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Question about hippocampal effect on HPA axis (self.neuroscience)
submitted 12y ago by electroreception
Hi /r/neuroscience,
I am currently doing some research that requires some knowledge about the relationship between the hippocampus and the hypothalamus. I've learned that the hippocampus inhibits most aspects of HPA (hypothalamic-pituitary-adrenalcortical) activity, mostly based on the measurements of corticosteroids, but I was wondering if it is exclusive to corticosteroids? For example, can actions of the hippocampus affect the expression of certain proteins in the hypothalamus (ex: BDNF - brain-derived neurotrophic factor)? If BDNF levels decreased in the hippocampus, can the hippocampus signal to the hypothalamus somehow and pose a feedback effect on the hypothalamus such that BDNF levels in the hypothalamus will increase?
Thank you for all your help!
I am currently doing some research that requires some knowledge about the relationship between the hippocampus and the hypothalamus. I've learned that the hippocampus inhibits most aspects of HPA (hypothalamic-pituitary-adrenalcortical) activity, mostly based on the measurements of corticosteroids, but I was wondering if it is exclusive to corticosteroids? For example, can actions of the hippocampus affect the expression of certain proteins in the hypothalamus (ex: BDNF - brain-derived neurotrophic factor)? If BDNF levels decreased in the hippocampus, can the hippocampus signal to the hypothalamus somehow and pose a feedback effect on the hypothalamus such that BDNF levels in the hypothalamus will increase?
Thank you for all your help!
bluewhale_moo 1 points
BDNF is an activity-dependent neurotrophin. This means that neuronal firing is required for it to be released into the synapse, and for it to increase dendritic branching.
Since the hippocampal innervations into the hypothalamus down-regulate hypothalamic activity, I think it makes sense that the hippocampus and hypothalamus would have opposite BDNF expression under conditions of chronic stress.
In rats or mice (I do human research so I can't honestly remember), under conditions where cortisol is released chronically (either by peripheral administration or by a chronic stressor) it has been shown that hippocampal size and function decrease. This is corroborated by lowered BDNF in the hippocampus. In humans, fMRI data has shown that depressed individuals have reduced hippocampal size, and they function more poorly on hippocampal dependent tasks (depression is associated with above average levels of cortisol in the blood). I think this reduction in hippocampal size is due to a reduction in the number of receptors for cortisol on hippocampal neurons, which leads to reduced firing in the hippocampus, and reduced release of BDNF into the synapse. With less BDNF, dendritic branches retract and communication breaks down between the hippocampus and other parts of the brain (including the hypothalamus).
Next, with less inhibitory signalling regulating the hypothalamus, it becomes over-active - leading eventually to enhanced cortisol release (through the HPA axis). Increased neuronal firing in this area would lead to more BDNF being released into the synapse and increased hypothalamic size and function (I have not read any studies which indicate this, but if things work the way I think they do then this would be true).
I hope that at least gets you started. The HPA-axis, while nice in that it is a simple feedback loop, could hardly account for the diverse and subtle ways stressors impact the brain. This is only one mechanism of action by which BDNF may be affect and be implicated in the relationship between your areas of interest.
Since the hippocampal innervations into the hypothalamus down-regulate hypothalamic activity, I think it makes sense that the hippocampus and hypothalamus would have opposite BDNF expression under conditions of chronic stress.
In rats or mice (I do human research so I can't honestly remember), under conditions where cortisol is released chronically (either by peripheral administration or by a chronic stressor) it has been shown that hippocampal size and function decrease. This is corroborated by lowered BDNF in the hippocampus. In humans, fMRI data has shown that depressed individuals have reduced hippocampal size, and they function more poorly on hippocampal dependent tasks (depression is associated with above average levels of cortisol in the blood). I think this reduction in hippocampal size is due to a reduction in the number of receptors for cortisol on hippocampal neurons, which leads to reduced firing in the hippocampus, and reduced release of BDNF into the synapse. With less BDNF, dendritic branches retract and communication breaks down between the hippocampus and other parts of the brain (including the hypothalamus).
Next, with less inhibitory signalling regulating the hypothalamus, it becomes over-active - leading eventually to enhanced cortisol release (through the HPA axis). Increased neuronal firing in this area would lead to more BDNF being released into the synapse and increased hypothalamic size and function (I have not read any studies which indicate this, but if things work the way I think they do then this would be true).
I hope that at least gets you started. The HPA-axis, while nice in that it is a simple feedback loop, could hardly account for the diverse and subtle ways stressors impact the brain. This is only one mechanism of action by which BDNF may be affect and be implicated in the relationship between your areas of interest.
bluewhale_moo 1 points
and I just saw this is 5-months after you posted. Haha, oh well.
Hannibal_Lecture 1 points
I don't know why you think that their would be a causal relationship between the level of BDNF in the hippocampus and the production of BDNF in the hypothalamus, but without associated evidence there is little value in making such an assumption. The inhibitory effects of the hippocampus would be systematic and many factors would be affected.
electroreception [OP] 1 points
Well, I've found that stress levels induced by poor diet increase BDNF in the hypothalamus but decrease BDNF in the hippocampus. I previously thought BDNF would decrease in the hypothalamus for rats exhibiting stress for obvious reasons, but it doesn't. I thought maybe there could be a connection between hippocampal BDNF and hypothalamic BDNF levels to explain the inverse relationship (since it is known hipp. can affect HPA), some kind of negative feedback in regards to neurotrophins.
Hannibal_Lecture 1 points
Possibly, but it's quite a leap. It could equally be that stress has a positive effect on a pathway in one and a negative effect on the other, quite independent of signaling between the two. In so much that stress modifies the entire system to make the inhibitory area more/less active, whilst doing the inverse to the area to be inhibited. Which stress factors specifically?
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