exam 2 (10,11,12,13,14,15,16,17,18)

neurotransmitters

released into the synapse, actions are limited (locality) and short (rapid uptake/breakdown)

hormones

released into bloodstream (circulates, widespread, not local) affecting a large number of cells, lingering actions

can a molecule act as a neurotransmitter AND a hormone?

yes

amino acid transmitters

derived from amino acids, from diet (like glutamate, GABA, etc)

peptides

transmitters that are amino acid chains

other transmitter types

steroids, gases, endocannabinoids

why do different neurotransmitters have different effects?

because they bind different receptors

neurotransmitter release

when spike reaches terminal, voltage gated calcium channels open and calcium ions enter, triggering SNARE proteins that cause exocytosis

exocytosis

presynaptic axon terminals contain vesicles (small, spherical membranes) that contain the neurotransmitters, and the vesicles fuse with the membrane and the neurotransmitters are released into the synaptic cleft

Dale’s “Law”

although ONCE BELIEVED a neuron to release only neurotransmitter, it is now known that a single neuron can release more than one transmitter

glutamatergic neurons / GABAergic neurons

cells that release glutamate/GABA

ionotropic receptors

neurotransmitter binds to one of these receptors and opens its ion channels, effects are fast

metabotropic receptors

when these receptors are activated, intracellular signaling cascades, ultimately changing how excitable the neuron is (and other things), effects are slower but longer lasting (no ion channel as part of receptor, activates metabolic processes instead, including changing the activity of an ion channel). they are coupled to a intracellular g-protein. gain-control (the net effect of this receptor activation is often increased or decreased excitability of the cell by ionotropic receptor activation)

AMPA receptor

glutamate acts on this ionotropic receptor, ligand gated, conformation changes when glutamate binds

NMDA receptor

glutamate acts on this ionotropic receptor, ligand (glutamate must bind to them) and voltage (the cell must be depolarized) gated. has channels permeable to Na and Ca

GABA-A receptors

GABA acts on these ionotropic receptors, inhibits

GABA-B receptors

GABA acts on these metabotropic receptors, inhibits

stages of synaptic transmission (5)

1. Synthesis - transmitter is created from raw materials

2. Storage - stored in vesicle

3. Release - vesicles fuse with the terminal membrane, releasing contents into synapse

4. Receptor binding/post-synaptic effect - the effect depends on the transmitter AND type of receptor

5. Inactivation - “uptake” - taken back up (often by same neuron), repackaged into vesicles, and recycled. Metabolism (broken down by enzymes)

endogenous ligand

the body produces it

exogenous ligand

the body does not produce it (drug, plant, etc.)

agonist

mimics the endogenous ligand, binds at same site, and activates receptor when it binds. Ex. nicotine (nicotinic acetylcholine receptors), THC (CB1 and CB2 receptors, all over body)

antagonist

binds to the receptor and prevents endogenous molecules from activating receptor. Ex: antipsychotics (first gen and second gen)

inverse agonist

induces opposite effects of the endogenous ligand. Ex: SR141716A (CB1 receptors that induces feeding, sometimes anxiolytic, this drug reduces appetite and induces depression and anxiety symptoms)

allosteric modulator

binds to a different site from the endogenous ligand, can increase/decrease the impact endogenous ligand has. Ex: alcohol (binds GABA-A receptors at the benzodiazepine binding site, increases amount of chloride influx when GABA binds at GABA site - MODULATES)

uptake inhibitor/transport blocker

blocks uptake of endogenous ligand, effectively increasing action at the synapse. Ex: cocaine (blocks dopamine uptake, increases amount of dopamine in synapse - also effects serotonin and norepinenphrine)

first generation psychotics

primarily D2 receptor antagonists, reduces positive (additive) symptoms of schizophrenia, side effects are sedation, motor side effects, “parkinsonism”

second generation antipsychotics

better tolerability, fewer and less extreme extrapyrimidal (motor) effects, tend to improve cognitive ability. Block D2 AND serotonin receptors (5-HT2A and 5-HT2C), reduces positive and negative symptoms

dopamine

D1, D2, D3, D4, D5 metabotropic receptors (D1 and 5 are excitatory, rest are inhibitory); primary source is from midbrain, Substantia Nigra (SNc), and Ventral Tegmental Area (VTA); nigrostratial pathway: SNc to caudate and putamen - movement generation and maintenance (parkinsonism); mesolimbic pathway: VTA to cortex and nucleus accumbens - appetitive and aversive motivation, cognitive control learning

acetylcholine

nicotinic (ionotropic, cation channel) and muscarinic (metabotropic) receptors; primary source is from the basal forebrain; neuromuscular junction, memory and attention (Alzheimer’s), autonomic nervous system

serotonin

5HT1-5HT7 most receptors metabotropic, 5HT3 ionotropic; primary source is the raphe nuclei; sleep and wakefulness, mood

norepinephrine

metabotropic alpha and beta receptors; primary CNS source is the locus coeruleus, in the PNS (hormone) is adrenal cortex; energy, arousal, attention, mood

non-stimulant ADHD medication

no direct effect on dopamine transmission, norepinephrine instead (uptake transporter)

brain divisions

forebrain, midbrain, and hindbrain

spinal cord

signals to and from the brain go mostly through here; cervical (neck), thoracic (between neck and abdomen), sacral (end of spine) - more axons to less axons, less grey matter to more gray matter

hindbrain

contains cerebellum and brainstem

cerebellum

critical for motor and other kinds of learning

brainstem

contains nuclei that are critical for several vital functions, such as breathing (pre-Botzinger complex), heart rate, blood pressure, sleep-wake, etc.

midbrain

important for stimulus driven behaviors (food approach, threat escape, orienting to loud sounds); contains superior colliculus, inferior colliculus, substantia nigra, ventral tegmental area

superior colliculus

important for vision driven, reflexive behaviors

inferior colliculus

auditory system relay, also important for hearing driven behaviors

substantia nigra

contains dopamine cell bodies

ventral tegmental area

contains dopamine cell bodies

forebrain (diencephalon)

the rest of the brain, includes cortex, thalamus, hypothalamus, pituitary gland

thalamus

relay center - relays sensory info to cortex and also recieves

hypothalumus

regulates critical survival behaviors

pituitary gland

releases hormones

basal ganglia

deep forebrain, important for motivated behaviors, composed of caudate nucleus, putamen, subthalamic nucleus, SNc (in midbrain, sends axons here); rich in dopamine/dopamind receptors

occipital lobe

visual perception and representation of the world; retinotopic map; dorsal stream - occipital to parietal lobe (WHERE/HOW); ventral stream - occipital to temporal lobe (WHAT)

temporal lobe

dorsal portion - auditory perception, understanding spoken language (Wernicke’s area); ventral - receives info from visual cortex; fear fear learning, appetitive learning, amygdala (attaching emotions to stimuli); memory, learning about places, forming memory sequences (hippocampus)

parietal lobe

integrates info from different sensory systems (dorsal pathway)

somatosensory cortex

receives sensations from all over the body

contralateral perception

how one side of the brain processes sensory input or perception from the opposite side of the body or the opposite visual field

somatopic map

an orderly, point-for-point representation of the surface of the body mapped onto a specific region of the central nervous system (sensory homunculus)

frontal lobe

how we interact with the world, controls movement (motor cortex and premotor cortex), ventrolateral prefrontal cortex (attention, response inhibition), dorsolateral prefrontal cortex (problem solving, decision making, planning, working memory), orbitofrontal cortex (decision making, planning, learning)

spiny neurons

typically excitatory glutamatergic neurons, have dendritic spines (sites of synaptic inputs)

pyramidal neuron

spiny neuron - 70-85% of cortical neurons, long axons that project to other cortical areas and sometimes all the way to the muscles (outputs, efferents, long range)

stellate neuron

spiny neuron - star-shaped interneurons, processes remain within the region where the cell body is located (local, short range)

aspiny neuron

do not have dendritic spikes, mainly inhibitory interneurons with short axons, primarily GABAergic (short, local range, releasing GABA)

basket neurons

aspiny neuron, looks somewhat like a basket

cortical layer IV

input - lots of interneurons - tend to be inhibitory - other layers act in parallel to this layer

cortical layers V and VI

output layers - sends axons to other cortical and brain areas - layer V has big pyramidal neurons called Betz cells that send axons all the way to spinal cord - layer VI generally contains neurons that project to the thalamus - motor cortex has larger layer V than sensory cortex

cortical layers II and III

receive inputs from other cortical areas and integrate them with layer IV outputs, send info OUT - lots of pyramidal neurons but not as large as in layer IV (smaller axons receive less input when layer IV is present/larger)

cortical layer I

“input layer” - function is less clear - primarily axon bundles and dendritic arbors - few cell bodies

specific afferents

brings information to a discrete cortical region, column, or layer. typically layers II, III, or IV

nonspecific afferent

serve general functions and terminate diffusely over large regions of the cortex (ex: dopamine neuromodulators)

cortical columns

most interactions between neurons take place vertically, within a single Layer I-VI column, neurons within are functionally similar, more apparent in primary sensory cortex than in association area of cortex

dorsal spinal cord

sensory axons and cell bodies

ventral spinal cord

motor neurons and cell bodies, lower motor neurons (drive skeletal muscles)

dermatome

each segment of the spinal cord maps onto one of these, with axons entering and leaving the spinal cord here

motor units

groups of these work together to generate movements

fast fatigable muscles

exert force very quickly following stimulation, but require lots of oxygen and amount of force tapers off very quickly (less and less force). ex: sprinting, jumping, weight training can develop this

slow muscles

engaged by activities such as standing for long periods, can be developed with distance and endurance training

muscle spindles

stretch receptors in muscles (how “stretched” they are), involved in passive stretch (a spinal reflex), baseline activity levels are decreased by contraction

golgi tendon organs

stretch receptors in muscles tendons, tell us how contracted our muscles are, activated by high contractive force, passive stretch does not activate them strongly (highjer activation threshold)

pain withdrawal reflex

ex: sharp sudden pain in right foot stimulates flexor muscles and inhibit extensor muscles on that side (ipsilateral), and extensor muscles on the contralateral side are simulated and flexor muscles are inhibited

central pattern generators

locomotion can occur without input from brain

pre-Botzinger complex

important for respiration rhythm

cranial nerves that are both sensory and motor

CN V, IX, X

cranial nerve I

olfactory nerve, sensory, sense of smell

cranial nerve II

optic nerve, sensory, vision

cranial nerve III

oculomotor nerve, motor, eye movements, papillary constriction + accommodation, movements of eyelid

cranial nerve V

trigeminal nerve, sensory and motor, somatic sensation in face

cranial nerve VIII

vestibulocochlear (auditory) nerve, sensory, hearing, sense of balance

dorsal column system

route that carries pressure and touch info - cell bodies are in dorsal root ganglion just outside spinal cord - unipolar cells (dendrite + axon is cell) - ascend spinal cord ipsilaterally, crossing the midline in the brain stem

spinothalamic system

route that carries pain and temperature information - cell bodies are also in dorsal root ganglia - ascend contralaterally, as they cross in the spinal cord

what is a word that can describe the way touch receptors work?

displacement

receptive fields

how large of an area of the skin is monitored by a single sensory neuron, indicating its sensitivity to stimuli.

what can determine/figure out the receptive fields (density of touch receptors) on a body?

two-point discrimination threshold

touch receptor transduction

pressure stretches cells’ lipid membrane, causing MECHANICALLY gated ion channels to open, depolarizing neurons, generating spikes (mechanoreceptive ion channels)

slowly adapting touch receptors

respond to stimuli that do not change much over time

rapidly adapting touch receptors

respond to stimuli that change quickly over time

pacinian corpuscle

looks like an onion - rapidly adapting - pressure and vibration responses - low threshold for activation - lower layer in skin

ruffini’s corpuscle

looks like a leek - slow adapting - stretch responses - middle of skin layers

Merkel’s disks

looks like ginger root - slow adapting - light (static) touch responses - upper area in skin layers

free nerve endings

looks like seaweed salad - slow adapting - pain and temperature responses - super close to surface of skin

thalamic touch relay

VPL (ventral posterior lateral) and VPM (ventral posterior medial) thalamus is where the thalamus relays pain and touch information

periaqueductal grey (PAG)

midbrain - spinothalamic tract sends a collateral here (in descending pain modulation), and it then projects a variety of pain sensing nuclei, leading to dorsal horn of spinal cord

local pain modulation

ex: you hit your shin, and then you rub the site of impact. this feels good because it stimulates mechanoreceptors (inhibiting the pain, as an inhibitory transmitter is released onto ascending nociceptive neurons)