Lesson 2. Neural communication PDF

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Bachelor´s Degree in Psychology, UEM. Subject: Physiology. Professor: Elena Velarde. Included in the Mid-term exam....

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Lesson 2. Neural communication 1. Synapsis Synapse: communication between two nerve cells. The action potential of a Presynaptic cell determines excitation or inhibition of a Postsynaptic cell. There are two types of synapses:  Electrical synapse o The cells are electrically coupled, allowing ions to spread between cytoplasm. o It does not require receptors or mediator molecules. o Cytoplasm are directly attached through their electric membranes (GAP junctions) o They are common in: Heart cells and smooth muscle cells.  Chemical synapse o Mediated by Neurotransmitters (NT) o The NT are molecules that are released by the presynaptic neuron and they bind specifically to a receptor located in the postsynaptic neuron. o Predominates in the CNS. o The information goes in one way. o NT binding to its receptor can induce depolarization of the postsynaptic cell. o The action potential of a presynaptic cell determines excitation or inhibition of the postsynaptic cell. Process: 1. Arrival of the action potential to the presynaptic terminal of the neuron. 2. Opening of voltage-gated Ca2+channels. 3. Exocytosis of NT vesicles. 4. Binding of NT to specific postsynaptic receptors. 5. Signal transmission to postsynaptic cell. Any transmission of a message means:  Stimulus recognition (specific binding receptor-NT)  Signal transmission. 6. Cellular response: gene expression, growth, action potential. 7. End of response: degradation or inactivation of the signalling molecule. Mechanisms to remove the NT from the synaptic cleft.  Diffusion of the NT to surrounding glial cells.  Enzymatic degradation of the NT in the synaptic cleft.  Re-uptake into the presynaptic terminal.  Mechanisms of synaptic transmission The binding of the NT to the postsynaptic neuron induces a change in the potential of that neuron called unitary postsynaptic potential. Postsynaptic potentials can be:  Excitatory postsynaptic potential (EPSP) o Generate depolarization that can reach the threshold potential (-55mV) and trigger AP opening Na+ channels. o Excitatory response.

Fisiología Physiology Elena Velarde Fernández [email protected] Inhibitory postsynaptic potential (IPSP) o Generates hyperpolarization that distances the membrane potential from the threshold potential. Opening of Clchannels (influx of Cl- to the cell) and K+ channels (outflux of K+ from the cell. o Inhibitory response. Summation  Triggering an action potential in the postsynaptic neurons requires the participation of several synapses: Summation.  Spatial summation  When two or more presynaptic afferents fire at the same time, each one produces its EPSP.  Each single EPSP does not reach the threshold potential.  By adding the three EPSPs, threshold is reached and AP is triggered.  No action potential is generated.  It may also happen that an IPSP from an inhibitory neuron decreases the value of the EPSPs generated by other excitatory neurons. Temporal summation When the same presynaptic fiber increases its firing frequency several in quick succession, the EPSPs overlap to reach the threshold. 8. Neurotransmitters 

Types of receptors:

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Ligand-gated ion channels: Ionotropic receptors o More Na+ influx = depolarization. o More Cl- influx = hyperpolarization-inhibition. o More K+ outflux = hyperpolarization-inhibition. G-protein coupled receptors: Metabotropic receptors o Channels opening/closing. o Activation-inhibition of second messengers.

Types of neurotransmitters: Drug Muscarine (fungi)

NT-receptor involved / action Acetylcholine-M1-5/ AG

Nicotine(tobaccodrug) Atropine (Belladonna) Clozapine(drug)

Acetylcholine-N ach/ AG Acetylcholine-M / ATG Dopamine-D1 / ATG

Bromocriptine(drug) Procaterol(drug) Atenolol(drug)

Dopamine-D2 / AG Adrenalin-β2 / AG Adrenalin-β1 / ATG

Effect / uses Toxicity parasympathetic Addiction Several medical uses Schizophrenia Treatment Parkinson Treatment Asthma Treatment Treatment cardiovascular

Fisiología Physiology Elena Velarde Fernández [email protected] Drug Buspirone (drug) Fluoxetine(drug) Caffeine (coffee) Cholera toxin (vibrio)

NT-receptor involved / action Serotonin-5-HT1 / AG Serotonin-ATG recapture Adenosine A1 / ATG Miscellaneous: D1, H2, A2, β/ Active AC GABA/ AG or ATG

Benzodiazepines (drugs) Alcohol (drug) GABA Anaesthetics (drug) GABA (more) Buprenorphine(drug) Opioids/ AG Naloxone(drug) Opioids/ ATG THC (marijuana-drug) Endocannabinoids-CB1 / AG

Effect / uses Anxiolytic Depression CNS excitation Diarrhea, cramps. Sedative, hypnotic Effects several SNC Sedation Analgesia Poisoning opiates Several CNS effects

Fisiología Physiology Elena Velarde Fernández [email protected] Pathology / etiology Epilepsy: Hereditary, Metabolic, failures or injuries during development.

Description

NT involved / area Seizures. GABA(Decrease Electrophysiol ) in the ogical hippocampus. abnormalities. Glutamate: NMDA alterations. Noradrenaline/s ystem opioidergic?

Treatment

Anticonvuls ants: -Diazepam (GABA stimulation). -Topiramate (NMDA antagonist). Carbamazepin e (Na+ channel inactivation). Tacrine: Miscellaneous: Dementia. Alzheimer: acetylcholines Degeneration mainly Destruction of of cortical and acetylcholine( terase neurons. Protein inhibitor. cortex). accumulation called subcortical AlsoD2 neurons. antagonists. β-amyloids. Symptomatol Catecholamin -MAO Emotional ogy: changes es: alteration in inhibitors disorders: and NT NA, serotonin, in mood, depression, reuptake ACh, DA and sleep, food bipolar and inhibitors. adrenaline intake, etc. anxiety: levels, mainly in -Lithium: for Alterationsin NT. bipolar. cortex. GABA, serotonin and neuropeptides in anxiety. DA Antipsychoti Psychosis, Schizophrenia: hallucinations hyperactivity cs: failures during and Glu risperidone or neurodevelopment, , cognitive and emotional hypoactivity haloperidol Stress, abnormalities (Others) inflammation, etc....