Amphetamines causing

The patty drug MDMA (3,4-methylene-dioxymetham-phetamine) as well as amphetamine causes efflux of all monoamine neurotransmitters. The effects of MDMA are described as psychostimulant and hallucinogenic and are judged differently from those of amphetamine. This difference is due to the stronger inhibition of SERT by MDMA as compared with amphetamine, which is a more potent dopamine releaser and moreaddictivethan MDMA. 

In anesthetized rats, amphetamine causes dose-dependent changes in neostriatal unit activity. Spontaneously aetive neostriatal cells are uniformly inhibited at low (<2.0 mg/kg, IP) doses. At intermediate doses, an initial exeitation precedes the inhibition, and, at high doses (>5.0 mg/kg, IP), the predominant effect is excitation (Groves and Rebec 1976). Regional differences in the direction, magnitude, and duration of the response of neurons in the neostriatum exist (Rebee and Curtis 1983). 

The side effects of amphetamine are related to its stimulant effects, especially at high doses and with long-term use. Side effects include irritability, insomnia, confusion, anxiety, paranoia, hallucinations, seizures, and aggressiveness. Amphetamines cause irreversible destruction of blood vessels in the brain, which can cause stroke—even in young people. These drugs also cause the potentially lethal side effects of increased heart rate, irregular heartbeat, and increased blood pressure. 

Monoamines include the catecholamines (dopamine and norepinephrine) and 5-hydroxytryptamine. Although these compounds are present in very small amounts in the CNS, they can be localized using extremely sensitive histochemical methods. These pathways are the site of action of many drugs for example, the CNS stimulants cocaine and amphetamine appear to act primarily at catecholamine synapses. Cocaine blocks the reuptake of dopamine and norepinephrine, whereas amphetamines cause presynaptic terminals to release these transmitters. 

Drugs that alter sleep produce their effects on the brain by altering the actions of neurotransmitters and consequently how neurons communicate with each other. However, different drugs can alter the actions of neurotransmitters in different ways. Stimulants such as amphetamine cause neurons to release excess amounts of neurotransmitters like dopamine and serotonin. Other drugs, such as the prescription sleeping pills Halcion or Ambien or antihistamines, can interact directly with the neurons receptors to either enhance or block the effects of the neurotransmitters. In later chapters, we will discuss how drugs that help you sleep or stay awake alter the chemistry of the brain. 

The stimulating and mood-altering effects of amphetamines give them a high abuse potential. Side effects include insomnia, irritability, loss of appetite, and paranoia. Amphetamines take a particularly hard toll on the heart. Hyperactive heart muscles are prone to tearing. Subsequent scarring of tissue ultimately leads to a weaker heart. Furthermore, amphetamines cause blood vessels to constrict and blood pressure to rise, conditions that increase the likelihood of heart attack or stroke. 

FIGURE 7-43. Adrenergic combo 4 NRI plus d,/-amphetamine. In this case, the NRI action at NE is double-boosted by a mixture of amphetamine salts containing the / as well as the d form of amphetamine. The /-amphetamine causes NE release. In addition, DA will be single-boosted by the (/-amphetamine, which causes DA release. 

A useful model of the action of these two drugs in the reward centers of the CNS is shown in Figure 32-1. Cocaine reduces reuptake of dopamine into the neuron by inhibiting the dopamine reuptake transporter. Amphetamine causes the intracellular release of dopamine within the terminal and reverses the transporter direction so that dopamine is released into the synapse by reverse transport rather than ordinary exocytosis. In addition, amphetamine inhibits intracellular MAO metabolism of dopamine. Note that both drugs result in an increase in the concentration of dopamine in the synapse. 

Some studies have shown that amphetamine causes a reduction in auditory gating of the P20/N40 components (Stevens et al., 1995), while others have argued that the effects are limited to amplitude of the... 

Ryan LJ, Linder JC, Martone ME, Groves PM (1990) Histological and ultrastructural evidence that d-amphetamine causes degeneration in neostriatum and frontal cortex of rats. Brain Res 518 61-11. 

Amphetamines release monoamines from the brain and thereby stimulate noradrenergic, serotonergic, and particularly dopaminergic receptors. Under certain circumstances this leads to psychosis and compulsive behavior, as well as auditory hallucinations similar to those experienced in paranoid schizophrenia. In addition, amphetamines cause an acute toxic psychosis with visual hallucinations, usually after one or two extremely large doses (54). 

F Amphetamines cause insomnia. They have been used as diet pills. 

DOM and DOET, in common with LSD, mescaline and (+ )-amphetamine, caused an increase in spontaneous activity of rats. Two of the phenylaminobutanes, those most closely resembling DOM, also produced activity increases. 

Amphetamines cause the release of dopamine and NE and block their re-uptake, thus aggravating psychotic... 

The continuous use of amphetamine causes tolerance, requiring higher doses, and hence there exists a high potential for its abuse. Amphetamine should not be used with a monoamine oxidase A inhibitor such as tranylcypromine, because the chance of inducing hypertension becomes magnified. 

The multi-slice technique of H MRI was used to study regional effects of amphetamine on rat brain [49], a two-coil system enabling three-dimensional perfusion imaging. Amphetamine caused a significant increase in perfusion in many areas of the brain, including the cortex, cingulate and caudate putamen. 

It has been demonstrated that amphetamine causes reverse transport of endogenous DA into the extracellular fluid [67]. This is consistent with Figure... 

---