Bio Psych Final

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Last updated 2:54 AM on 4/27/26
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52 Terms

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neuropharmacology

animals and humans

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spinal cord

damage causes paralysis and numbness

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meningitis

phototopia, phonophobia

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language and spatial navigation areas

asymmetrical

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sensory areas

symmetrical

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cerebrovasculature

supplies the brain with oxygen and nutrients

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meninges

surround and protect the brain

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physiology

study of how living systems function

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peripheral NS

all of the components of the nervous system outside the skull and spine, the nerves and ganglia

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parasympathetic NS

just the parts of the NS that regulate day-to-day functions like digestion

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sympathetic NS

just the parts of the NS that regulate “fight-or-flight” responses to threats and stressors

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dorsal roots

afferent pathways, damage causes numbness or loss of sensory info

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ventral roots

damage causes paralysis, efferent pathways, carry motor info

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dura mater

outermost meningeal layer

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pia mater

innermost meningeal layer

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schwann cells and oligodendricytes

increase speed of axonal conduction, production of myelin

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microglia

acting as the brain’s immune cells and removing microorganisms and dead and dying cells

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ependymal cells

produce cerebrospinal fluid

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leukodystrophy

Defective production of myelin by his oligodendrocytes or Schwann cells

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ions

atoms or molecules that are charged, become charged by gaining or losing protons 

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pumps

move ions against their concentration gradient, can move ions into or out of the cell, depending on the one 

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Na+/K+ pump

it pumps both Na+ and K+ AGAINST their concentration gradients, it moves Na+ out of the cell and K+ into the cell 

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non-gated K+ channel

allows K+ to move down its concentration gradient, The non-gated K+ channel does not require energy, at rest, K+ flows out of the cell through the non-gated K+ channel

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resting membrane potential

non-gated K+ channel, Na+/K+ pump

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pumps and ion channels

Pumps but not ion channels require energy to move ions, Both pumps and ion channels can move ions into or out of the cell, depending on the pump/ion channel and ion 

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action potential propogation

During the refractory period, the previous membrane patch can't reform the action potential because the voltage-gated Na+ channels are inactivated, the action potential moves can move in only one direction, down the axon toward the synapse. 

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peptide

synthesized and packaged in the cell body

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synaptic transmission

voltage-gated Ca2+ channels are opened by depolarization allowing Ca2+ to flow into the cell 

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ionotropic receptors

it is an ion channel that directly opens or closes and allows ions to flow into or out of the cell, they do NOT require a G protein to open or close ion channels, they are ligand-gated ion channels

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EPSP

depolarization, inside of cell less negative, close K+, open Na+

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IPSP

hyperpolarization, inside of cell more negative

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temporal/spatial summation of multiple EPSPs

more likely to fire action potential

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uptake

the transport into and deactivation of neurotransmitter by glial cells

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reuptake

transporter proteins move NT back into pre-synaptic neuron axon terminal (amino acids and monoamines)

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neuromodulation

It is associated with monoamines and neuropeptides, It is associated with metabotropic receptors 

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classical neurotransmission

It produces a more rapid and shorter lasting electrical response, associated with amino acid and monoamine neurotransmitters

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neural tube

the structure that eventually forms the spinal cord and brain

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neural crest

the cells that migrate out to form the peripheral nerves

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cell migration

before birth

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synapotgenesis

after birth, long term memory

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cell death and synaptic pruning

after birth, neurotrophins

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chemoattractants and adhesion molecules

Axonal extension during morphological differentiation

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master regulatory genes

chemical differentiation

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defects in tangential migration

defects in peripheral nerve formation

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excessive synaptic pruning

epilepsy, schizophrenia

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insufficient synaptic pruning

ADHD, over-connectivity of autism, epilepsy

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explicit memory

The medial temporal cortex and hippocampus, PFC, basal forebrain

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implicit memory

The basal ganglia and cerebellum 

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synaptic plasticity

It refers to changes in the strength of communication between neurons that can be increases or decreases, It refers to changes in the strength of communication between neurons that may involve changes to existing synapses or that involve adding new synapses. 

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implicit memory amnesia

Physical trauma to the basal ganglia or cerebellum, Huntington’s disease

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encoding

refers to the creation of a very transient record of the received sensory information

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consolidation

short-term stabilization of memory after its initial acquisition