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Neuropeptides
Uni of Notts, Neurobiology of Disease, year 2, topic 15
| Term | Definition |
|---|---|
| Neuropeptides | Small protein-like molecules enabling communication between neurons as well as other cell types (such as pancreatic beta cells) |
| Autocrine cellular signaling | Occurs when a cell secretes a signaling molecule that binds to its own receptors |
| Paracrine cellular signaling | Occurs when a cell releases signal molecules to target neighboring cells |
| Endocrine cellular signaling | Involves signaling molecules traveling through the bloodstream to act on distant cells |
| Neuropeptide release locations | Released at many points along the cell membrane rather than solely at presynaptic terminals |
| Neuropeptide recycling? | Unlike neurotransmitters, are never recycled by neurons back into presynaptic vesicles. |
| Neuropeptide functional classes | endoopioids (endorphins), peptide hormones (oxytocin & vassopressin), & hypothalamic releasing hormones (CRH) |
| Neuropeptide synthesis | Long prepropeptides contain signal peptides, prompt cleavage into propeptides by signal peptidases, propeptides cleaved by endo- & exopeptidases into simple peptides, then modified by glycosylation or nitrosylation |
| Synthesis sites compared to neurotransmitters | Synthesized as prepropeptides in the rough ER & Golgi, whereas standard neurotransmitters are made in cytosol |
| Neuropeptide vesicle storage | Stored in large dense-core vesicles (LDCVs), whereas common neurotransmitters utilize small secretory vesicles (SSVs) |
| Response speed & duration neuropeptides vs neurotransmitters | High molecular weight causes slow-acting, prolonged responses compared to neurotransmitters |
| Axonal transport & release delay neuropeptides vs neurotransmitters | Move slowly across axons centimeters per day; neurotransmitters release milliseconds after action potentials |
| Cytosolic calcium requirements | Require much lower cytosolic calcium concentrations for vesicle release than standard neurotransmitters |
| Diffusion pattern during neurotransmission | Diffuse outward multidirectionally instead of directional release across a tight synaptic cleft |
| Potency compared to neurotransmitters | Roughly 1000x more powerful than classic neurotransmitters but behave as slow neuromodulators |
| Stimulation requirements for release | Stored in fewer large dense core vesicles (LDVCs), requiring a prolonged period of high-frequency stimulation |
| Neuropeptide degradation mechanism | Lack specific enzymatic degradation; must be endocytosed & broken down by lysosomes |
| Tachykinin & primary structure characteristic | Largest neuropeptide family, neurokinin that can help reduce chemotherapy nausea. Position 4 on the primary structure is always a hydrophobic residue, usually phenylalanine (F) |
| Neuropeptide Y (NPY) G-protein coupling characteristics | Receptors 2 & 4 utilize Gq pathways; receptor subtypes 1, 3, & 5 utilize Gi pathways |
| BDNF downstream cascade functions | Activates TrkB & CREB pathways to control neurogenesis, cell survival, & long-term potentiation. Also activates mTor to increase lipid biosynthesis for expanding the membrane in synaptogenesis |
| Somatostatin & tissue isoforms | Inhibits release of hormones like insulin & glucagon. Brain isoform contains 14 amino acids; gastrointestinal isoform contains 28 amino acids. Helps clear beta-amyloid plaques which reduces Alzheimer's |
| Corticostatin stimulation behavior | Part of the somatostatin family; pathway activation in rodents triggers anxiogenic (anxiety-inducing) behaviors. Is also involved in analgesia & sleep |
| Neuropeptide Y | One of the most abundant neurotransmitters. Regulates: brain activity, mood, stress coping, ingestion, digestion, metabolism, vascular & immune function; often in the ANS |