This session provides an in-depth review of the structure and functioning of neurons, neurotransmitters, and cranial nerves. Topics include synaptic transmission, the effects of neurotoxins, post-synaptic receptors, and the process of inactivation. You'll additionally explore the roles of different types of neurotransmitters, including glutamate and GABA, and how their balance is crucial to maintaining normal brain function. The session also covers cranial nerves, their respective functions and pathways, and their significance in the medical field. Through this engaging session, you'll gain a deeper understanding of the fundamental neurobiology that underpins human health.
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Neurotransmitters and cranial nerves mk2922@ic.ac.ukFAA KHANTILO'S COVERED I. Intercellular II. Organization of the communication Nervous System LECTURE TIMELINE Synapses Neurotransmitters GABA and Cranial Nerves Glutamate synapses 1. 2. 3. 4.Structure of a Neuron • Signals are received by dendrites Spines Soma Synaptic • Dendrites have Dendrites terminal spines with proteins which increase Axon surface area to receive neurotransmitters • Signal integration by Soma • Transmitted via axonSynaptic Transmission Stages of Synaptic Transmission 1. Synthesis and Packaging 2. Neurotransmitter release 3. Receptor activation 4. Inactivation Characteristics of synapse a. Rapid timescale b. Diversity c. Plasticity d. Learning Release of Neurotransmitter 3. Complex formation between 1. Packaging into proteins on vesicle vesicles involves ATP and presynaptic cell membrane. This is ATP called docking- priming. Ca2+ 4. Fusion with cell membrane allows 2. Action potential causes exocytosis Ca2+ influx which triggers neurotransmitter vesicle releaseNeurotoxins Alpha Latrotoxin • Activates Ca2+ ion channels • Stimulates GABA release until depletion Endocytosis • Spasms Alpha Budding Botulinum Latrotoxin • Inhibits membrane + Ca2+ Docking Budding proteins • Preventing the release of glutamate Priming Fusion Botulinum Exocytosis • Flaccid (muscles relaxed) - paralysisPost-Synaptic Receptors Ion-linked receptor (ligand gated) G-coupled protein receptor Multiple subunit combinations result in different properties CNS: CNS & PNS → ACh at muscarinic receptors (e.g. in heart), dopamine, • GABA receptors (GABAR- linked to Cl- channels)l) noradrenaline, serotonin and neuropeptides like enkephalin • glycine receptors (GlyR- linked to Cl- channels) NMJ: • channels) on skeletal muscle fibres receptors (nAChR- linked to Na+Post-Synaptic Receptors • Excitatory allow Na+ through which depolarises the post-synaptic membrane • Inhibitory ion channels allow Cl- through which hyperpolarises pos- synaptic membrane All of these are ion linked receptors (as opposed to G- coupled proteinInactivation There are two ways we inactivate a synapse: • Enzyme degradation (hydrolytic) Reuptake • Reuptake channels Enzyme DegradationQs - Synapses Types of Neurotransmitter Types of Molecules Glutamate GABA & Glycine Amino acids - glutamate, GABA and glycine Amines – dopamine and noradrenaline Neuropeptides Excitatory vs inhibitory Excitatory neurons depolarise (which increases membrane potential) and inhibitory hyperpolarise (which decreases membrane potential) Glutamate Glutamate is the most important excitatory GABA neurotransmitter in the brain GABA is the most important inhibitory neurotransmitter in the brain Glycine is an inhibitory neurotransmitter in the brainstem and spinal cord GlycineGlutamate Synapse A-Ketoglutarate Glutamate (transamination) 1. Glutamate synthesised 3. Reuptake viaexcitatory amino acid transporters (EAATs) into presynaptic neuron and nerve terminal glial cells 4. Glutamine synthetase converts glutamate to glutamine in glial cells Na + Postsynaptic nerve terminal Glial cell 2. Glutamate binds to ion channels (NMDA orAMPA) Glutamate GlutamineGlutamate Receptor AMPA receptor • Faster • Allows Na+ ions to enter through channel NMDA receptor • Slower Gly • Allows Na+ and Ca2+ ions to enter through channel • Calcium ions act as “second messengers” as they can have separate effects within the neurons • Requires a glycine co-agonist GABA Synapse GABA-T GABA Succinic Semialdehyde 1. GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD) GAD 4. GABA Glutamate GABA GAT GAT enzymatically modified by GABA- transaminase (GABA- 3. Rapiduptake of GABAby T) to succinic GABAtransporters (GATs) cells & GABA nervel - terminals) Cl 2. GABAreversibly binds post- synaptic receptors (linked to ion channels) Glial cell Epilepsy Diagnosis Pathophysiology Pharmacology Epilepsy is abnormal Epilepsy is caused by an excess • Drugs that decrease glutamate brain activity and can of glutamate causing excitation be observed on an • Drugs that increase GABA EEG which measures within the brain electrical activity Glutamate Glutamate GABA GABAQs – GABA and GlutamateCN: 2, 3, 4, 6 (eye nerves) • Cranial nerve 2 is the optic nerve. Visual information travel down it • Cranial nerve 3 (ocular sphincter pupillae, ciliary motor) controls most parasympathetic and eye muscles and some levator palpabrae extra parasympathetic superioris • Cranial nerve 4 (trochlear) controls superior oblique • Cranial nerve 6 (abducens) controls lateral rectusCN: 5 and 7 (branchy) CN 5 - Trigeminal nerve • Ophthalmic, maxillary, mandibular CN 7 - Facial nerve • Muscles of facial expression • Sensation of the face • Parasympathetic for lacrimal and • Muscles of mastication (V3) salivary glands • TasteCN: 1 and 8 (senses) CN 1 Olfactory CN 8 Vestibulocochlear • Smell • Hearing • BalanceCN: 9 and 12 (the “gloss”) CN 9 Glossopharyngeal CN 12 Hypoglossal • Parasympathetic salivary gland Muscles that move tongue • T aste and sensation to tongue • Swallowing (stylopharyngeus) • *all these also done by other nervesCN: 10 and 11 (other) CN 10 Vagus CN 11 Accessory • Parasympathetic heart • Innervate neck muscles regulation (sternocleidomastoid and • Parasympathetic trapezius) digestion • Swallowing muscles Multiple cranial nerves • (Taste and tongue sensation) • Salivary glands • Swallowing muscles Glossopharyngeal Facial FacialCranial Nerves Nuclei Motor Sensory • Our brainstem has Nucelli Nucelli motor and sensory nuclei • Cranial nerves pass through. • Some only have motor or sensory and some both. Multiple cranial nerves may derive fibres from a single nucleusSpecial CN Pathways • “Special” is opposed Nerve type Definition to the general nerve pathways Special somatic afferent Fibres that carry special senses of • Afferent is still hearing and balance senses but: • Somatic is for Special somatic efferent Non existent hearing and balance while Special visceral afferent Fibres that carry taste sensation visceral is taste Special visceral efferent Fibres that innervate skeletal • Efferent muscles of the jaw, face, larynx and • All special cranial nerves efferent pharynx are visceralSummary Synapses and neurotransmitter GABA and Glutamate • Transmission at glutamate • Parts of neurons and their synapses functions • Glutamate receptors • Characteristics of a synapse • Transmission at GABA synapse • Stages of synaptic transmission • Cause and treatment of epilepsy • Release of neurotransmitters and the effect of neurotoxins • Post-synaptic receptors • Inactivation Cranial Nerves • Amino acid, amine and peptide • The functions of each cranial nerve neurotransmitters • Cranial nerve nuclei • Excitatory and inhibitory • Special cranial nerve pathways neurotransmittersQuestions – Cranial Nerves
