anatomy midterm 4 - lecture 18 - synapses

what are the 5 structures that comprise a chemical synapse?

pre-synaptic neuron, neurotransmitters, synaptic vesicles, synaptic cleft, and post-synaptic neuron

what are the 4 steps of neurotransmitter release?

action potential arrival → calcium influx → vesicle fusion and neurotransmitter release → neurotransmitter binding and postsynaptic response

what is acetylcholine?

a neurotransmitter that plays a crucial role in muscle movement at the NMJ, as well as in the ANS and other areas of the brain

what are the 3 molecules that act as neurotransmitters?

amino acids, monoamines, and peptides

what are the 4 types of amino acid NTs?

glycine, GABA, glutamate, and acetylcholine

what are the 5 types of monoamines?

dopamine, epinephrine, norepinephrine, histamine, and seratonin

what are the 2 types of peptides?

substance P and opioid peptides

what are catecholamines?

a group of neurotransmitters that share a common chemical strucutre; dopamine, norepinephrine, and epinephrine

what is the process of conversion for catecholamines?

tyrosine → DOPA, DOPA → dopamine

what is the breakdown of catecholamines catalyzed by?

COMT and MAO-A

what are the two types of graded potentials?

excitatory (EPSPs) and inhibitory (IPSPs)

function of EPSPs

neurotransmitters that open sodium ion channels, leading to depolarization; e.g. glutamate

function of IPSPs

neurotransmitters that cause hyperpolarization by increasing permeability of the membrane to potassium or chloride ions; e.g. GABA

what are GABA-A receptors?

ionotropic receptors that are activated by GABA to open the chloride channel, which causes hyperpolarization of the membrane

are ionotropic receptors voltage or ligand gated?

ligand

what are 3 ways of concluding synaptic transmission?

enzymatic degradation, diffusion, and reuptake

what is enzymatic degradation?

enzymes breaking down NTs, like acetylcholinesterase, MAO, and COMT

what is diffusion that ends synaptic transmission?

NTs can diffuse away from the synaptic cleft and into extracellular fluid, which dilutes the NT concentration

what is reuptake?

NTs are reabsorbed back into the presynaptic neuron or into glial cells through specific transporter proteins

what are the 4 dopaminergic pathways in the brain?

nigrostriatal, mesocortical, mesolimbic, and tuberoinfundibular

what is nigrostriatal pathway?

pathway that connects the substantia nigra to the striatum and is involved in voluntary motor control

what is the mesolimbic pathway?

originates in the ventral tegmental area in the midbrain and projects to the nucleus accumbens in the limbic system and is associated with reward, motivation, and pleasure; reward pathway

what is the mesocortical pathway?

originates in the ventral tegemental area in the midbrain but projects to the prefrontal cortex and is involved with executive control, attention, and working memory

what is the tuberoinfundibular pathway?

it originates in the arcuate nucleus in the hypothalamus and extends to the anterior pituitary gland and exerts inhibitory control over prolactin secretion

what is neuroplasticity?

the brain’s ability to change and adapt throughout life by forming new connections, strengthen existing ones, and reorganize itself in response to experiences, learning, and injury

what is synaptic plasticity?

the specific mechanism that involves changes in strength and efficiency of synapses; fundamental to learning and memory, as well as recovery from damage

what is short-term plasticity?

neurons temporarily enhance their connections by increasing the amount of NTs released and increasing the number of postsynaptic receptors available

what is long-term plasticity?

strong and sustained activities that cause the growth of new dendritic spines and synaptic connections

how do the hippocampus and cerebral cortex interact?

the hippocampus forms memories while the cerebral cortex stores them

what principle does synaptic plasticity follow?

use it or lose it

what is long-term potentiation?

the strengthening of synaptic connections by high frequency stimulation or repeated experiences, essential for forming new memories

what is long-term depression?

weakened synaptic connections when a memory becomes irrelevant

what is the possible mechanism of LTP in the hippocampus

initial glutamate release, binding to AMPA and NMDA → depolarization and NMDA receptor activation → calcium influx and cellular signaling → synaptic strengthening

describe the proposed mechanism of LTD at the glutamatergic synapse

postsynaptic neuron is less responsive to glutamate which induces dendritic spine shrinkage and synaptic loss