Ligand Gated: Byrant et.al [1] notes that a rapid response is initiated by a ligand/drug binding to a receptor on the ligand gated channel on the cell surface. This binding of the ligand results in the ligand gated channel to open or close, triggering the entry or exit of ions into or out of the cell, along a concentration gradient, causing a cellular response the cell. [2]. Cocaine is an example of a drug which blocks sodium channels. This causes blocked neural transmission and localized loss of sensation [3]. G-Protein Coupled: These receptors are also called metabotropic receptors, which Bryant [1] states act within seconds to bring about a response, slower than the responses seen with ligand-gated receptors. These receptors become activated when a ligand binds to a receptor, located externally on the cell membrane. The G-protein becomes activated from the inactive GDP to the active form, GTP. This causes a change in the effector protein, such as an ion channel, resulting in a response in the cell [1]. Milligan [4] states that LY-404,039, an amino acid analogue drug, acts on the 5-HT2A receptor, to treat schizophrenia. Kinase Linked: …show more content…
This is due to the fact that the binding of a ligand to this receptor triggers processes which change the synthesis of proteins, such as enzymes, through gene transcription in order to bring about a response at a cellular level [5]. An example of a drug that acts on this receptor is Pazopanib, which Stenberg [6] states acts on vascular endothelial growth factor and platelet derived growth factor receptors as well as c-Kit to block tumour growth and inhibit
Chemistry of Psilocybin and Synaptic Transmitters Involved Psilocybin is a type of hallucinogenic mushroom that is ingested by eating the raw fungi. The mushroom can also be made into a tea and drunk. In some of the later studies done on psilocybin, the drug was synthetically produced and then either inhaled or injected by an IV. The drug enters the blood stream and can cross the blood brain barrier because of it relative metabolic similarity to serotonin (Fuller 1985). This means that since psilocybin is chemical resemblance to the neurotransmitter serotonin, psilocybin can trick the protein channels embedded in the membrane of the blood vessel and pass through as if it were serotonin and not a drug.
Synaptic Transmitters Involved in LSD Administration The nearly concurrent discovery of serotonin (5-HT) and LSD-25 in the 1950 's encouraged a lot of research to be done on the relationship between LSD and serotonin, which helped to develop a greater understanding of the role serotonin plays as a neurotransmitter in the brain (Nichols, 2004). Today it is believed that LSD (and other hallucinogens) stimulate 5-HT2A receptors (Kalat, 2004). Activation of these receptors causes cortical glutamate levels to increase. This is presumed to be a result of a "presynaptic receptor-mediated release" from neurons in the thalumus (Nichols, 2004).
Pharmaceuticals have examined and found to ”work by changing the biological functions of the target cells in the body through chemical agents“ (Doweiko, 2015, p. 16). ”Many people in the past have thought that drugs that
The Role of Dopamine Receptors in Schizophrenia. Retrieved March 3, 2005, From Stanford University, Chemistry department web site, http://www.chem.csustan.edu/chem44x0/SJBR/Mann.htm Naheed, M., & Green, B. (2000). Focus on Clozapine. Retrieved February 7, 2005. From http://www.priory.com/focus14.htm Waddinton, J.L., & Buckley, P.F. (1996).
...s to interfere with bonding to the receptors. The final possibility uses CNP, which downregulates the activation in MAP kinase pathways in the chondrocytes (4).
The dopamine theory behind the cause of schizophrenia states that in part excess dopamine is a possible factor or there is more than an average number of dopamine, Type 2 receptors. Risperidone acts on the dopamine D2 receptor (Sarason, et al, 2001, pg. 368). Risperidone is a psychotropic drug and is part of the chemical class of benzisoxazole derivatives used as a treatment for schizophrenia, with some results for bipolar manic disorder, as well.
When something changes in the inner environment it sends information to the receptor. The receptor sends information to the control center and then the control center sends instructions to the effector once the information is received from the control center it proceeds to either oppose or increase the stimulus. This process is designed to repeatedly work at restoring or maintaining homeostasis.
Barbiturates fall into the class of sedative-hypnotics. Some of the medical uses include: short-acting barbiturates that can be used for anesthesia induction, while the long acting barbiturates are utilized in anti-convulsant therapy. Barbiturates attach to the β subunit of the GABAA receptor. Stimulation of this inhibitory receptor causes an influx of chloride into cell membranes, which affects the threshold potential of the postsynaptic terminal. Barbiturates at high doses can actually cause direct opening of the chloride channel, essentially mimicking GABA without the actual presence of GABA. Barbiturates also have the ability to suppress depolarization, which is induced by glutamate, an excitatory neurotransmitter within the CNS. These drugs are highly effective at causing neuronal inhibition within the CNS. Barbiturates have a very narrow therapeutic window, which can result in life threatening side effects if not monitored properly. Some of the serious side effects corresponding to the cardiovascular system include: hypotension, decreased cardiac contractility, decreased cardiac output and decreased cerebral blood flow. In long-term barbiturate use cytochrome P450 enzymes are induced which can rapidly metabolize and affect other drugs utilizing this pathway. Tolerance to the depressant effects is common amongst chronic users. Barbiturates have both a tissue specific tolerance and metabolic tolerance. Tissue specific tolerance occurs in the reticular activating
Its ability to inhibit sodium channels within brain cells thereby protecting the cells from hypoxia (lack of oxygen)
glutamate receptors using antibodies, that tag on to the receptor itself. The proteins that make up the
γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the CNS. GABAA is a ligand gated ion channel composed of five subunits. Through positive allosteric modulation ethanol binds to the δ subunit of the receptor and enhances the inhibitory effect of GABA. Once ethanol has bound to the GABAA receptor, chloride ions enter the post-synaptic neuron. This cascade of ions hyperpolarises the neuron, thus increasing inhibitory effects and makes the neuron less excitable. Ethanol alters the enzyme kinetics enabling the ion...
Comparison of the Effects of Antidepressants and Their Metabolites on Reuptake of Biogenic Amines and on Receptor Bindings. Cellular and Molecular Neurobiology, Vol.19, No.4.Denmark: Plenum Publishing Co. Science Direct, (2003).Fluoxetine inhibits A-type Potassium Currents in Primary Cultured Rat Hippocampal Neurons. Department of Physiology, Medical Research Center, South Korea.
The occurrence of action potential is a very short process. When action potential occurs in the neuron the sodium channels open along the axon and sodium comes in. Because the sodium is positive it make the inside of the axon positive. When both the inside and outside are comparative in charge the sodium storms rushing in and starts the depolarization of the action potential. After this happens the sodium channels begin to close and the potassium channels begin to ...
Action potential is another method of transmission of chemical information from one neuron to another. It takes place in an area of plasma membrane in which high concentration of voltage-gated 〖Na〗^+ and K^+channels. The only ions involved in action potential are 〖Na〗^+ and K^+. As chemical reach a certain level, the neuron will eject the extra concentration into the adjacent neuron. One of the keen differences between graded and action potential is that the presence of refractory period does not make summation possible because of its “all or none” nature.
When using a drug like cocaine it causes the nerve cells to release an abnormal large amount of natural neurotransmitters and also prevents the normal recycling of brain chemicals which are needed to shut off the signal between neurons. Such disruption produces an amplified message that disrupts the normal communication patterns in the brain.