (IPSP)
The phenomena of temporal and spatial summation?
Summation
of EPSPs
-
Temporal Summation:
Several times: rapid, repeated stimuli at the same synapse.
-
Spatial Summation:
Several places: many stimuli, arriving at several synapses
The different types of modulation of synaptic transmission?
1.Presynaptic inhibition
GABA release from nearby neuron- inactivation of Ca+ channels - less Ca+ in presynaptic neuron - less neurotransmiter
2 .Presynaptic facilitation
Serotonin release- activation of Ca+ channels - more Ca+ - more neurotransmiter released
The different types of synaptic plasticity?
Types of changes in synaptic strength:
- Synaptic Facilitation / Augmentation / Potentiation
- Synaptic Depression
Duration of the changes:
- Short-term (milliseconds to minutes)
- Long-term (hours to days or longer):
Long-term potentiation (LTP)
Long-term depression (LTD)
EEG?
EEG we get electrical activity diagrams of brain regions
Age makes EEG different
The main categories of ion channels?
leak chanels
Four main classes of gated ion channels
1.
Voltage-gated
2.
Chemically-gated / ligand-gated (e.g., by neurotransmitters)
3.
Mechanically-gated (stretch)
4.
Temperature-controlled (heat, cold)
The mechanisms involved in the production of graded potentials?
-
Also called local potential, receptor potential, postsynaptic potential.
-
Changes in the membrane potential.
-
Amplitude is proportional to stimulus strength.
-
Spread passively in the membrane but the amplitude decreases with distance.
-
Produced by a stimulus that opens ”gated” channels
key words
The mechanisms involved in the conduction of action potentials?
nodes of ranvier,voltage activated gated ion chanels
electrical and chmical synapses
Extracellular and intracellular ion concentrations?
Intracellular fluid =I
Extracellular fluid=E
Potassium (K+)
High (140 mM) =I
Low (5 mM)=E
Sodium (Na+)
Low (5-15 mM)=I
High (145 mM)=E
Chloride (Cl-)
Low (4-30 mM)=I
High (110 mM)=E
Calcium (Ca2+)
Low (0.0001 mM)=I
1-2 mM=E
Four main classes of gated ion channels:
1.
Voltage-gated
2.
Chemically-gated / ligand-gated (e.g., by neurotransmitters)
3.
Mechanically-gated (stretch)
4.
Temperature-controlled (heat, cold)
what is Graded potential?
-
Also called local potential, receptor potential, postsynaptic potential.
-
Changes in the membrane potential.
-
Amplitude is proportional to stimulus strength.
-
Spread passively in the membrane but the amplitude decreases with distance.
-
Produced by a stimulus that opens ”gated” channels
LTP in the hippocampus CA1early phase: induction and expression
Induction of LTP:
→ tetanus (rapid, intense stimulation)
→ strong postsynaptic depolarization
→ activation of NMDA receptors
→ flood of Ca2+ through NMDA receptors
→ activation of PKC and CaMKII
Expression of LTP
→ insertionofAMPA receptors at the synapse
→ strengthening of synaptic transmission (LTP)
Threshold for action potential is ?
-50 to -55
Absolute refractory period
= during that period a second stimulus can not activate a second action potential cause the Na+ ion gated channels are inactivated
Why an action potential can not go the other direction ?
refractory period
Explain how total body water (TKV) is normally distributed between the intracellular (ICV) and extracellular (ECV) spaces, and describe osmolarity in the ECV and ICV, under normal conditions.
2/3 intracelular and 1/3 extracelular
3/4 of extracellular water is intersitial and 1/4 is plasma.
Osmolarity Intracellular = Osmolarity extracellular
