Thalamus

The effects of VIP and PACAP are mediated by three GPCR subtypes, VIP, VIP2, and PACAP receptor, coupled to the activation of adenjiate cyclase (54). The VIP subtype is localized ia the lung, Hver, and iatestiae, and the cortex, hippocampus, and olfactory bulb ia the CNS. The VIP2 receptor is most abundant ia the CNS, ia particular ia the thalamus, hippocampus, hypothalamus, and suprachiasmatic nucleus. PACAP receptors have a wide distribution ia the CNS with highest levels ia the olfactory bulb, the dentate gyms, and the cerebellum (84). The receptor is also present ia the pituitary. The VIP and PACAP receptors have been cloned. 

Dementia with Lewy bodies (DLB) is considered the second most common cause of dementia after AD. The disorder is characterized by progressive fluctuating cognitive impairment, visual hallucinations and motor features of Parkinsonism. Neocoitical cholinergic activity is more severely depleted in DLB than in AD, and DLB also affects the caudate nucleus, the thalamus and the brain stem. Tolerability of ChEI in DLB appears similar to AD, with some gastrointestinal effects and muscle cramps. 

Mice lacking the 8 subunit, which is mainly expressed in cerebellum and thalamus, display an attenuation of ssatrighting reflex time following the administration of the neurosteroids, alphaxalone and pregnanolone, while the responses to propofol, etomindate, ketamine and the benzodiazepine midazolam were unaffected. This demonstrates the role of GABAa receptors containing the 8 subunit for neurosteroid action. 

Hi-receptors in the adrenal medulla stimulates the release of the two catecholamines noradrenaline and adrenaline as well as enkephalins. In the heart, histamine produces negative inotropic effects via Hr receptor stimulation, but these are normally masked by the positive effects of H2-receptor stimulation on heart rate and force of contraction. Histamine Hi-receptors are widely distributed in human brain and highest densities are found in neocortex, hippocampus, nucleus accumbens, thalamus and posterior hypothalamus where they predominantly excite neuronal activity. Histamine Hrreceptor stimulation can also activate peripheral sensory nerve endings leading to itching and a surrounding vasodilatation ( flare ) due to an axonal reflex and the consequent release of peptide neurotransmitters from collateral nerve endings. 

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. 

Highest concentrations of MOPs are found in the thalamus, caudate, neocortex in the brain, but the receptors are also present in gastrointestinal tract, immune cells, and other peripheral tissues. 

Major efferent projections of the hypothalamic orexin system comprise descending and ascending, dorsal and ventral pathways that terminate preferentially in aminergic, endocrine, and autonomic control centers in the hypothalamus, midbrain, brainstem, and spinal cord, as well as in limbic cortical and subcortical structures, including sqDtum, amygdala, thalamus,... 

Afferent input from cutaneous and visceral nociceptors is known to converge on spinal neurons, which accounts for the referral of pain between visceral and cutaneous structures (e.g. cardiac pain gets referred to the chest and left upper arm in patients suffering from angina pectoris). Projection neurons in the spinal dorsal horn project to cell nuclei in supraspinal areas such as the thalamus, brainstem and midbrain. Of these, the synaptic junctions in the thalamus play a very important role in the integration and modulation of spinal nociceptive and non-nociceptive inputs. Nociceptive inputs are finally conducted to the cortex where the sensation of pain is perceived (Fig. 1). The mechanisms via which the cortex processes nociceptive inputs are only poorly understood. 

Nociceptive neurons in the spinal cord as well as in higher centres such as the thalamus and cortex can also undergo alterations in activity following chronic peripheral changes and trauma (Table 1). These changes are typically long-term in nature and lead to the clinical syndromes of centrally maintained pain (secondary hyperalgesia, allodynia, spontaneous pain). Alterations... 

Localization CNS Hippocampus (CA1, CA3, DG), septum, amygdala, raphe nuclei CNS Striatum, hippocampus (CA1), substantia nigra, globus pallidus, superior colliculi, spinal cord, raphe nuclei CNS like 5-HT1B but at lower densities. CNS Caudate putamen, parietal cortex, fronto-parietal motor cortex, olfactory tubercle, amygdala CNS Cortex, Thalamus, olfactory bulb (rat), claustrum (g-pig), hippocampus (CA3), spinal cord. 

Localization CNS Cortex, hippocampus, striatum, olfactory bulb, spinal cord CA/S not present in adult. CNS Choroid plexus, medulla, pons, striatum, hippocampus (CA1, CA3), hypothalamus, spinal cord CNS Striatum, hippocampus (CA1), substantia nigra, globus pal-lidus. CNS Striatum, brainstem, thalamus, hippocampus, olfactory bulb, substantia nigra... 

Localisation CA/S Hippocampus (CA1, CA3, DG), cortex, cerebellum (granular layer), olfactory bulb, habenula, spinal cord CA/S Caudate putamen, olfactory tubercle, nucleus accumbens, cortex, hippocampus (CA1, CA3, DG) CA/S Hippocampus (CA1, CA2), hypothalamus, thalamus, superior colliculus, raphe nuclei... 

The synchronised oscillatory activity between the intrinsically linked thalamus and cortex. Under normal circumstances there is a level of activity which changes during the sleep-wake cycle increasing during periods of slow wave sleep. Excess synchrony occurs in conditions such as epilepsy. Thiazolidinedione... 

The LVA channels are expressed in a wide variety of tissues. In the cardiac sinus node and the thalamus, activation of LVA channels seems to be necessary to generate action potentials upon depolarising the membrane. 

FIGURE 2.11 Matched diffusion and perfusion abnormalities. An early DWI image (a) shows an acute infarct in the left thalamus. An MTT map (b) shows a small perfusion abnormality that is no larger than the diffusion abnormality. When diffusion and perfusion lesions are matched, there is usually minimal if any infarct extension. Indeed, in this case, a follow-up CT scan (c) shows no enlargement of the infarct. 

McCormick, DA and Prince, DA (1986b) Inhibitory effect of acetylcholine in the thalamus. Nature 319 402-405. 

McCormick, DA, Pape, HC and Williamson, A (1991) Actions of norepinephrine in the cerebral cortex and thalamus implications for function of the central noradrenergic system. Prog. Brain Res. 88 293-305. 

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. 

---