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135 Cards in this Set

  • Front
  • Back
The study of the effects of drugs on the nervous system and on behavior
Drug effects
2. Sites of Action
The changes a drug produces in an animal’s physiological processes and behavior
2. The locations at which molecules of drugs interact with molecules located on or in cells of the body, thus affecting some biochemical processes of these cells.
The process by which drugs are absorbed, distributed throughout the body, metabolized, and cleared.
Routes of Drug Administration (1)
Intravenous (IV) injection
Injection of a substance directly into a vein (the ultimate goal is to get a drug to the site of action; the easiest way to do this is get it into the bloodstream)
Intraperitoneal (IP) injection * USU ANIMALS
The injection of a substance into the peritoneal cavity-the space that surrounds the stomach, intestines, liver, and other abdominal organs. Easy for animal use but not typical for humans.
Intramuscular (IM) injection
Injection of a substance into a muscle. Usu for diabetes/insulin. Absorbed into bloodstream from capil vents.
Subcutaneous (SC) injection* USU ANIMALS
2. Oral administration
Injection of a substance into the space beneath the skin. Often animals vs humans. 2. Administration of a substance into the body by swallowing (to stomach enzymes to bloodstream, as nutrients are)
Sublingual administration
2. Intrarectal administration
Administration of a substance by placing it beneath the tongue
Usu when swallowing is risky (gag reflex) or unable. 2. Administration of a substance into the rectum
2. Intranasal
Administration of a vaporous substance into the lungs (or burn a solid to release gases, e.g. cigarettes) 2.“Snorting”…powder delivered to bloodstream via capillary beds in the nasal epithelium [not usu into lungs?]
Transdermal administration
2. Intracerebral administration* (ANIMALS)
Administration of a substance absorbed through the skin (not topical administration)
2. Administration of a substance directly into the brain *(Usu in animals)
Intracerebroventricular (ICV) administration
Administration of a substance into one of the cerebral ventricles. (More likely to be in humans vs animals, ICV)
Routes of Drug Administration: Comparison of Plasma concentration
Intravenous (most concentrated and fastest), intranasal; smoked (less long lasting but fast), oral. Different amounts per route; lower amount for intraven.
Dose-Response Curve
Amount of drug nec for some effect (effect changes in response to drugs). The working range: straight portion; systematic, incremental effects w/ dose inc. Start dosage in wking range.
Dose-Response Curve: Margin of Safety
Between dose-resp curve for analgesic effect of morphine and depressive effect on respiration. Ex. Ibuprofine, large margin of safety.
Effects of Repeated Administration
1. Tolerance
A decrease in the effectiveness of a drug that is administered repeatedly.
A larger dose of drug is required to get the same behavioral/therapeutic effect
“Reverse Tolerance”
**Tolerance shifts dose-resp curve right. (These effect the margin of safety, unless curve for side effects shifts too)
2. Withdrawal
An increase in the effectiveness of a drug that is administered repeatedly.
A smaller dose of drug is required to get the same behavioral/therapeutic effect
Shift d-r curve left.
2. Symptoms opposite to those produced by the drug
Appears when drug is administered repeatedly and then suddenly no longer taken
Placebo effect
An inert substance given to an organism in lieu of a physiologically active drug
Used experimentally to control for the effects of mere administration of a drug
Rarely used clinically (ethical issues)
Two Broad Classes of Drugs
1. Antagonist 2. Agonist
Opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell 2. Facilitates or mimics the effects of a particular neurotransmitter on the postsynaptic cell.
Potential Sites for Drug Action 1)
1) Drug serves as a precursor (AGO); Inc amount of NT by providing precursor. 2) Drug could block/inactivate synthetic enzymes (inhibits syn of NT) Blocks conversion of precursor to NT (ANTAG)
Potential Sites for Drug Action 3) 4)
3) Drug prevents storage of NT/TS in vesicles (ANTAG) 4) Drug stimulates release of NT (AGO), release of NT already in vesicle vs 1) for increased amount.
Potential Sites for Drug Action 5) 6)
5) Drug that inhibits release of NT (ANTAG) 6) Drug that stim post-syn receptors (AGO) (after binding)
Potential Sites for Drug Action 7) 8)
7) Drug that blocks post syn receptors (ANTAG) 8) Drug that stimulates autoreceptors (on presyn mem, reg feedback for NT release), inhibits synthesis.
Potential Sites for Drug Action 9) 10)
9) Drug that blocks autorecep; inc syn/release of NT (AGO) 10) Drug that blocks reuptake (AGO), Prolong life of NT
Potential Sites for Drug Action 11)
11) Drug that inactivates acetylcholinesterase. AGO; NT not degraded, still effective.
Sites of Action on Ionotropic Neurotransmitter Receptors
Agonist (ex. ion channel opens)
Binding site
Ion pore (ex. act at binding site to NT receptor to shut off ion channel or plug up pore)
Metabotropic Neurotransmitter Receptors
Many potential drug interac sites (to G proteins; intracell messenger; ion channels; downstream messages) vs two of ionotropic recep.
Classification of drugs that act directly on NT receptors
Competitive binding (w/ same or opp effect) Direct AGO or ANTAG. Noncompet binding: Indirect AGO (not binding at same receptor pt as NT; still binds at recep) Inverse AGO (drug that is noncompet, produces opp effect of NT (ex channel to close). (*ANTAG effects but termed AGO b/c binds to postsyn recep.)
Drug exposure leads to:
2) Withdrawal effect:
The deveol of adaptive neural changes that produce tolerance by counteracting the drug effect. 2) With no drug to counteract them, the neural adaptations produce w/drawal effects opposite the effects of the drug.
Tolerance as a learned behavior
Contingent Tolerance
2) Conditioned Tolerance
Drug tolerance that develops as a reaction to the experience of drug effects rather than to drug exposure alone 2)
Tolerance effects are maximally expressed when a drug is administered in the same situation in which it has previously been administered.
Therapeutic uses of drugs
Addictive properties of drugs
Effects on behavior
Effects on neurotransmitter systems. Well funded area of research.
Monoamines and “Good Times”
Many drugs that are associated with addiction affect the monoaminergic systems—why?
Three major dopaminergic systems:
2) Catecholamines
2) All from Tyrosine precursor->L-Dopa->Dopamine(DA) (precursor molecule for:) -> Norepinephrine (NE) (Precursor for:) -> Epinephrine. *AMPT blocks conversion of Tyro to LDopa and affect the following three NTs (Antag)
Mesolimbic DAergic System
Soma lie in the Ventral Tegmental Area (VTA) in the brainstem
Axons project to the nucleus Accumbens and amygdala; associated with reward
Implicated in addictive properties of drugs (usu) See diagram.
Mesocortical DAergic system
Soma lie in the VTA
Axons project to prefrontal cortex; involved in planning behavior and remembering the significance of stimuli
Also may play a role in short-term memories (Difficult to find areas of brain NOT affected -> highly distributed pathway) Ex. cocaine (~memory, reward, planning, ex. seeing razors)
Nigrostriatal DAergic system
Soma lie in the substantia nigra (“dark substance”)
Axons project to the Corpus Striatum, which is involved in coordinating movements
Loss of DAergic cells in the substantia nigra in Parkinson’s disease leads to progressive motor deficits
Drugs that affect Catecholamines
Inhibition of storage: (Reserpine;
Makes synaptic vesicles “leaky”)
Block reuptake:
(Cocaine blocks dopamine reuptake, AGO, stays in synapse longer)
Block reuptake + facilitate release:
(Amphetamine—reverses reuptake mechanism, spills into synapse)
Serotonin Synthesis:
Tryptophane converted to 5-hydroxytryptophan converted to 5-hydroxytryptamine (aka, 5-HT or Serotonin). PCPA blocks conversion to 5-hydroxy...phan.
Serotonergic system
Raphe nuclei: moderate-size cluster of nuclei found in the brain stem, and releases serotonin to the rest of the brain.[1] Selective serotonin reuptake inhibitor (SSRI) antidepressants are believed to act in these nuclei, as well as at their targets; cell bodies projecting through cortex, cerebellum, and thalamus, and basal ganglia (involved in motor func).
Drugs that affect Serotonin
At least nine different receptor types
Reuptake Inhibitors
Selective Serotonin Reuptake Inhibitor (SSRI)
Example: Fluoxetine (Prozac)
Effective antidepressants
Drugs that affect Serotonin
Reuptake Inhibition + Release Facilitation
Fenfluramine (Half of “Fen-Fen”)
MDMA (“Ecstacy”)
Reverses the reuptake mechanism
Also affects norepinephrine
Direct Agonists
ACh Receptors
see slide 2) Nicotinic
Found in brain, skeletal (striated) muscle
Found in the brain, salivary glands, sympathetic ganglia, heart (smooth) muscle, eye, stomach, colon, bladder
Drugs that affect ACh: Curare and Botulinum toxin
Curare—blocks nicotinic receptors
Results in paralysis due to inability to get signals from motor neurons to muscles
Botulinum toxin—prevents ACh release
Results in paralysis due to inability to get signals from motor neurons to muscles
Drugs that affect ACh: Black Widow Spider venom & Atropine
Black Widow Spider venom—Facilitates ACh release
Results in a myriad of symptoms due to its non-specific effects
Atropine—blocks muscarinic receptors
Results in mouth dryness, pupillary and bronchial dilation, decrease in secretions
Glutamate (Glu; Glutamic Acid)
Amino acid neurotransmitter
Most important excitatory neurotransmitter in the brain
Produced in neurons by metabolism
No effective way to block synthesis without disrupting other cell activities
Glutamate Receptors
Four major kinds:
Kainate (Ionotropic)
Metabotropic glutamate receptor (mGluR)
-Excitatory effect if stimulated.
2) Kainate
Stimulated by AMPA (a-amino-3-hydroxy...) Most common Glu receptor
Ionotropic; Na+ channel 2) Stimulated by Kainic acid
Ionotropic; Na+ channel; EPSP
NMDA and has *Binding sites for:
Activated by NMDA (n-methyl-d-aspartate)
Ionotropic; permeable to Na+ and Ca2+
Includes six different binding sites
Four on extracellular surface
Two deep within ion channel (w/in pore) See diagram. *Binding sites for: Glu, Zn 2+, Glycine, Polyamine, PCP, MG 2+, the latter two are inside.
When Mg or PCP bind to binding sites the flow of ions through channel is blocked, does not happen often for PCP. When neurons are at rest, MG 2+ is binding -> blocking NMDA channel under normal conditions. (Glu does not need to be present; sep binding site) High affinity; when Glu binds as well - no ion flow... Diagram 2. During postsyn depol: Mg 2+ becomes unblocked from receptor - expelled. Glu binding DOES allow ions to flow into postsyn cell. **Voltage dep. (Mg 2+ binding only at resting poten). NA+ and Ca 2+ entry only after postsyn mem depol; important for learning and mem. Only takes Glu or another to open. PCP probably not voltage dep.
Activated by NMDA
Includes six different binding sites
Four on extracellular surface
Two deep within ion channel
Ionotropic; permeable to Na+ and Ca2+
Blocked by Mg2+ at rest
Dynamic Regulation of Synapses

1)Strong EPSP
2)AMPA + NMDA activation (unblocked recep)
3)Ca2+ influx (can be used by many intracell 2nd messengers); Leads to phosphor of other substrates -> AMPA recep become inserted into post syn mem. Inc number of AMPA recep. Contribution to learning: The next presyn action poten -> postsyn poten will be greater than before b/c more Na+ influx after Glu binds -> stronger depol. Quicker rise to max voltage b/c more Na+ ch oppen, inc EPSP at synapse. Ex. More likely to respond; NTs recog. Strengthed synapse, info through more often and quickly. Not nec long-term storage but short-term acquisition. ***Longterm potentiation, LTP.
Dynamic Regulation of Synapses

[LTP: process of strengthening synapse; by an AMPA recep-dep mechanism; when no longer blocked by Mg+]
4)Intracellular signaling
5)AMPA receptors inserted in the postsynaptic membrane adn become active/functional. [Depol of cell due to Na+ vs Ca 2+]
Synaptic Regulation: Silent Synapses
A) Stimulation (voltage clamp method) Post syn current. Ion eff/in(Na through AMPA recep)flux for 3 ms. B) Influx of Ca 2+ via NMDA recp (Before, pore blocked; depol of mem; ejected Mg)
Synaptic Regulation: Silent Synapses
*A lot more NMDA recep than AMPA along dendrites. Silent syn more prevalent along NMDA; usu info would not get through->only NMDA rec present->no EPSP since Mg would block Na&Ca entry. Many silent syn in brain. Function: possibly waiting for appropriate info exchange. (Silent syn converted to AMPA for important info to get through) Devel in part (silent syn) from aging. -Juv vs Adult rat brain (more AMPA-R) Process allows silent syn (only NMDA-r present) to become more responsive w/ maturation.
Two main receptor types
-- Synthesized from Glutamate:
Glu + Glutamic Acid Decarboxylase (GAD) -> GABA
Two main receptor types
Ionotropic; Cl- channel
Metabotropic; K+ channel
--Activation of either receptor -> IPSP
GABA A Receptors
Binding sites for: GABA, Picrotxin, Steroids, Benzodiazepine, Barbiturate (the latter three are indirect AGO of GABA A recep; do not block binding of GABA) All potentiate effects of GABA binding; other sites besides GABA enhance effects of NT) {Barbiturates: Anti-anxiety, anesthesia, anti-convulsant; site of action for alcohol?] [Benzos” Anti -anxiety]
Longer molecules made up of many amino acids
Peptides are manufactured in the soma and transported to terminals
Most neuropeptides are Neuromodulators, but some are neurotransmitters (e.g. some are classified as endogenous opioids)
Endogenous Opioids
Receptors are stimulated by opiates (Heroine, opium, morphine)
Three types of receptors
Enkephalins: first discovered endogenous opioids
Important for analgesic effects
Often abused because of its effects on the “reward pathway”
Lipid Neurotransmitters
Derived from fat molecules
Endogenous ligands for the Cannabinoid receptors
Very little is known about function of these systems in the normal brain
Agonists such as THC (active ingredient in marijuana) produce analgesia, sedation, and relieves nausea
Also interferes with cognition, concentration, memory, alters visual and auditory perception
Anandamide: first endogenous cannabinoid discovered
1) Example: Adenosine
Based on a sugar molecule
Converted to nucleotides by specific kinases
1) Neuromodulator not NT;
Present in all cells;
Released when cell is short of fuel or oxygen; causes dilation of nearby capillaries
Three different types of adenosine receptors
Receptors usually suppress neural activity (IPSP)
Activation of adenosine may be associated with controlling sleep
Adenosine receptor (blocking results in) antagonists result in increased alertness and improved mental function Ex. Cup of Aden recep blocker -> Coffee => Stimulates GABA A Recep while blocking Aden.
Soluble Gases
- Not strictly NTs. Example: Nitric oxide
Synthesized by nitric oxide synthase (NOS)
Used as a chemical messenger (for other cells but cannot receive N. oxide signal)
No Receptors
Diffuses out of the cell as soon as it is produced (Nitric Oxide is used as a retrograde signal->back on pre-syn cell influencing transmission; regulatory role in)
Activates an enzyme responsible for producing a second messenger molecule (cGMP)
An imaginary line drawn through the center of the central nervous system, between the front of the forebrain and the bottom of the spinal cord
All directional terms that are used in neuroscience describe locations relative to the neuraxis
Direct AGO: 1.
Direct Antag: 2.
LDOPA vs DA: 3.
1. Mimics NT 2. Receptor blockers. 3. Can cross BBB
ACh receptors: Ionotropic (1) vs Metabotropic (2)
1) Stim by nicotine/nicotinic recep. Rapid. Blocked by Curare (paralysis, faster than botulinumtoxin) 2) Stim by muscarine/Muscarinic recep. Slower/prolonged, more numerous in CNS. Atropine blocks Muscarinic recep.
Monamines: Catech (Tyrosine-LDOPA-DA-NE) DA: 1) 2) 3)
From midbrain; 1) Nigrostriatal sys (movement; Parkinsons) 2) Mesolimbic sys (VTA; reinf) 3) Mesocortical sys (VTA; planning; prefrontal)
DA: Two Receptors 1. 2.
1. D1; postsyn. 2. D2; presyn & postsyn; blocked by Chlorpromazine.
DA Agonists:
1) Amphetamines (rel of DA and NE to cleft) 2) Cocaine (blocks NA channels; ex. as topical anesthetic) 3) Methylphenidate (Ritalin)
-Overactivity of DA leads to Schizophrenia; Chlorpromazine blocks D2 recep.
NE (cell bodies begin in: ___) 2) Released through: ___ 3) Receptor types/Adrenergic receptors (usu CNS or as hormones in PNS):
1) Locus Coeruleus (in dorsal pons; vigilance) 2) Axonal Varicosities (vs terminals) 3) [Metabotropic] B 1, B 2, alpha 1, alpha 2; Autorecep. blocked by idazonan (AGO)
Deprenyl is an DA AGO, esp rel in terminal. Destroys:
MAO B. MAO regul/destroys catech.
Trytophane -> Serotonin. AGO for 5-HT:
1) Fluoxetine/prozac 2) fenfluramine 3) LSD is a direct AGO for recep. 4) MDMA (also norad. ago; excit and halluc; backwards; NE release and inhib reuptake)
Most common NTs in CNS: 1) Glutamate 2) GABA
[evolved first]
1) Receptor types: NMDA, AMPA, Kainate, Met. Glut. recep. 2) Recep types: GABA A (w/ 5 binding sites) and GABA B.
Another common NT in CNS:
Glycine (inhib; spinal cord; low brain) Recep (iontro); Cl- channel.
5 binding sites for GABA A:
1) GABA 2) Benzod (AG) 3) Barbit (AGO) (No natural ligands?) 4) Steriods 5) Picrotoxin (ANTAG) (No natural ligands?)
The fastest way to have a drug reach the brain is through: 2) The most common route for small animal drug injec: 3) The therapeutic index:
1) Intravenous injec. 2) Intraperitoneal 3) A measure of a drug's margin of safety.
1) Drugs that bind w/ and stimulate dendritic autorecep: 2) For most NTs, termination of the postsyn poten occurs when molecules of the NT are: 3)*Acetylcholine:
1) Produce in inhib depol. 2) taken back into the terminals. 3) The first NT discovered; all muscle movement is stim by its release; once deactiv, choline is returned to terminals and recycled.
1) The precursor of DA and NE is __ and their synthesis is interrupted by __. 2) The halluc. LSD produces its effect by interacting w/ __ neurons.
1) Tyrosine; AMPT 2) serotonergic.
1) One of the nec condit for NMDA recep to open is: 2) Benzod bind w/ __ recep and __. 3) Many peptides are rel along w/ a NT may serve to regulate the: 4) Endogenous opiods are:
1) Depol of mem. 2) GABA A, have an anxiolytic effect. 3) Sensitivity of nearby postsyn recep. 4) neuromodulators produced in brain.
Rostral/Anterior: ___ Caudal/Posterior: ___
1) Toward the head from the neuraxis. 2) Toward the tail; more specific.
Dorsal: ___ Ventral: ___
1) Toward/on the back. 2) Toward the belly. Ex The hindfeet are caudal to forefeet.
Lateral: ___ Medial: ___
1) Toward the side. 2) Toward the middle (dep on what side you are) Heart is medial in respect to arms. Right eye in dorsal laterally to neuraxis.
Bend 90 degrees in neuraxis. 2) Toward the feet. Ex. back of head - caudal end of brain. 3) vs rostral in brain. 4) Toward chin.
Directional Terms in Brain
Rostral (face side) Dorsal north of brain. Cerebellum on ventral end.
- Subdural hematoma:
On the same side as…
On the opposite side of…
- Nerve damage-blood spills onto brain.
The Meninges (Gr.; “membranes”)
1) Dura mater 2) Arachnoid mater 3) Subarachnoid 4) Pia mater
1) Outside of mem; 'tough mother.' In humans as thick as paper. 2) spider mother; difficult to locate 3) Blood vessels in brain and where cerebrospinal fluid flows. 4) very close contact w/ brain and follows grooves and blood vessels.
Cerebrospinal Fluid (CSF)
Ventricles (“little bellies”)
Four hollow spaces located inside the brain
Each ventricle contains a specialized network of blood vessels called the choroid plexus that produces CSF
The CSF supports the weight of the brain (ex. air in balloon)
CSF helps reduce shock to the CNS caused by sudden head movements (w/ mininges) PAD: pia, ar, dura.
Human devel
Stages 1-12 -> first month; most func of/neural devel (cannot reliably det if preg).
1) 16 days after fertilization
1) Neural plate, flat struc. Primitive node: primitive streak (fold in plate) Notochord: beneath neural plate (Makes us chordates, vertebrates subgroup) Cells around NC rel chem so above cells thicken and prim streak forms (groove)
2) 20 days
Thicken cells scrunch up (Neural groove of plate) Neural plate elongated; neural groove where chord was.
3) 22 days
3) Cells fuse, NG closes to neural tube. Neural fold. Tube begins from middle. Former plate becomes brain struc vs end of spinal cord. Cardiac bulge becomes heart.
4) 24 days
4) Almost completely closed. Neural folds will become cerebral hemis. Neural tube formation and closure complete by day 24.
Neural Tube Closure Defects
Brain (vs stem) does not develop. No skull. Occurs once every 2000 preg (may not be still born) Live up to a couple of days. Neural tube does not fully close.
Water Brain. Enlarged cerebral ventricles. Affects one out of every 500 live births to varying degrees (maybe cured).
Spina Bifida
Meningocele: mild outcropping. Myelocele: protrusion of spinal cord out through back. Still may be repaired maybe even in utero. May be paralyzed. Occurs in 1/1000 live births (not very rare).
Related to above; about 1/5000. Protrusion of brain outside skull. 2) Folic acid (veg; vitamins)
10 week human fetus
2) 20 week human fetus
Brain is 1.25 cm (0.5 in) long and mostly ventricle
2) 5 cm (2 in) long with basic brain shape (still mostly ventricles)

See Diagrams!!!
End product is approximately 1400 g (3 lb) (Most new neurons/tissue to forebrain vs hind/mid)
Neuron Birth and Proliferation
-Founder cells
Cells of the ventricular zone that divide and give rise to cells of the central nervous system
Symmetrical division (mitosis)
Division (in first 20 wks) of a founder cell that gives rise to two identical founder cells; increases the size of the ventricular zone (vs struc) and hence of the brain that develops from it.
Number of cycles of symmetrical division may account for the enlargement of the brain across species evolution
Asymmetrical division (mitosis)
Division of a founder cell that gives rise to another founder cell and a neuron, which migrates away from the ventricular zone towards its final place in the brain (usu too many neurons...) 2. Apoptosis (literally, a “falling away”)
Death of a cell caused by a chemical signal that activates a genetic mechanism inside the cell
Also known as “programmed cell death”
Radial glia
Special glia with fibers that grow radially outward from the ventricular zone to the surface of the cortex
1) Gyri
2) Sulci and fissures
3) Gray vs white
1) Bulges betwn sulci/fissures; often contain cells that have a specific function. 2) Delineate brain sec; small vs large grooves. 3) Cell bodies vs axons/myelin.
1) Central sulcus
2) Forebrain
1) Sep the frontal and parietal lobes. 2) Telencephalon (gray matter/cerebrocortex) and diencephalon (subcortical structures/thalamus)
1) Midbrain 2) Hindbrain
1) Mesencephalon 2) Metencephalon (cerebellum) and mylencephalon (superior: main vision center in animals w/o neocortex; inferior: hearing...)
Important struc of limbic sys: 1 and 2
3) Dienceph. surrounds:
1) Hippocampus 2) Amygdala 3) Third ventricle, has the thal and hypothal.
1) Neurons in hypothal: 2) Ant pit gland 3) Tectum structures:
1) Autonomic and endocrine sys. 2) gonadotropic hormones 3) Sup/Inf Colliculi
1) Vagus nerve controls: 2) Preganglionic axons:
1) Parasym func of organs in thoracic and ab cavities. 2) Leave the spinal cord through the ventral root.
1) Ventricles 2) Cerebralcortex 3) Meninges
1) Hollow spaces w/in brain. 2) Outmost layer of gray matter in the cerebral hemis. 3) Three tissue layers encasing the CNS
1) Autonomic 2) Fornix 3) Nucleus
1) Controls vegetative func. 2) Fiber bundle connec the hippocampus w/ other parts of brain. 3) Group of neural cell bodies in CNS.
Unilateral neglect is
2) Frontal Section
3) Midsagittal
Associated with damage to the right parietal lobe. 2) A slice through the brain parallel to the forehead. 3) Parallel to ground.
1) Cross section 2) Brain stem 3) Dorsal root
1) Right angles to neuraxis. 2) From medulla to dienceph (Not cerebellum) 3) Spinal root w/ afferent sensory fibers.
1) Limbic sys 2) Spinal cord
1) Ant. Thalamic nuclei, amygdala, hippocampus, limbic cortex, parts of hypothal. 2) Extends caudally from medulla.
1) Thalamus 2) Dorsal root ganglion 3) Lateral fissure
1) Largest portion of dienceph above hypothal; w/ nuclei proj info to regions of cerebral cortex. 2) Cells of afferent spinal nerve neurons. 3) Sep temporal from overlying frontal and parietal lobes.
1) Neocortex 2) Midbrain 3) Red nucleus
1) Prim sensory cortex, prim motor cortex, and assoc cortex 2) Mesenceph. 3) Of midbrain w/ inputs from cerebellum and motor cortex and sends axons to motor neurons in spinal cord.
1) Parietal lobe 2) Spinal roots caudal to end of spinal cord.
1) Region of cerebral cortex cadual/behind to frontal lobe and dorsal/above to temporal lobe. 2) Cauda equina
1) Region of midbrain surrounding cerebral aqueduct; contains neural circuits involved in species-typical beh. 2) Peripheral nerve attached directly to brain.
1) Periaqueductal gray matter. 2) Cranial nerve
1) Nucleus of thal receiving inputs from cerebellum and sending axons to prim motor cortex. 2) Hindbrain
1) Diencephalon-Thalamus: (vs Lateral Geniculate Nucleus and Medial G. N) Ventrolateral nucleus 2) Contains met and myelenceph.
1) Temporal lobe 2) Center of metenceph, located btwn cerebellum and dorsal pons. 3) Spinal root with efferent motor fibers.
1) Rostral/(in front of) the occip lobe and Ventral/below to parietal/frontal lobes. 2) Fourth ventricle 3) Ventral root.
Major divisions of CNS vs PNS 1)
2) The Subarachnoid space...
1) Brain and spinal cord vs. Nerves and Peripheral ganglia. 2) Filled w/ cerebrospinal fluid and Arachnoid trabeculae.
1) Midbrain -> Ventricle:
2) Hindbrain -> Ventricle:
1) Cerebral aqueduct -> Mesen. -> Tectum/Tegmentum. 2) Fourth -> Meten -> Cerebellum (pons)
1) Forebrain -> Ventricle:
1) Lateral -> Telenceph -> Cerebral cortex, (basal ganglia), limbic sys.
1) Parietal-occipital
2) Central
3) Sylvian or lateral fissure
Lobes of brain:
The parietal lobe lies caudal to the central sulcus rostrally and rostral to the parieto-occipital sulcus caudally, dorsal to the Sylvian (lateral) fissure.
The occipital lobe
The occipital lobe is situated caudal to the same imaginary line of the parieto-occipital sulcus.
The frontal lobe
- The temporal lobe is
The frontal lobe is defined as the area rostral to (in front of) the central sulcus and above the Sylvian (lateral) fissure.
-The temporal lobe is located ventral to the Sylvian (lateral) fissure and rostral to the imaginary line extending from the parieto-occipital sulcus.
The postcentral gyrus (AKA ___)
2) The MOTOR CORTEX or ____:
The postcentral gyrus (or somatosensory cortex), delimited rostrally(in front) by the central sulcus and caudally/in back by the postcentral sulcus.
2) The precentral gyrus (or motor cortex), delimited rostrally by the precentral sulcus and caudally by the central sulcus.
Telencephalon—the Forebrain
2) Limbic cortex
The phylogenetically newest cortex, including the primary sensory cortex, primary motor cortex, and association cortex.
2) Phylogenetically old cortex, located at the medial edge of the cerebral hemispheres; part of the limbic system.
Prefrontal cortex
2) Corpus callosum
Frontal lobe, rostral to the precentral (motor) cortex
Involved in formulating plans and strategies
2) Large bundle of axons that interconnects corresponding regions of the cortex on each side of the brain
Limbic System
2) Cingulate gyrus
Lies in the interior of the rostral temporal lobe
Involved in emotions 2) A strip of limbic cortex lying along the medial walls of the cerebral hemispheres
Just dorsal (ABOVE) to the corpus callosum
Basal Ganglia
Part of the telencephalon
Includes caudate nucleus, the globus pallidus, and the putamen
Implicated in Parkinson’s disease
Normal function is to provide fine control of movement
Subcortical structures
Division of the forebrain
Includes the thalamus and hypothalamus
Located between the telencephalon and the mesencephalon
These forebrain structures surround the third ventricle
Thalamus (Greek thalamos, “inner chamber”)
Largest portion of the diencephalon
Located above the hypothalamus
Contains nuclei that receive information from specific sensory systems, process it, and send the result on to the cerebral cortex:
Lateral geniculate nucleus (Vision)
Medial geniculate nucleus (Hearing)
Ventrolateral nucleus (Motor)
Also receives information from the cortex
Hypothalamus (“beneath the thalamus”)
- Pituitary gland
A group of nuclei in the diencephalon situated beneath the thalamus
Controls the autonomic nervous system
Organizes the “four fs” behavior
Controls the anterior and posterior pituitary glands
- (Hypophesis)
Anterior pituitary gland (Adenohypophesis)
2) Posterior pituitary gland (Neurohypophesis)
The “master gland”
Endocrine gland whose secretions are controlled by the hypothalamic hormones.
2) Contains hormone-secreting terminal buttons of axons whose cell bodies lie within the hypothalamus
“Neurosecretory cells”
A region of the brain that surrounds the cerebral aqueduct; includes the tectum and tegmentum
Tectum (“roof”)
The dorsal part of the midbrain
Superior colliculus (vision)
Inferior colliculus (hearing)
Tegmentum (“covering”)
The ventral part of the midbrain
Periaqueductal gray matter (pain fibers)
Reticular formation (sleep, arousal, attention)
Red nucleus (motor control)
Substantia nigra (motor control)
The most caudal part of the brain; includes the metencephalon and myelencephalon.

Cerebellum (“little brain”)
A major part of the brain located dorsal to the pons, containing the two cerebellar hemispheres, covered with the cerebellar cortex; important component of the motor system.
Medulla oblongata
The most caudal portion of the brain, located in the myelencephalon, immediately rostral to the spinal cord.
Includes nuclei that control vital functions such as the cardiovascular system, respiration, and skeletal muscle tone.