Psychopharmacology, Effect of Drugs on Behaviour - Essay Example

? Psycho-pharmacology Questions Psycho-pharmacology Questions Sleep comprises of five stages and stage of sleep best resembles the brain activity of being awake. This represents the beginning of sleep and it is considerably a light stage. It is a transition between sleep and wakefulness. An awakened individual might not realize that he/she was dreaming. This is the stage of light sleep where an individual easily drifts into and away from sleep. One can easily be awakened and the eyes exhibit slow movement and decreased muscle activity. Most individuals will experience abrupt muscle contractions and will be drawn to falling. This can be attributed to abrupt muscular contraction also referred to as hypnic myoclonia. The brain waves of the individual are highly irregular. These are theta waves with high amplitude and this makes the brain waves are very slow (Rang & Dale, 2007). The stage falls in the state of non-rapid eye movement (non-REM). 2. The brain waves in stage I differ from those in stage 4. Stage 1 is characterised by slow brain waves that are theta waves with high amplitude. Conversely stage 4 also forms the session of delta sleep. This is named after the slow delta waves experienced in this session of sleep. Consequently an individual is immersed in deep sleep and it is hard to wake such an individual. This is unlike stage one which is the stage of light sleep which is triggered by the slow theta brain waves experienced in this session (Rang & Dale, 2007). 3. Stage 2 forms the second sleep stage which lasts for around 20 minutes. An individual’s brain engages in the activity of producing fast rhythmic brain waves also referred to as sleep spindles. According to polysomnographic readings, this session of light sleep is characterized by intermittent negative and positive waves. These waves depict abrupt periods that are marked by sessions of muscle relaxation in combination with muscle tone. These brain waves progressively become larger and slower. The body temperature gradually decreases and the heart rate also slows down. Individuals are likely to experience subjective sleep spindles. The intensity of these rhythmic brain waves varies amongst individuals. Moreover, individuals might experience longer periods of muscle relaxation as compared to muscle tone and vice versa. Furthermore, individuals also experience theta, delta and K-complexes waves in combination with sleep spindles. These other waves may be experienced for a longer duration than sleep spindles (Rang & Dale, 2007). 4. On the basis of brain waves, stage 3 can be referred to as the stage of deep sleep for the following reasons. Stage 3 is characterized by slower and larger brain waves as compared to those exhibited in stage 2. The brain begins to produce delta waves during stage 3. This marks the beginning of deep sleep (Rang & Dale, 2007). 5. The brain waves in stage 3 vary from those experienced in stage 4. Stage 3 is characterised by delta waves that are initially produced during this stage to usher in deep sleep. It marks the transition from light sleep to deep sleep. However, these delta waves occur in combination with faster and smaller waves. In stage 4, the brain exclusively produces delta waves. This session is devoid of both muscle activity and eye movement. In fact it is during this period when individuals experience nightmares, sleepwalking and bedwetting. In this respect, individuals are likely to be more perceptive of stimuli (including noise in the immediate environment) in stage 3 as compared to stage 4 when an individual is fully immersed in deep sleep (Rang & Dale, 2007). 6. Sleep is manifested by the two main states of non rapid eye movement (NREM) and rapid eye movement (REM). The later comprises of deep sleep and comes after NREM. REM is marked by higher brain activity than NREM. The brain waves generated during REM are much slower and irregular as compared to those in REM. This is consistent with research concerning dreaming. Dreaming occurs in the state of very deep sleep and hence the need for the brain to generate slow and large waves (Rang & Dale, 2007). 7.Opiates have a profound impact on pain and mood. With regard to pain, opiates are antinociceptive. The opiates bind to numerous opioid brain receptors with a higher affinity than endogenous peptides such as dynorphin, Met-enkephalin, leu-enkephalin and ?-endorphin thereby mediating their analgesic effect. Opiates also trigger a sense of wellbeing and contentment. This is crucial since anxiety and agitation is associated with pain. This mediated by µ opiate receptors in the brain (Rang & Dale, 2007). 8. Heroin (diamorphine) is a very addictive opiate. Treatment for dependency can be provided by an opiate agonist. Opiate agonists produce an opiate effect via their interaction with opioid receptors. Consequently, the body will not experience any withdrawal symptom that is normally caused by the terminated consumption of heroin. An opiate antagonist will not be effective as it will bind and occupy the opiate receptor sites and prevent the binding of an agonist. The addict will not experience any opiate effect and will be greatly affected by withdrawal symptoms after ceasing from heroin consumption (Rang & Dale, 2007). 9.Dopamine is abundant in the hypothalamus, limbic system, and corpus striatum. It is elased from the dopaminergic neurons into the synapse. It’s synthesized from tyrosine to form dopa and subsequently decarboxylated. This neurotransmitter is recaptured after release from the nerve terminals by a dedicated dopamine transporter. It is degraded by catechol-O- methyltransferase and monoamine oxidase into homovanillic acid(HVA) and dihydroxyphenylacetic acid(DOPAC) (Rang & Dale, 2007). 10. For persons suffering from conditions resulting from excess dopamine, it would be not be effective to administer a drug that would interfere with reuptake as this would result in more dopamine in the synapse and hence more sensitization (Rang & Dale, 2007). 11.Reuptake helps in the removal of neurotransmitters such as dopamine to prevent the perpetual stimulation of neurons (Rang & Dale, 2007). 12.Amphetamines trigger the release and contribute to increased levels of dopamine. They are structurally similar to dopamine and bind to dopamine receptors to and directly diffuse via the neural membrane and are subsequently in the presynaptic neuron terminal. Consequently, amphetamines cause the release of dopamine from the storage vesicles and there is high concentration of dopamine in the synaptic gap (Rang & Dale, 2007). 13.Reuptake is the process through which a neurotransmitter is absorbed by the specific neurotransmitter protein after the neurotransmitter has fulfilled its function of propagating action potential/nerve impulse. This is crucial as it facilitates neurotransmitter recycling and allows for the regulation of neurotransmitter levels at the synapse. This also regulates the signal duration as a consequence of neurotransmitter release. Neurotransmitters bind and are transported by transport proteins that are highly specific and these transport proteins are vital in neurotransmitter reabsorption. .14. Reuptake reduces the synaptic dopamine levels. Dopamine is transported by a dopamine transporter which specifically binds to dopamine and this transporter is a member of the monoamine transporter family (Rang & Dale, 2007). 15. TCH (tetrahydrocannabinol) mimics the effects produced by anandamide in the following mechanism. Both agents have an affinity and bind highly to cannabinoid receptors. Anandamide is the neurotransmitter that activates cannabinoid receptors. THC is present in marijuana and mimics the activity of anandamide by binding to cannabinoid receptors thereby activating neurons. Cannabinoid receptor activation inhibits the release of neurotransmitters by inhibiting Ca+ entry as well as depolarization following the activation of potassium channels. This leads to behavioral and psychological effects (Rang & Dale, 2007). 16. For a scientist, seeking to counteract marijuana effects, it would be appropriate for him/her to design a drug that is based on anandamide. Anandamide binds to the same cannabinoid receptors (CB1) as THC, the main active compound contained in marijuana (Rang & Dale, 2007). The structure of this drug will be compatible with the cannabinoid receptors. The drug will be an antagonist and prevent the binding of THC thereby counteracting the effects of marijuana. Reference Rang, H.P.& Dale,M.M.(2007). Pharmacology. Philadelphia: Elsevier Publishers. Read More