Please reword in your own words this whole figure.... thank you A hypothetical m

Question

Please reword in your own words this whole figure.... thank you

A hypothetical model of how neuromodulator-amygdala interactions mediate stress effects on hippocampal plasticity. Stress activates the hypothalamus-pituitary adrenal (HPA axis, resulting in elevated secretion of glucocorticoids, catecholamines, enkephalins and other neuromodulators, which affect the hippocampus and amygdala. The influence that stress hippocampus, denoted by his), and the effects of these neuromodulators on the amygdala, denoted by gts). The output from the amygdala (variable m) is a crucial component of the stress induced modulation of hippocampal plasticity. The interaction between m and h(s) is denoted by f(m, h(s)). The model shows that when there is an experimentally induced reduction in the amygdalar input to the hippocampus (as a result of damage or inactivation of the amygdala, m = 0, plasticity in the hippocampus is intact under stress conditions (upper right. However, with intact amygdalar input in response to stress (m> 0), plasticity in the hippocampus is disturbed for example, impaired long-term potentiation (LTP) and enhanced long-term depression (LTD) lower right). The green circles on the matrices represent synapses with normal capacity to generate plasticity for exam normal LTP, thereby accommodating normal hippocampus- dependent memory. The pink circles represent synapses with altered properties of plasticity (for example, impaired LTP and enhanced LTD), which impair subsequent hippocampus-dependent memory. The conjunction of inputs m and his) is required for plasticity n the hippocampus to be disrupted. The model predicts that stress effects on the hippocampus can be prevented by reducing the amygdalar input (upper part of the figure) to the hippocampus. Conversely, the model predicts that these stress effects can be exacerbated by increasing the amygdalar input to the hippocampus

Explanation / Answer

“Amygdala” region of the brain is a neuro-modulator. It further affects the hippocampus region of the brain. This model talks about “amygdala-neuromodulator interaction” and its effect on the brain.

Stress is the stimulus. Stress activates adrenal glands, which further activate hypothalamus, which sends this signal to the pituitary gland. This results in secretion of a variety of neuromodulators including glucocorticoids, catecholamine, enkephalins etc. These neuromodulators affect ‘Amygdala’ and ‘Hippocampus’.

Neuromodulator has an effect known as ‘m’ on amygdala. It has an effect known as ‘h(s)’ on the hippocampus. ‘m’ and ‘h(s)’ combine together to give a requisite response. If there is a damage to amygdala then “m=0”. In such a case, hippocampus plasticity remains intact, even under stress conditions.

On the other hand, if m>0, this means that amygdala is sending signal to hippocampus; in such a case, the plasticity of hippocampus will be disturbed. Impaired LTP (long term potentiation) and enhanced LTD (long term depression) will be observed.

So, if plasticity of hippocampus is disrupted, it means that “Amygdala” and “Hippocampus” regions of brains have given some or the other combined input.

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