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We can work on 8 steps to having fruitful conversations about immigration
o The Immigration table give us 8 steps to having fruitful conversations about immigration. Please read the 8 steps. Then answer one of the four questions proposed as conversation starters.
âHave you ever been in a circumstance where you were a newcomer or felt out of place?â
âWhat factors do you think most influence your perspective? Your personal experience with immigrants whom you know? The media? The Bible?âFor me, I think it is the media mostly.
âHow do you think you might respond if you faced the circumstances that many immigrants were in prior to their decision to come to the U.S.?â
âCan you tell me about an immigrant you know in our community that youâve worked with, served or learned from?â
Sample Solution
Drugs has been known to induce structural plasticity of dendrites since 1997 (Robinson & Kolb, 2004; Russo et al., 2009; Dietz et al., 2009; Russo et al. 2010). Since then, researches on various drugs of abuse have shown to induce a structural change in the brainâs reward circuitry such as opiates decreasing number of NAc medium spiny neurons (MSN) in contrast to stimulants which increases NAc MSN numbers. Early withdrawal after exposure to chronic cocaine induces expression of N-methyl-D-aspartate (NMDA) glutamate receptors at MSN surface causing silent synapse formation and long-term depression (LTD). Prolonged withdrawal will cause retraction of the NMDA receptors to be replaces by α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors changing structure of the spine to become mushroom shaped and promoting long-term potentiation (LTP). This change however can be reversed easily by a challenge dose of cocaine (Figure 2) (Russo et al.,2010). Figure 2. Cocaine-induced synaptic and structural plasticity (Russo et al., 2010) At a molecular level, this is caused by regulation of actin cytoskeleton via scaffolding proteins as well as GTPases and they are activated by transcription factor ÎFosB and cyclic AMP response element binding protein (CREB) which induces spinogenesis (Heiman et al., 2008; Kim et al., 2009). On the other hand, ÎFosB also regulates cyclin dependent kinase 5 (Cdk5) (Kumar et al., 2005) as well as nuclear factor κB (NFκB) (Russo et al., 2009) where both molecules play a role in cocaine-induced spine formation showing the major role of ÎFosB in cocaine-induced structural changes. The only paradox here is that both opiates and cocaine induce similar behavioural phenotypes (Russo et al., 2010) as well as drug administration and withdrawal symptoms although they have completely opposite effect on the NAc MSNs. A few possible hypothesises include changes in synaptic plasticity having a bidirectional property where a change in both directions result in similar behavioural phenotypes, decrease in neuronal complexity in one brain area is compensated by a strength>
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Drugs has been known to induce structural plasticity of dendrites since 1997 (Robinson & Kolb, 2004; Russo et al., 2009; Dietz et al., 2009; Russo et al. 2010). Since then, researches on various drugs of abuse have shown to induce a structural change in the brainâs reward circuitry such as opiates decreasing number of NAc medium spiny neurons (MSN) in contrast to stimulants which increases NAc MSN numbers. Early withdrawal after exposure to chronic cocaine induces expression of N-methyl-D-aspartate (NMDA) glutamate receptors at MSN surface causing silent synapse formation and long-term depression (LTD). Prolonged withdrawal will cause retraction of the NMDA receptors to be replaces by α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors changing structure of the spine to become mushroom shaped and promoting long-term potentiation (LTP). This change however can be reversed easily by a challenge dose of cocaine (Figure 2) (Russo et al.,2010). Figure 2. Cocaine-induced synaptic and structural plasticity (Russo et al., 2010) At a molecular level, this is caused by regulation of actin cytoskeleton via scaffolding proteins as well as GTPases and they are activated by transcription factor ÎFosB and cyclic AMP response element binding protein (CREB) which induces spinogenesis (Heiman et al., 2008; Kim et al., 2009). On the other hand, ÎFosB also regulates cyclin dependent kinase 5 (Cdk5) (Kumar et al., 2005) as well as nuclear factor κB (NFκB) (Russo et al., 2009) where both molecules play a role in cocaine-induced spine formation showing the major role of ÎFosB in cocaine-induced structural changes. The only paradox here is that both opiates and cocaine induce similar behavioural phenotypes (Russo et al., 2010) as well as drug administration and withdrawal symptoms although they have completely opposite effect on the NAc MSNs. A few possible hypothesises include changes in synaptic plasticity having a bidirectional property where a change in both directions result in similar behavioural phenotypes, decrease in neuronal complexity in one brain area is compensated by a strength>
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