Most drugs and toxins that affect psychological functions Essay

            Most drugs and toxins that affect psychological functions alter the transmission of chemicals across the synapses.  Some substances impede the release of transmitter chemicals from neurons into the synaptic space.  For example the toxin produced by the microorganism that causes botulism prevents the release Ach.  The result is paralysis and sometimes rapid death.  Drugs such as reserpine cause transmitter chemicals to leak out of the synaptic vesicles and be rapidly broken down, creating a shortage of transmitters and decreased activity at the synapse.  Reserpine is often prescribed to reduce blood pressure because it decreases the activity of the neurons that excite the circulatory system.

            Some drugs speed up the release of transmitter chemicals into the synaptic space.  For example, the poison of the black widow spider causes Ach to spew into the synapses of the nervous system.  As a result, neurons fire repeatedly, causing spasms and tremors.

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  Caffeine increases release of excitatory, arousing neurotransmitters by blocking the action of adenosine, a transmitter substance that inhibits the release of these substances.  Two or three cups of coffee contain enough caffeine to block half the adenosine receptors for several hours, producing a high state of arousal in the nervous system.  In some cases, the arousal is so intense we say the person is suffering from coffee nerves (Nehlig, Daval & Debry, 1992 p.

139).            Some chemicals produce their effects by increasing or decreasing the quantity of neurotransmitters in the synapse.  Other substances work directly on the receptor sites at the other side of the synaptic gap.  The drug LSD for example, attaches to receptor sites on neurons that receive serotonin, inhibiting the activity of those neurons.  LSD may also affect levels of dopamine, although scientists do not know exactly how.

  Some scientists have speculated that a number of these neurons suppress dreaming.  When LSD inhibits or interferes with those neurons, a kind of dreaming occurs, even though the user is awake.  Some drugs act by blocking receptors so that neurotransmitters can neither excite nor inhibit their targets.  For example, atropine, a poison derived from belladonna and other plants, blocks receptor sites for Ach in the brain, often disrupting memory functions.  Curare, the poison with which some native peoples of South America traditionally have tipped their arrows, blocks the Ach receptors that control skeletal muscle function and rapidly produces paralysis (Shepard, 1994).

            Still other drugs interfere with the removal of neurotransmitters from the synapse after they have done their job.  Once transmitter chemical have bonded to receptor sites and have stimulated or inhibited the neuron, they are normally either removed from the body or returned to the axon terminals from which they came.  A number of stimulant drugs interfere with this process.  Cocaine, for example, prevents dopamine from being reabsorbed.

  This excess amount of dopamine accumulates in the synapses, producing heightened arousal of the entire nervous system.            Drug effects can lead to surprising discoveries about the brain and its neurotransmitters.  For example, in attempting to explain the effects of opiates or painkilling drugs like morphine and heroin that are derived from the opium plant scientists have discovered that the central nervous system contained receptors sites for these substances.  They reasoned that such receptor sites would not exist unless the body somehow was able to produce its own natural painkillers.

  This has become apparent when researchers discovered that our brains actually do produce such substances, the endorphins.  It turns out that morphine and other narcotics lock into the receptors for endorphins and have the same painkilling effects.  Similar findings have been noted by people researching the effects of marijuana found brain receptors for a chemical called tetrahydrocannabinal (THC).  The reasoning should be that there should be a natural substance in the body that would fit into these receptors.  Although its natural functions are not yet known, anandamide should have at least some of the effects of marijuana because it locks into the same receptors as THC (Restak, 1993).            Another discovery in recent times is that imbalances in some neurotransmitters may contribute to certain kinds of mental illness.

  Schizophrenia seems to be associated with an overabundance of dopamine.  Some drugs that have been developed to treat schizophrenia seem to reduce the symptoms of this disorder by blocking dopamine receptors.  Some theories link depression to reduced serotonin activity.  Antidepressant drugs such as Prozac alleviate the symptoms of depression by blocking re-absorption of serotonin, increasing the overall level of serotonin in the synapses of the nervous system (Pasinetti & Hiller-Sturmhofel, 2008).            The National Institute of Mental Health labeled the 90’s as the “Decade of the Brain” (Goleman, 1996) and encouraged researchers to push back the frontiers of knowledge about the brain.

  One of the expected payoffs will be a new generation of “designer drugs”.  The miracle of drugs of the previous decade, such as Prozac for depression and Xanax for anxiety, may be little more than chemical dinosaurs in the new millennium.  Current research has shown that there are many different kinds of receptors for neurotransmitters.

  For example, there are at least 15 kinds of receptors for serotonin, a neurotransmitter implicated in mood disorders, eating disorders, sexual response and other aspects of behavior and mental activity.  There are at least five kinds of receptors for dopamine, a neurotransmitter involved in schizophrenia.            One of the problems with the current generation of psychiatric drugs is that they affect all of the receptors for the neurotransmitter they target, rather than the one or two they ought to be targeting.  Such as with depression and serotonin, only one or a few of serotonin’s receptors are likely to be involved in depression.  Current antidepressant drugs therefore cause unwanted side effects, such as digestive and sexual problems.  Once scientists know exactly how each kind of receptor is involved in psychological disorders, we may be able to increase the potency of drug therapies and reduce the side effects.

  The ultimate goal would be to prevent psychological disorders altogether (Pasinetti & Hiller-Sturmhofel, 2008).            Biological treatment, a group of approaches that include medication, may be used to treat psychological disorders in addition to or even instead of psychotherapy.  Patients and therapists select biological treatments for several reasons.  First, therapists sometimes find that they cannot help clients with any of the psychotherapies because the clients are extremely agitated, disoriented, or totally unresponsive.  In these cases, therapists may decide to use some kind of biological treatment to change client’s behavior so they can benefit from therapy.  Second, biological treatment is virtually always used for disorders that have a strong biological component.  Schizophrenia, mentioned earlier and bipolar disorders cannot be effectively treated with psychotherapy, but often do respond to medication.

  For other disorders such as depression, psychotherapy can be effective, but the patient may prefer to take medication because of costs and is more convenient, and allows them to avoid possible stigma of seeing a psychotherapists.  Third biological treatment is often used for clients who are dangerous to themselves and others, especially if they are residing in institutions where only a few therapists serve patients.  But whatever the reason in recent times drug companies have conducted research that is certainly very interesting and hopeful to the future of psychology.Reference:Goleman, D. J. (1996, November 19).  Research on brain leads to pursuit of designer      drugs.  New York Times, pp.

C1, C3.Nehlig, A., Daval, J.L., & Debry, G.  (1992). Caffeine and the central nervous system:   Mechanisms of action, biochemical, metabolic and psychostimulant effects.           Brain Research Reviews, 17.

 139-170.Pasinetti, G. M. & Hiller-Sturmhofel, S.  (2008)  Systems biology in the study of            neurological disorders: focus on Alzheimer’s disease.

  Journal of Alcohol          Research and Health, 30(1),  p. 60-65.Restak, R (1993, Sept/Oct.).  Brain by design.  The Sciences, 27-33.

Shepard, G.M. (1994).  Neurobiology, 3rd. Ed.

  Oxford: Oxford University Press.


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