Methamphetamine_A Disrupted Dialogue Between Memory and Reward

Heysieattalab and colleagues(2016) delve into the neurological underpinnings of addiction, specifically how amphetamine disrupts communication within the brain's reward and memory systems, and here is a closer look (Heysieattalab et al., 2016): 

• Hijacking the Reward System: Our brains naturally have a reward system that reinforces positive experiences by strengthening connections between neurons. This system helps us learn and remember pleasure-related things, motivating us to repeat those actions. Addictive drugs like methamphetamine interfere with this system, essentially hijacking it and causing it to prioritize the drug above all else. 
• Focus on the Hippocampus:  Heysieattalab and colleagues focused on the hippocampus, a critical brain region for memory function. It's like the brain's filing cabinet, storing information and helping us consolidate memories. Their research investigates how METH use disrupts this process. 
• METH and Impaired Memory: Normally, the hippocampus strengthens connections between neurons through a process called Long-Term Potentiation (LTP). This allows us to learn and form lasting memories. However, the study finds that METH disrupts LTP in the hippocampus, hindering its ability to function effectively. This can explain the cognitive deficits often observed in people struggling with METH addiction. 
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  The Reward Circuit Connection: The hippocampus doesn't operate in isolation. It communicates with other brain regions, including the nucleus accumbens (NAc), a key player in reward processing. The NAc is like the brain's pleasure center, registering and amplifying feelings of reward. METH disrupts dopamine levels in both the hippocampus and NAc. Dopamine is a neurotransmitter heavily involved in motivation, reward, and movement. By altering dopamine function in these areas, METH can further manipulate the reward system and drive addictive behaviors.
• Potential Therapies: Heysieattalab and colleagues (2016) explore using medications targeting specific NAc receptors. These medications could potentially counteract the adverse effects of METH on memory function by regulating dopamine signaling within the reward circuit. This research paves the way for developing treatments that address not just the addictive aspects of drugs like METH but also the associated cognitive impairments.

In conclusion, Heysieattalab and colleagues' (2016) study highlighted how Meth addiction disrupts communication within the brain's memory and reward circuitry, and by understanding these changes, scientists can develop more comprehensive treatment strategies to combat addiction and its consequences.

References

1. Heysieattalab, Soomaayeh & Naghdi, Nasser & Hosseinmardi, Narges & Zarrindast, Mohammad-Reza & Haghparast, Abbas & Khoshbouei, Habibeh. (2016). Methamphetamine-Induced Enhancement of Hippocampal LTP Is Modulated by NMDA and GABA Receptors in the Shell-Accumbens. Synapse (New York, N.Y.). 70. 10.1002/syn.21905.