Download Free Medical Nervous System PowerPoint Presentation

Nervous System PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Neurology, which is titled "Nervous System", to know about the nervous system including central nervous system and peripheral nervous system.

Tags : Neurology, Nervous System, central nervous system, peripheral nervous system

Published on : Aug 18, 2021 | Views : 2831 | Downloads : 7

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ppt slide no 1 content not found
Slide 2-

ppt slide no 2 content not found
Slide 3-

ppt slide no 3 content not found
Slide 4-

A fresh brain with dura removed. Note the numerous superficial blood vessels running in the arachnoid.
Slide 5-

If we strip off the meninges we see the brain has a heavily folded surface or cortex (in latin: cortex =bark)
Slide 6-

The outwardly rounded ridges of cortex are GYRI (singular GYRUS) The grooves between the gyri are SULCI (singular SULCUS)
Slide 7-

The two main sulci are also known as fissures. These are the central sulcus (fissure) between the frontal and parietal lobes, and the lateral sulcus (fissure) between the frontal and temporal lobes
Slide 8-

Recall that the main bones of the cranium are the frontal, parietal, occipital and temporal.
Slide 9-

The forebrain (cerebrum) can be divided into lobes that rest in the corresponding cranial fossa. The frontal lobe lies under the frontal bone in the anterior cranial fossa, the temporal lobe lies under the temporal bone in the middle cranial fossa and the occipital lobe lies under the occipital bone in the posterior cranial fossa, along with the cerebellum. The parietal lobe lies under the parietal bone. The cerebellum (little brain) lies below the occipital lobe. It has much thinner gyri than the cerebrum
Slide 10-

Note appearance of cerebellum; the gyri are thinner and straighter than in cortex
Slide 11-

Most of the gyri and sulci have individual names but for now we only need to remember the central and lateral sulci.
Slide 12-

Inside the lateral fissure there is a hidden area of cortex, the insula or ‘Island of Reil’.
Slide 13-

Before we can investigate the interior of the brain by cutting it up we need to define the planes of the brain that we will cut (section) in. Ggoing to a higher horizontal (axial) plane is going rostral. Going down towards the spinal cord and cauda equina is going caudal. The coronal plane is also known as the frontal plane
Slide 14-

This is a brain cut in the frontal plane. Unstained brain tissue shows up as grey (actually pinky-grey) and white matter
Slide 15-

Staining the brain tissue is essential to differentiate structures. In this stain cell bodies are stained blue. Thus the cortex can be seen to contain large numbers of nerve cell bodies
Slide 16-

Grey matter = cell bodies & processes White matter = axons
Slide 17-

Nowadays MRI enables us to see a histology-like picture in the living brain. Stained post-mortem Living
Slide 18-

The corpus callosum is the most important landmark in the brain. It is a bridge of axons that joins the two hemispheres and allows communication between them. Corpus Callosum
Slide 19-

The corpus callosum is very easy to identify in the mid-sagittal plane (below). Corpus callosum is easy to see on an MRI
Slide 20-

Underneath the anterior part of the corpus callosum we can see the lateral ventricles
Slide 21-

Note that the corpus callosum folds back on itself rostrally. This region ends in the anterior commissure ‘Folded back’ region Anterior commissure
Slide 22-

CRITERIA NT found in axon terminals NT released by action potentials Synthesis identified External application mimic normal Response Pharmacology same for normal and externally applied NT ~
Slide 23-

Lock & Key Model NT binds to receptor NT = key Receptor = lock Receptor changes shape determines if EPSP or IPSP receptor subtypes NOT NT ~
Slide 24-

ligand binds to receptor activation: + or - ~
Slide 25-

Same NT can bind to different -R different part of NT ~
Slide 26-

Specificity of drugs Drug A Drug B
Slide 27-

Acetylcholine - ACh Most abundant NT in Peripheral N.S. also found in Central N.S. Precursor = choline nutrient Degraded by acetylcholinesterase- AChE Membrane bound - pre- & postsynaptic Nicotinic receptor - ionotropic Muscarinic receptor - metabotropic ~
Slide 28-

Acetylcholine Synthesis choline + acetyl CoA
Slide 29-

Ach - Distrubution Peripheral N.S. Excites somatic muscle Autonomic NS Ganglia Parasympathetic NS Neuroeffector junction Central N.S. - widespread Hippocampus Hypothalamus ~
Slide 30-

Cholinergic Agonists Direct Muscarine Nicotine small doses Indirect AChE Inhibitors ~
Slide 31-

Physostigmine Organophosphates - irreversible DFP Soman & Sarin Malathion* Agonist or Antagonist? indirect agonist ~ AChE inhibitors
Slide 32-

Cholinergic Antagonists Direct Nicotinic - Curare Muscarinic - Atropine Scopolamine Indirect Botulinum Toxin Black Widow Spider Venom ~
Slide 33-

ACh N M AChE AChE Botulinum toxin BWSV curare atropine
Slide 34-

Monamines Amino acid precursors single amine group 2 groups Catecholamines - catechol ring Indolamine - indole ring Affected by many of same drugs ~
Slide 35-

Monoamines Catecholamines Dopamine - DA Dopaminergic Norepinephrine - NE Noradrenergic Epinephrine - E Adrenergic ~ Indolamines Serotonin - 5-HT Serotonergic
Slide 36-

Monoamines Terminated by... reuptake monoamine oxidase - MAO catechol-O-methyltranferase - COMT also in liver Reserpine ---> leaky vesicles depletes monoamines ~
Slide 37-

A Monoamines MAO MAO COMT Reserpine
Slide 38-

MAOIs Iproniazid Reuptake blockers Tricyclic antidepressants Imipramine Desipramine Cocaine & Amphetamine ~ Indirect Monoamine Agonists
Slide 39-

Dopamine Only in central nervous system mostly inhibitory systems Reward Schizophrenia Movement Nigrostriatal Pathway At least 5 DA-R types: D1, D2, etc. ~
Slide 40-

Dopaminergic Drugs Agonist L-dopa Antagonists Chlorpromazine D1 Haloperidol D2 ~
Slide 41-

Dopamine Synthesis Tyrosine
Slide 42-

Norepinephrine Peripheral N.S. Sympathetic neuroeffector junction Adrenal glands Central N.S. Hypothalamus Locus coeruleus Alpha & Beta receptor subtypes NEa & NEb ~
Slide 43-

Noradrenergic Drugs Agonists Mescaline Ephedrine Antagonist Propranalol - beta receptors ~
Slide 44-

Norepinephrine Synthesis Tyrosine
Slide 45-

Serotonin NOT a catecholamine Peripheral 98% in blood & smooth muscle Central N.S. Raphe nucleus Hypothalamus R subtypes: 5HT1 & 5HT2 ~
Slide 46-

Sertonergic Drugs Agonists SSRIs Selective Serotonin Reuptake Inhibitors Buspirone MDMA Ecstacy ~
Slide 47-

Sertonergic Drugs Antagonists Psilocybin LSD in CNS Inverse agonist ketanserin ~
Slide 48-

Tryptophan Serotonin Synthesis
Slide 49-

Gamma-aminobutyric acid GABA - GABAergic Major NT in brain inhibitory system Receptor subtypes GABAA - controls Cl- channel GABAB - controls K+ channel Precursor = glutamate ~
Slide 50-

GABAergic Drugs Agonists Benzodiazepines Barbiturates Ethyl alcohol (ETOH) Antagonists Picrotoxin Inverse agonist Ro 15-4513 ß CCM ~
Slide 51-

GABA Synthesis & Reuptake From Krebs cycle metabolism of glucose in mitochondria From Glial cells GABA ---> Glutamate ---> Glutamine Glutamine into neurons After release GABA back into glia ~
Slide 52-

Glutamate GABA GABA Synthesis
Slide 53-

Neuropeptide Chains of amino acids Synthesis in soma Often neuromodulators alters sensitivity of neurons slower, longer-lasting effects Substance P - pain signaling Endorphins - analgesia, euphoria ~
Slide 54-

Endorphins Opioids Dynorphin met-enkephalin leu-enkephalin Beta-endorphin Receptor subtypes: mu1, mu2, kappa, delta, omega ~
Slide 55-

Agonists morphine heroin codeine Antagonists naloxone naltrexone ~ Endorphins (cont.)
Slide 56-

Other NTs Excitatory amino acids Glutamate & Aspartate Histamine Inflammatory Response Nitric Oxide - It’s a gas Carbon Monoxide? Anandamide ligand for THC-R ~
Slide 57-

Why would anyone want to be a neuroscientist?
Slide 58-

The scientific study of the nervous system and its relationship to cognition and behaviour.
Slide 59-

ppt slide no 59 content not found
Slide 60-

Associative Learning Mechanisms Classical Conditioning Discovered by Ivan Pavlov (1920s) Passive learning Operant Conditioning Discovered by B.F. Skinner (1960s) Active learning
Slide 61-

Types of Memory Explicit (conscious) Implicit (unconscious)
Slide 62-

How is the Brain studied? Case Studies Gene Splicing Imaging PET EEG (electrical current detection) Transcranial Magnetic Stimulation (causes temporary disruption of a brain region) MRI fMRI CAT
Slide 63-

How is learning and memory enabled? Signal Transduction: Inter-Neuron communication occurs via Neurotransmitters at the synaptic gap Neural Plasticity: Through experience, Neurons can change the way they function Long Term Potentiation: Cellular mechanism through which associations can be detected and recorded in the brain
Slide 64-

Sensory Memory Working Memory LTM Sensory Input Indefinite duration Retrieval Stage Theory of Memory