Brain structure thalamus

Brain structure below the thalamus and main portion of the ventral region of the diencephalon, controlling homeostatic and nonhomeostatic basic body and brain functions, including circadian and feeding rhythms, energy metabolism, thermogenesis, sympathoadrenal, and neuroendocrine outflow (secretion of hormones by the pituitary gland), behavioral state and memory functions. 

Although sleep and wakefulness are global states, specific brain structures are known to be involved in their regulation. These sites include areas within the brainstem, hypothalamus, and the thalamus, and Glu plays an active role in the control of sleep and waking in these areas. 

There are numerous GABAergic neuronal pathways in the CNS. y-Aminobutyric acid is found in high concentrations in the cerebellum, is also found in the hypothalamus, thalamus, and hippocampus, and occurs in low concentrations in practically all brain structures as well as in the spinal cord. The amounts present are relatively high—on a pmol/g order of magnitude— rather than the nanomolar quantities seen with most major neurotransmitters. y-Aminobutyric acid also occurs in glial cells, where its role is less well defined. 

Moruzzi (9) already clearly dissociated activation from arousal. Stimulation from the sensory terminals leads to monosynaptic and more often polysynaptic reflexes. These polysynaptic reflexes relay in subcortical structures. Depending on the intensity of stimulation, the degree of neuronal recruitment, and so forth, the number of brain structures involved will vary. Stimulation may affect the thalamus, basal forebrain, and a newly recognized loop called the cor-ticothalamocortical loop (10). 

Khorram et al. (2006) found that conventional antipsychotics caused a dose-dependent increase in the volume of the thalamus compared to normal volunteers. The thalamic volumes returned to normal when the patients were switched from the older antipsychotic drugs to olanzapine. However, the doses of olanzapine are not provided. The authors conclude, Antipsychotic medication could contribute to the wide range of thalamic volumes reported in schizophrenia (p. 2007). In other words, the drugs and not the disorder are causing the brain structure abnormalities. This, of course, confirms the brain-disabling principles of neuroleptic effects. 

For the first time, we watched the human brain develop from birth to adulthood...at birth, the areas that were functioning in the newborn child were, not surprisingly, the phylogenetically older parts of the brain the cerebellum, the central structures of the brain the thalamus, and the old motor cortex... as you watch (the child grow) one structure after the other matures,... 

Although CDV targets specific brain structures such as hypothalamic nuclei, thalamus, limbic system, substantia nigra, pars compacta, locus ceruleus, and raphe nuclei (Bernard et al, 1993), viral transcripts are only present in few structures, including hypothalamus (Bernard et al, 1999). 

The determination of fhe embryonic "critical period of development" for the brain structures involved in learning and memory processes in mice is based on the original work by Rodier (1976). This study identified fhe embryonic time frames for peak neurogenesis and neuroepithelial proliferation for cerebral corfex, hippocampus, septum, amygdala, corpus striatum, thalamus, hypothalamus, cerebellum, and olfactory bulb as the period from embryonic day E14 fhrough E17. Rodier documented almost 40 years ago that the specific time of the central nervous system (CNS) insult is an important factor in subsequent effects on both anatomy and behavior. Therefore, this early work established what we refer to as the embryonic "critical period of development." The report suggested that the behavioral effects of toxicants such as benzo(a)pyrene (B(a)P) are similar in both rats and mice. This study was one of the first to demonstrate that mice could be used successfully as subjects in a variety of behavioral evaluation experiments. 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

The thalamus has one of the highest densities of nicotinic acetylcholine receptors in the brain and is thought to be a critical structure in nicotine dependence (Clarke 2004 Rubboli et al. 1994a, b). As mentioned, Durazzo et al. (2004) obtained... 

The thalamus is the gateway to cortical processing of all incoming sensory information, represented in Figure 2.1 by the three major systems somatosensory (S), auditory (A), and visual (V). Primary sensory cortices (SI, Al, VI) receive information from the appropriate input modules (sensory organ -I- thalamus). The association cortex integrates information from primary cortices, from subcortical structures, and from brain areas affiliated with memory to create an internal representation of the sensory information. The medial temporal lobe (i.e., hippocampus, amygdala) serves two major... 

Serotonergic neurons are found only in midline structures of the brain stem. Most serotonergic cells overlap with the distribution of the raphe nuclei in the brain stem. A rostral group (B6-8 neurons) projects to the thalamus, hypothalamus, amygdala, striatum, and cor-... 

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