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• Dorsal root-- somatosensory
• Ventral root--motor
+Amygdala --stria terminalis--> hypothalamus
+Amygdala--> hippocampus, entorhinal cortex and frontal cortex
+entorhinal cortex<--> hippocampus
+hippocampus <--fornix--> septal nuclei
+hippocampus --fornix--> mammillary bodies--> mammillothalamic tract--> anterior nucleus of thalamus --> cingulate gyrus--> entorhinal cortex
1. olfactory: sensory smell
2. nerve: sensory eyes
3. occulomotor: motor sise to side, in, dilation
4. trochlear: motor eyes down
5. trigemenical: sensory face, motor mastication
6. abducens: side to side eye movement, lateral,
7. facial: motor facial expression, sensory 2/3 anterior tongue
8. vestibulocochlear: sensory hearing and balance
9. glossopharyngeal sensory poster 1/3 tongue, motor throat
10. vagus: sensory and motor viscera
11. spinal accessory: motor shoulder and neck
12. hypoglossal: motor tongue
has a single branch that leaves the cell body and then extends in two directions one end is the receptive pole, the other end the output zone
Parietal: Somatosensation (Touch), Spatial Cognition.
– Damage can cause hemineglect
meninges=layers of spinal cord/brain protective membrane
inner= pia mater
middle = arachnoid
outer = dura mater
liquid that is inside of your meninges
-chemical composition close to seawater
compares levels of activity across different brain regions by using a powerful magnetic field to measure Blood Oxygen Level Dependent (BOLD) signals
fMRI is a non-invasive
function magnetic resonance imaging
-measures brain's BOLD signal (blood O2 level dependent signal)
-measures brain activity indirectly
-good spatial resolution
-bad temporal resolution
The sum of the electrical and chemical forces is called the driving force. The direction of the driving force determines which way an ion “wants” to flow across the membrane.
An ion is said to be at equilibrium when the driving force upon that ion equals zero. Note that it is possible (indeed, common) for one ion to be at equilibrium while others are not.
-55 to -80 mV, meaning that the inside of the cell is more negatively charged than the outside.
If spatial and/or temporal summation can depolarize the axon hillock above spike threshold, then an action potential occurs and the story begins all over again
Local anesthetic drugs (such as lidocaine and novocaine) block somatosensation by blocking the active zone sodium channels
Metabotropic G-protein coupled Receptors
igand is a second messenger molecule that binds the channel inside the cell rather than outside the cell
Glutamate can be synthesized from the amino acid glutamine by an enzyme called glutamine aminohydrolase
An enzyme called glutamate decarboxylase (GAD) converts glutamate into GABA by removing carbon dioxide from the molecule.
So both excitatory and inhibitory neurons produce glutamateThe only difference between them is whether they express the gene for the GAD enzyme!!!!!
ligands of a receptor are chemicals normally found in the body which bind to the receptor
ligands of a receptor are compounds not found in the body that, when introduced into the body, can affect the receptor in one of two ways:
• Agonists bind to the receptor and activate it in much the same way as its normal endogenous ligands (sometimes even more so)
• Antagonists bind to the receptor and prevent it from being activated by its normal endogenous ligand. (competitive or non competitive)
egulates the docking and fusion of neurotransmitter vesicles in synaptic boutons (found in all neurons).
we could make GABA neurons expresses GFP by conjugating the GAD67 promoter to the DNA sequence that encodes GFP.
To control which cells a gene is expressed in, we attach it to a cell-specific promoter sequence.
Blue light opens the channel to excite the neuron. OPENS THE CHANNEL TO DEPOLARIZE THE NEURON, WHICH GENERATES EPSPs OR SPIKES, DEPEND- ING ON STRENGTH OF THE LIGHT
So blue light will generate a Light-evoked Excitatory Potential (LEP) at all locations throughout the cell. If the LEP depolarizes the cell above spike threshold then the neuron will fire an action potential.
GREEN LIGHT CAUSES THE NEURON TO GIVE OFF A FLOURESCENT GLOW (SO WE CAN SEE THAT IT CONTAINS THE CHANNELRHODOPSON PROTEIN)
So yellow light will generate a Light-evoked Inhibitory Potential (LIP) at all locations throughout the cell. The LIP hyperpolarizes the cell and prevents it from reaching spike threshold.
The brain is supplied with oxygen and nourishment by a network of blood vessels (capillaries) that permeate the entire brain
cAMP is inactivated by an enzyme called phosphodiesterase (D2 inhibition)
Caffeine (the world’s most widely used drug) blocks cAMP PDE and thus
increases cAMP (similar to D1 receptor activation)
Norepinephrine participates in controlling arousal and attention:
• low NE levels are associated with sleep.
• medium NE levels are associated with waking
• high NE levels are associated with anxiety and distractibility
G-proteins coupled to inhibition of the postsynaptic cell, or release of calcium from intracellular stores
• a-adrenergic agonist drugs are used as decongestants, pupil dilators, and to increase blood pressure
• a-adrenergic antagonist drugs (“alpha-blockers”) are commonly used to lower blood pressure in patients suffering from hypertension
G-proteins coupled to second messenger pathways that usually produce excitation of the postsynaptic cell
• b-adrenergic agonist drugs have important medical uses (e.g., albuterol inhalers for asthma), but can cause side effects such as hyperactivity, attention deficit, and panic attacks
• b-adrenergic antagonist drugs (“beta-blockers”) can be anxiolytic
mechanisms for disabling the transmitter:
A) Catabolism (chemical breakdown by enzymes)
B) Active transport (re-uptake of the transmitter into the presynaptic cell or into glia)
Catecholamine reuptake inhibitors
psychoactive drugs increase availability of dopamine, noradrenalin, and adrenalin at synapses by blocking reuptake in three ways:
The drug causes the transporter to be internalized into the presynaptic cell membrane, so it is no longer able to remove transmitter from the synapse
The transporter sucks up the drug instead of the neurotransmitter, which prevents the transmitter from being taken up
The drug causes the transporter to reverse direction and push neurotransmitter in the opposite direction across the membrane:
• Vesicular transporters dump transmitter out of vesicles into the cytoplasm
• Synaptic transporters dump transmitter out of the cytoplasm into the synapse
synthesized from the amino acid tryptophan
agonists treat anxiety, depression, LSD, antidepressant, molly
n the peripheral nervous system, acetylcholine is the excitatory neuro- transmitter release by motor neurons to activate muscle fibers at the neuromuscular junction
• muscle relaxants
• Muscarine (for which the receptor is named) is a nerve toxin found in some species of poisonous mushrooms
• Atropine is used for surgical anesthesia and
to treat bradycardia (slow heart rate)
• Scopalamine is used in low doses to treat motion sickness; at higher doses it causes amnesia
activation causes analgesia, euphoria, addiction,
Endogenous agonists: endorphins, enkaphalins
Exogenous agonists: morphine, fentanyl
Exogenous antagonists: naloxone (used to treat acute opiate overdose), naltrexone (used to treat chronic addiction to various drugs), oxycodone, hydrocodone
surround the canal is therefore called the ventricular zone. divide and create new cells
The outer regions of the neural tube are called the marginal zone
Once cells have chosen a fate they stop dividing and migrate from the ventricular zone by radial glia to to enter the marginal zone, where they will form the brain and spinal cord
1) Time of birth: When a cell is born in the ventricular zone cells born early end up in deep layers (near ventricles) and cells born later end up in superficial layers (near brain surface).
– 2) Cell-to-cell signaling: Cells can communicate with one another via growth factors, adhesion molecules, hormones, neurotransmitters, etc. to influence one another’s fate during development.
neurons grow in size by extending growth cones outward from their cell bodies, which form the long processes that will become the neuron’s dendrites and axons.
– Controls reflexive behaviors such as coughing, gagging, vomiting, swallowing, sneezing
Hypothalamus and its hormone systems are involved in certain weight and sleep disorders, and may also contribute to anxiety disorders, violent behavior, and other mood problems.
Known as the “gateway to the cortex.” Sensory/motor information passes through the thalamus on its way to/from the cortex:
– Damage can cause blindness
Temporal: Hearing, Taste, “Declarative” Memory.
– Damage can cause hearing loss, amnesia
Frontal: Motor Control, Planning, Decision Making
– Damage can cause paralysis, personality disorders
Cingulate: Motivation, Emotion, Memory
Ischemia: Caused when a blood vessel is blocked by an embolism or blood clot, starving the brain of oxygen and glucose
– Hemorrhage: Caused when blood vessel bursts and bleeds into the brain
Nuclei - collection of soma in CNS
Ganglia - Collection of soma in PNS (not basal ganglia motor commands)
-slow but long
-Na and K channels all the way down the axon
very fast but not very far
can be ionotropic or metabotropic
-Na+ and K+
-ionotropic (Cl-) or metabotropic (K+)
in neurons located in the raphe nuclei and other nearby areas,