What Is the Relationship Between the Amygdala and Hippocampus?

The amygdala, also known as the amygdala, is amygdala and is part of the limbic system. It is the brain tissue that generates emotions, recognizes and regulates emotions, and controls learning and memory, and studies have found that autism in young children also seems to be associated with enlarged amygdala.

The amygdala, also known as the amygdaloid body, is located in the dorsal medial part of the anterior temporal lobe, slightly anterior to the top of the inferior corner of the hippocampus and lateral ventricle. Mainly through the lateral olfactory lines, terminal lines, and ventral almonds, and the medial frontal lobe, orbitofrontal gyrus,

Generally, the amygdala is divided into two parts, namely the outer basal nucleus group and the inner cortex group.

Cortex

The amygdala is an important nucleus of the basal nucleus of the brain. It is a component of the limbic system and contains 13 nucleus of different sizes. According to its position and function, it is divided into four parts: lateral basal nucleus, medial cortical nucleus, anterior amygdala region and cortical amygdala transition region. Afferent fibers of the amygdala mainly originate from cholinergic neurons in the olfactory bulb and preolfactory nucleus, Meynert nucleus of the basal forebrain, brain stem, midbrain nucleus, parabranchial nucleus, pontine plaque, midbrain raphe nucleus Ventral dorsum, ventromedial nucleus of hypothalamus, midline nucleus of thalamus and medial ventral nucleus of thalamus. Most of the outgoing fibers of the amygdala are connected back and forth with the afferent fibers.It is generally believed that the amygdala sends signals through two paths: the terminal striatal pathway, which starts from the medial cortex nucleus and is arched between the medial margin of the caudal nucleus and the thalamus. It terminates forward in the terminal striatum, hypothalamus (especially the paraventricular nucleus, supraoptic nucleus), preoptic region, and septal nucleus.The ventral amygdaloid nucleus mainly originates from the lateral basal nucleus, with many and scattered fibers. Stops inwardly at the medial portion of the terminal striate bed nucleus; some anteriorly stop at the preoptic zone, hypothalamus (ventral medial nucleus), dorsal medial nucleus of the thalamus, and then reach the prefrontal cortex and other cortical contact areas [

A University of Iowa study was surprised to find that three fearless female volunteers with damaged amygdala can experience internal fear. This shows that the amygdala is not the area of the brain that causes fear and panic. Decades of research on humans and animals have shown that the amygdala plays an important role in fear. Related research was published in the recently published journal Nature-Neuroscience.

Researchers tested three rare patients with damaged amygdala and never experienced fear. After inhaling carbon dioxide, the three patients were stimulated to breathe, developed fear and developed panic attacks. One of the patients experienced fear as a child, and this was the second time he had developed a feeling of fear. Previous studies of this patient and patients with similar problems have shown that damage to the amygdala causes patients to lose their sense of fear in a variety of fearful stimulation experiments and life-threatening traumatic events. This study by Wemmie et al. Showed that the amygdala is not the organizational structure necessary to produce fear.

Researchers still don't know why carbon dioxide alone can cause fear in the absence of amygdala. However, most of the things that can cause fear are projected into the amygdala through visual and auditory means, and are felt. In contrast, high concentrations of carbon dioxide are felt by receptors in the brainstem and cause a series of physiological changes, which may stimulate other brain regions including the amygdala. ^[2]

According to scientists, benzodiazepines have great benefits in improving amygdala function. From the basic electrophysiological properties, the effect of BZ on the electrical activity of neurons, the effects of benzodiazepines on amygdala have been experimentally proven. And benzodiazepine has been

A large number of practices have proved that the amygdala is related to emotion, behavior, visceral activity and autonomic nerve function. The basis is that there are many neurochemical transmitters in the amygdala.

(1) Choline (Acetylcholine). Focusing on ABL is related to the amygdala ignition process, and electrical stimulation can increase acetylcholine levels. Amygdala is one of the brain areas involved in convulsions. After Soman poisoning, acetylcholine in the brain quickly accumulates in peripheral areas, causing excitement in local brain areas and convulsions.

(2) Monoamines (MAO). Afferent fibers come from the substantia nigra and ventral tegmental areas. This is consistent with a significant gender difference in the incidence of Parkinson's disease. The density of serotonin (5-HT) energy fibers and receptors in the amygdala decreases, and the increase of 5-HT in ABL not only has obvious antidepressant effects, but also can increase slow wave sleep and deepen sleep. Accompanied by sleep disorders, sleep also returns to normal after the depression is relieved, so some people think that 5-HT deficiency in the amygdala may be one of the common foundations of the two.

(3) Amino acids. The coordinated balance between excitatory glutamate and inhibitory GABA plays an important role in the normal function of the amygdala. Glutamate activates NOS to increase NO synthesis, which acts on adjacent presynaptic nerve endings, activates guanylate cyclase, and increases cGMP production and effects.

(4) Nitric oxide (NO). Most of the amygdala contains NOS-positive neurons, of which the back of AME and ABL is more. The relationship between NO and sleep is reported differently. Some scholars have separately conducted experiments and concluded that NO has the effect of increasing arousal and reducing slow-wave sleep.

(5) Cyclic nucleotide (cGMP). There are a large number of opioid receptors in the amygdala, which can increase cGMP concentration and reduce production. Injecting cGMP into the amygdala can increase wakefulness, reduce slow-wave sleep and total sleep time, and has no effect on fast-wave sleep. The effect caused by cGMPase inhibitors is exactly the opposite of cGMP, indicating that cGMP has an important role in regulating sleep arousal.

(6) Peptides. SOM neuroactive substances can enhance the hippocampal LTP, promote learning and memory, and some cognitive and intellectual impairments in clinical dementia are related to a decrease in SOM content in the brain. SOM can change the nervous system is one of the specific pathogenic mechanisms of Alzheimer's disease. Some people think that its function may affect the memory process by acting on two neurotransmitters, choline acetate and norepinephrine. ^[2]