# Discussion Guideline

## Aim of Discussion
The aim of discussion is to fulfill the promise made in introduction. The discussion section should flow as: (A) conclusion first, (B) relevant results of this work and how they relate to that conclusion, and (C) relevant literature.

## Rules
Discussion must:
- Follow the format of the template below.
- Conform to the language style typical of a scholarly article in the field.
- Use technical language suitable for the target journal.
- Spell out abbreviations and acronyms considering previous sections.
- Include a clear, concise topic sentence in each paragraph.
- Use transition phrases between paragraphs for coherence.
- Explicitly indicate species.
- Maintain quantitative measurements as they are written.
- Avoid unnecessary adjectives like "significantly", "well".
- Use LaTeX format.
- Ensure at least 1000 words.

## TEMPLATE

[1. Summarizing Key Findings]
This section will provide a clear and brief overview of your main results. State why this particular study was needed to fill the gap stated in Introduction and why that gap needed filling in the first place.

[2. Comparison with Previous Evidence]
Here, you'll place your findings in the context of existing research, reinforcing the validity and relevance of your work.

[3. Supporting Your Findings]
In this part, you address potential counterarguments or contradictory findings, enhancing the robustness of your research by explaining why your results are preferable or more accurate.

[4. Limitations]
Acknowledging limitations in methodology or approach helps strengthen your credibility as a researcher. Study limitations are not simply a list of mistakes made in the study. Rather, limitations help provide a more detailed picture of what can or cannot be concluded from your findings.

[5. Implications]
This final section is crucial for illustrating the broader impact of your work, discussing its biological significance, practical usefulness, and potential applications. End with a concise summary explaining the big-picture impact of the current study on our understanding of the subject matter.

## Examples

For example, the discussion below is well-written, following the provided template.

## With tags

[START of 1. Summarizing Key Findings] We have generated a knockout mouse strain lacking the NMDAR1 subunit in the CA1 region of the hippocampus. These mice seem to grow normally and do not present obvious behavioral abnormalities. We have shown that the mutant mice lack NMDAR-mediated EPSCs and LTP in the CA1 region and are impaired in the hidden-platform version of the Morris water maze (a measure of spatial memory) but not in nonspatial learning tasks. [END of 1. Summarizing Key Findings]

[START of 4. Limitations] We cannot exclude the possibility that the NMDA receptor-dependent synaptic plasticity crucial for memory formation is LTD, given that the CA1-KO mice seem to lack NMDAR-dependent LTD. [END of 4. Limitations]

[START of 3. Supporting Your Findings] However, we think that this is unlikely because spatial learning is apparently intact in knockout mice deficient in protein kinase A that lack CA1 LTD (Brandon et al. 1995). [END of 3. Supporting Your Findings]

[START of 2. Comparison with Previous Evidence] Previous work has used pharmacological and genetic tools to examine whether synaptic plasticity is the mechanism for memory formation. Although the evidence is consistent with this notion many issues have remained unresolved. Our work circumvents these concerns because the deletion of the NMDAR1 subunit occurs in a restricted manner, only in the CA1 region. [END of 2. Comparison with Previous Evidence]

[START of 5. Implications] The plasticity of the EC-CA3 synapses has not been well studied, but our proposed scenario predicts that they are important in implementing the memory system. Thus, it is desirable to generate a CA3 region-specific knockout of the NMDA receptor to allow direct examination of the contribution of these synapses to learning. [END of 5. Implications]

## Without tags

We have generated a knockout mouse strain lacking the NMDAR1 subunit in the CA1 region of the hippocampus. These mice seem to grow normally and do not present obvious behavioral abnormalities. We have shown that the mutant mice lack NMDAR-mediated EPSCs and LTP in the CA1 region and are impaired in the hidden-platform version of the Morris water maze (a measure of spatial memory) but not in nonspatial learning tasks.

We cannot exclude the possibility that the NMDA receptor-dependent synaptic plasticity crucial for memory formation is LTD, given that the CA1-KO mice seem to lack NMDAR-dependent LTD.

However, we think that this is unlikely because spatial learning is apparently intact in knockout mice deficient in protein kinase A that lack CA1 LTD (Brandon et al. 1995).

Previous work has used pharmacological and genetic tools to examine whether synaptic plasticity is the mechanism for memory formation. Although the evidence is consistent with this notion many issues have remained unresolved. Our work circumvents these concerns because the deletion of the NMDAR1 subunit occurs in a restricted manner, only in the CA1 region.

The plasticity of the EC-CA3 synapses has not been well studied, but our proposed scenario predicts that they are important in implementing the memory system. Thus, it is desirable to generate a CA3 region-specific knockout of the NMDA receptor to allow direct examination of the contribution of these synapses to learning.
