An example of this type of autonomic reflex is the baroreceptor reflex. Baroreceptors located in some of the major systemic arteries are sensory receptors that monitor blood pressure. If blood pressure decreases, the number of sensory impulses transmitted from the baroreceptors to the vasomotor center in the brainstem also decreases. As a result of this change in baroreceptor stimulation and sensory input to the brainstem, ANS activity to the heart and blood vessels is adjusted to increase heart rate and vascular resistance so that blood pressure increases to its normal value.
neuroscience exploring the brain 4th edition pdf 49
These neural control centers in the hypothalamus and the brainstem may also be influenced by higher brain areas. Specifically, the cerebral cortex and the limbic system influence ANS activities associated with emotional responses by way of hypothalamic-brainstem pathways. For example, blushing during an embarrassing moment, a response most likely originating in the frontal association cortex, involves vasodilation of blood vessels to the face. Other emotional responses influenced by these higher brain areas include fainting, breaking out in a cold sweat, and a racing heart rate.
The preganglionic neurons that arise from the brainstem exit the CNS through the cranial nerves. The occulomotor nerve (III) innervates the eyes; the facial nerve (VII) innervates the lacrimal gland, the salivary glands and the mucus membranes of the nasal cavity; the glossopharyngeal nerve (IX) innervates the parotid (salivary) gland; and the vagus nerve (X) innervates the viscera of the thorax and the abdomen (eg, heart, lungs, stomach, pancreas, small intestine, upper half of the large intestine, and liver). The physiological significance of this nerve in terms of the influence of the parasympathetic system is clearly illustrated by its widespread distribution and the fact that 75% of all parasympathetic fibers are in the vagus nerve. The preganglionic neurons that arise from the sacral region of the spinal cord exit the CNS and join together to form the pelvic nerves. These nerves innervate the viscera of the pelvic cavity (eg, lower half of the large intestine and organs of the renal and reproductive systems).
The pathologic diagnosis of AD remains the gold standard for diagnosis. While certain features of AD can be ascertained on macroscopic examination, no single feature or combination of features is specific, but certain features are highly suggestive of AD. The AD brain often has at least moderate cortical atrophy that is most marked in multimodal association cortices and limbic lobe structures. The frontal and temporal cortices often have enlarged sulcal spaces with atrophy of the gyri, while primary motor and somatosensory cortices most often appear unaffected [18]. There is increasing recognition of atrophy in posterior cortical areas in AD, most notable the precuneus and posterior cingulate gyrus, driven in part by functional imaging studies [19, 20]. As a result of this atrophy, there is often enlargement of the frontal and temporal horns of the lateral ventricles as shown in Fig. 1, and decreased brain weight is observed in most affected individuals. None of the macroscopic features are specific to AD, and unaffected clinically normal people may have moderate cortical atrophy, especially affecting frontal lobes, with volume loss mostly affecting white matter [21]. Medial temporal atrophy affecting amygdala and hippocampus, usually accompanied by temporal horn enlargement is typical of AD [18, 22, 23], but can be seen in other age-related disorders such as hippocampal sclerosis or argyrophilic grain disease. Another macroscopic feature commonly observed in AD is loss of neuromelanin pigmentation in the locus coeruleus as shown in Fig. 1 [23]. None of these observations alone are specific to AD, but often they can be highly supportive, especially in the absence of macroscopic changes specific for other neurodegenerative diseases.
Microglial cells are phagocytes that operate within the brain, monitoring their territories for pathogen exposure or deteriorating neurons, which promotes their migration to the site and subsequent activation and at times antigen presentation [84, 85]. Normally they play a role in synaptic monitoring and turnover, but under conditions of stress or deterioration (e.g., protein aggregates such as Aβ amyloid fibrils and tau paired helical filaments) they become activated and are observed around senile plaques, and their numbers increase in promotion to neuronal damage associated with NFTs and NT [86, 87]. Microglial activation is characterized as an innate immune response, which can be activated by multiple factors in the local environment. Receptors on microglia can bind Aβ fibrils, driving an inflammatory response similar to the M1 (proinflammatory) phenotype observed outside the central nervous system [84]. Activated ameboid microglia are frequently observed juxtaposed to amyloid deposits in plaques. This may explain the risk association of TREM2 with AD, as this microglial and astrocytic receptor is thought to mediate microglial phagocytosis [84]. Reactive astrocytes represent the other inflammatory response observed in the brains of AD patients, and they are thought to function in the neuroprotection of damaged neurons and maintaining homeostasis. Astrocytes normally function to provide trophic support for the neurons and synapses directly connecting these structures to the critical blood supply and nutrients. In AD, they also are often observed around senile plaques, though in lower abundance compared to microglia, and at a greater distance from the plaque epicenter. It is thought they react to the cytokines and other agents produced by pro-inflammatory M1 microglia, and these changes in the astrocytes are thought to be neurotoxic [88, 89]. Reactive astrocyte burden occurs later in AD when dementia develops, and is considered to be correlate with tau burden [90]. It should also be noted that neurons and oligodendrocytes are involved in regulation of glia [85].
The Mayo Clinic brain bank operates under the auspices of the Mayo Clinic Institutional Review Board (IRB), which has determined that research on postmortem material is exempt from human subjects research. All autopsies are approved by the next-of-kin or someone with legal standing to grant permission for postmortem examinations.
Neuroscience Online is an open-access electronic resource for students, faculty, and those interested in neuroscience. The project began in 1999 and the first section, Cellular and Molecular Neurobiology, was released in 2007.
Connections in the central auditory system are complex, but a simple summary is that information proceeds from the Organ of Corti to spiral ganglion cells and the VIIIth nerve afferents in the ear, to the cochlear nuclei, many crossing in the trapezoid body to the superior olive in the brain stem. Then all ascending fibers stop in the inferior colliculus in the midbrain and the medial geniculate body in the thalamus, before reaching the cortex in the superior temporal gyrus. All auditory afferents synapse in the cochlear nuclei and in the thalamus. Beyond that simplification, second order fibers from the cochlear nuclei proceed rostrally in several different pathways. Afferents are generally distributed bilaterally so unilateral damage at any level does not usually result in deafness in either ear.
Close, but incorrect. Auditory afferents from the medial geniculate body travel to primary auditory cortex in the sublenticular portion of the internal capsule, but this structure is in the forebrain. 2ff7e9595c
Comments