MIDTERM 2 REVIEW action potential electrophysiology Graded potentials in dendrite Epsp ipsp is local change to membrane as it travels down membrane it degrades More ligand binding greater the depolarization What happens when synaptic potentials degrade and spread As it moves across membrane it degrades Action potential doesn t degrade Linked neurons direct electrical connections through gap junctions allows ions to go through so you can have direct electrical charges go through Ions in high concentration outside cell sodium Other element high outside cell calcium High concentration inside is potassium Negative proteins make cell inherently negative because they are too big to move through membrane Sodium channels opening cause epsp chloride channels cause ipsp Why is potassium inside and sodium out Potassium is more selectively permeable than sodium is most sodium channels are voltage gated whereas most potassium channels are leaky membranes Absolute refractory period voltage gated channels are closed continues as long as they are closed Once some are reactivated it is then the relative refractory period At epsp channel activation happens gradually Pretty much every sodium channel requires same activation energy to reach threshold Ttx blocks voltage gated sodium channels Mtx blocks voltage gated potassium channels Firing rate Two things that affect speed of ap diameter of axon whether it is myelinated larger diameter is faster Calcium binds to axon terminal spaces causes activation for exocytosis NEUROCHEMISTRY nucleus NMDA channel Disbindin sp is prob root cause of schizophrenia inhibits glutamate reuptake GABA and glutamate have no central nucleus spread everywhere over brain Ach in basal GABA opens chloride ion channels which leads to ipsp hyperpolarization Too much gaba builds up and eventually shuts things down Serotonin too much too little treat depression by increasing serotonin levels Having reuptake inhibitor increases levels in synapses reuptake is primary way these synapses are shut down Pills meds don t have anything to do with disorder drug actually makes the brain refine a different system i e a few synapses away the serotonin is malfunctioning so you take pill and brain accommodates to fix it 5HT1A receptor in synapse linked with anxiety inherited deficiency and religiosity Anandemide peptide made by brain on stem cells Know these receptors nicotine muscarinic ach serotonin 5HT1A live in raffe nuclea turn off during REM sleep norepi and dopamine didn t give us receptors Know role of sodium and calcium after release of transmitters Calcium causes vesicles to fuse sodium depolarizes the membrane Dopamine live in cell bodies project to basal ganglia projects to frontal lobe NE lives in floor of the fourth ventricle fat pads are innervates by NE from sympathetic nervous system enhanced metabolism some are born to be obese because the receptor is blocked Ach learning memory attention when activated in frontal lobes you activate contingency anticipation wave attention degenerates with Alzheimers Signals that activate NE ach glutamate Signals that shut off NE gaba serotonin sleep DEVELOPMENT Radial glial help move the progenitor cells turn into astrocytes when done 6 layers of cortex formed inside out starts at ventricular zone proliferative zone Limiting factor need space for wiring which is why we are limited to 6 layer cortex as humans Big brains longevity trade off is less offspring Central sulcus is formed first by primary sensory and primary motor gyro Myelination last frontal lobe degenerate first If neuron A dies neuron B may die because no connection transneurona degeneration anterograde and retrograde degeneration anterograde is like going down stream from one cell to the other Retrograde is when cell damages own nucleus Stem cells formed in hippocampus lack of stem cells causes depression lack of attention
View Full Document
Unlocking...