Neurotransmitters and Synaptic Plasticity Overview

Glutamate

Main excitatory neurotransmitter in the CNS.

GABA

Primary inhibitory neurotransmitter in the CNS.

Glycine

Inhibitory neurotransmitter in CNS and PNS.

Acetylcholine

Excitatory neurotransmitter in the PNS.

Indirect transmitters

Transmitters acting on GPCRs, not ion channels.

Histochemical methods

Techniques to visualize neurotransmitter presence.

Immunohistochemical methods

Use antibodies to detect specific neurotransmitters.

Neurotransmitter Mapping

Identifies neurons expressing specific neurotransmitters.

AMPA Receptors

Fast-opening glutamate receptors with GLuA1-4 subunits.

NMDA Receptors

Slow-opening, Ca2+ permeable glutamate receptors.

Kainate Receptors

Modulate glutamate release, not primary excitatory.

Metabotropic glutamate receptors

mGluRs, act via G proteins, modulate synaptic activity.

Group 1 mGluRs

Excitatory, couple to Gq proteins, activate PLC.

Group 2 mGluRs

Inhibitory, located presynaptically, reduce transmitter release.

Group 3 mGluRs

Inhibitory, also presynaptic, modulate neurotransmitter release.

GABA expression areas

Predominantly in cortex and midbrain.

Glycine expression areas

Predominantly in brainstem and spinal cord.

IPSP

Inhibitory postsynaptic potential produced by GABA or glycine.

Inhibitory ionotropic receptors

Control excitatory output via negative feedback.

GABAB receptors

Metabotropic receptors with pre and postsynaptic effects.

Cholinergic neuron populations

Found in various CNS regions, release ACh.

ACh release in CNS

Triggered by action potentials in cholinergic neurons.

Cholinergic System

Involves acetylcholine for cognitive functions.

Nucleus Basalis

Associated with learning, attention, and memory.

Tegmental Area

Involved in arousal, reward, and motor control.

Medial Habenular Nucleus

Processes reward, nicotine addiction, and stress.

Striatum

Controls movement and reward behaviors via dopamine.

Alzheimer's Disease

Characterized by degeneration of cholinergic neurons.

ACh and Memory

ACh enhances attention to sensory information.

Volume Transmission

Neurotransmitter release diffuses through extracellular space.

Adrenergic Neurons

Located in locus coeruleus, enhance attention.

Autoinhibition

Negative feedback mechanism via K+ channel opening.

Serotonergic Neurons

Located in raphe nuclei, regulate mood and arousal.

5-HT Receptors

Include ionotropic and G protein-coupled types.

Dopaminergic Neurons

Located in brainstem, control reward and movement.

Parkinson's Disease

Degeneration in basal ganglia affects movement.

L-DOPA

Supplement that increases dopamine levels.

Ventral Tegmental Area

Key region for reward signaling in the brain.

Histamines

Mediates cortical arousal and inflammation.

Tuberomammillary Nucleus

Histamine-producing neurons found here.

Purinergic Neurons

Release ATP as a neurotransmitter.

P2X Receptors

Ligand-gated cation channels for ATP.

P2Y Receptors

G protein-coupled receptors for ATP.

P2X receptors

Fast-acting transmitter receptors in specific brain neurons.

P2Y receptors

Stimulated by ATP/ADP, induce cation current.

ATP

Key regulator of glia, increases glial Ca2+ levels.

Glia

Cells that release ATP and transmitters.

Adenosine buildup

Causes sleepiness after prolonged wakefulness.

Caffeine

Blocks adenosine receptors, increases dopamine levels.

Ketamine

NMDA antagonist, inhibits excitatory neurotransmitters.

Benzodiazepines

Target GABAa receptors, induce sedation and relaxation.

EtOH

Targets GABAa and NMDA, causes depression and sedation.

Nicotine

Targets nAChRs, leads to dopamine release.

Fluoxetine

SSRI, inhibits serotonin reuptake, increases serotonin.

Cocaine

Blocks reuptake of dopamine, norepinephrine, serotonin.

Choline

Precursor for ACh, transported back into axons.

Choline acetyltransferase

Enzyme synthesizing ACh from choline and AcCoA.

Acetylcholinesterase

Enzyme degrading ACh in synaptic cleft.

DOPA

Precursor for catecholamines like dopamine.

Dopamine β-hydroxylase

Converts dopamine to norepinephrine in vesicles.

Monoamine oxidase

Degrades catecholamines, located in mitochondria.

Aromatic L-amino acid decarboxylase

Converts DOPA to dopamine and 5-HTP to 5-HT.

Tryptophan

Initial precursor for 5-HT from amino acids.

Phenylethanolamine N-methyltransferase

Converts norepinephrine to epinephrine in vesicles.

Tryptophan

Amino acid linked to aggression and sleep changes.

Krebs Cycle

Pathway converting GABA to glutamate and vice versa.

Glutamate Synthesis

Produced from glutamine by glutaminase in neurons.

Glutamate Uptake

Glia convert glutamate to glutamine for neurons.

Neuropeptide Synthesis

Occurs on ribosomes, modified in ER and Golgi.

Propeptide Processing

Cleavage in vesicles yields active neuropeptides.

Solute Carrier Transporters

Transporters for multiple neurotransmitter types into vesicles.

Axoplasmic Flow

Transport mechanism for organelles along microtubules.

Kinesin

Motor protein for anterograde transport to axon terminal.

Dynein

Motor protein for retrograde transport to cell body.

Neuropeptide Transporter (NPT)

Transports neuropeptides back into nerve terminals.

Synaptic Vesicle Transport

Uptake by presynaptic terminal via specific transporters.

Synaptic Facilitation

Increased neurotransmitter release from Ca2+ accumulation.

Synaptic Depression

Depletion of readily releasable transmitter with stimulation.

Augmentation

Moderate stimulus trains enhance transmitter release over seconds.

Post-Tetanic Potentiation (PTP)

Increased synaptic potential after high-frequency stimulation.

Long-Term Potentiation (LTP)

Persistent synaptic efficacy increase from repetitive activation.

Long-Term Depression (LTD)

Long-lasting decrease in synaptic efficacy.

Calcium's Role

Ca2+ accumulation influences neurotransmitter release dynamics.

Vesicle Fusion

Process where vesicles release neurotransmitters into synapse.

Neurotransmitter Repackaging

Recycling of neurotransmitters for subsequent release.

Glial Cells

Support cells involved in neurotransmitter uptake and recycling.

LTD

Long term depression; decreased synaptic efficacy.

Calcium Imaging

Technique to visualize calcium dynamics in neurons.

Homosynaptic LTP

Potentiation at only the activated synapse.

Associative LTP

Potentiation from simultaneous weak and strong inputs.

Silent Synapses

Inactive excitatory synapses activated by depolarization.

AMPA Receptors

Receptors that mediate fast synaptic transmission.

Homosynaptic LTD

Depression from repetitive activity in the same pathway.

Heterosynaptic LTD

Depression from activity in a different pathway.

Associative LTD

Weak input depression due to combined stimuli.

Dendritic Spines

Small protrusions where synapses form on neurons.

NMDA Receptors

Receptors that mediate synaptic plasticity via calcium influx.

CaMKII

Enzyme activated by calcium; crucial for synaptic changes.

LTP

Short term potentiation lasting minutes to hours.

L-LTP

Long term potentiation lasting hours to months.