Neurons

Week 3

nodes of Ranvier

channels concentrated here

interneurons

advantage - modulation and flexibility

cytoskeleton in a neuron

keeps everything in the soma attached, structure and strength of long axon, ion channels

intelligence

efficiency of neural networks, synaptic plasticity, sophistication of neurons

ionotropic receptor

subunits that make an ion channel

open a channel directly

faster, modulation

metabotropic receptors

coupling site for intracellular signaling proteins

i.e G protein-coupled receptors

cascades, slower, longer term reaction

G protein-coupled receptor

neurotransmitter binds to receptor, activating the G protein

part of subunit detaches, modulating ion channels on the effector protein activating it

ion channel opens and ions flow across the membrane

electrical synapse

faster than chemical, direct pathway (junction)

cannot modulate

fast way to coordinate cells to perform a function

chemical synapse

allows modulation

slower than electrical

saltatory conduction

in myelinated neurons, only unmyelinated regions depolarize

impulse moves faster

EPSP

depolarize neuron

open gated channels causing Na+/K+ pump to work

IPSP

hyperpolarize neuron

open gated channels allowing K+ to leave cell and Cl- to diffuse into cell

GABA

spatial summation of EPSP/IPSP

IPSP dips membrane potential → hyperpolarize, less excitable (less likely to trigger AP)

brain functions - frontal lobe

thought, memory, emotion, behavior

brain function - parietal lobe

sensory processing

brain function - brain stem

autonomic regulation

Broca’s aphasia

broken speech, can understand

Wernicke’s aphasia

cannot understand speech, nonsense

neuroglia

non-neurons

provide support to neurons

do not transmit electrical impulses

maintain homeostasis, protect neurons

neuroglia in CNS

ependymal cells, oligodendrocytes, astrocytes, microglia

neuroglia in PNS

satellite cells, Schwann cells

reflex

autonomic response

involve interneurons - can modulate to an extent, i.e keeping hand over flame

NMJ

APs arrive at presynaptic terminal and open VG Ca2+ channels → uptake into terminal → ACh released into cleft, binds to ligand gated ACh nicotinic receptors → ligand gated Na+ channels open

AChE

ends ACh activity

myasthenia gravis

autoimmune disease, antibodies made by body against own end plate ACh receptors bind to receptors → ACh stays in cleft longer but then gets destroyed by AChE

nociceptive pain

somatic, visceral

nociceptors activated by noxious stimuli that cause tissue damage

neuropathic pain

damage/dysfunction of somatosensory NS

ischemic pain

CV - insufficient O2 supply

referred pain

pain felt in different location

inflammatory mediators

initiation, amplification, maintenance of pain

i.e anti-inflammatory cytokines (IL-10)

VEG-F

released by cancer cells