Nicotinic receptors thalamus

Court J, Spurden D, Lloyd S, McKeith I, Ballard C, Cairns N. et al. 1999. Neuronal nicotinic receptors in dementia with Lewy bodies and schizophrenia Alpha-bungarotoxin and nicotine binding in the thalamus. J Neurochem 73 1590-1597. 

Bohr IJ, Ray MA, McIntosh JM, Chalon S, GuiUoteau D, McKeith IG, Perry RH, Clement F, Perry EK, Court JA, Piggott MA (2005) Cholinergic nicotinic receptor involvement in movement disorders associated with Lewy body diseases. An autoradiography study using [(125)l]alpha-conotoxinMII in the striatum and thalamus. Exp Neurol 191 292-300... 

Court J, Spurden D, Lloyd S, McKeith I, Ballard C, Cairns N, Kerwin R, Perry R, Perry E (1999) Neuronal nicotinic receptors in dementia with Lewy bodies and schizophrenia alpha-bungarotoxin and nicotine binding in the thalamus. J Neurochem 73 1590-1597 Couturier S, Bertrand D, Matter JM, Hernandez MC, Bertrand S, MiUar N, Valera S, Barkas T, Ballivet M (1990) A neuronal nicotinic acetylcholine receptor subunit (alpha 7) is devel-opmentally regulated and forms a homo-oligomeric channel blocked by alpha-BTX. Neuron 5 847-856... 

Other approaches, some of which are still in clinical development, include restoration of the acetylcholine-dopamine balance in the basal ganglia, neuronal nicotinic receptor agonists, neurotrophic immunophilins, dopamine transport inhibitors, COMT-inhibitors, and adenosine A2A receptor antagonists.162,163 Also surgical therapies are used or under development, including stereotactic thalamotomy, continuous electric thalamus stimulation,164 posteroventral pallidotomy and transplantation of embryonal substantia nigra cells. 

In the thalamus, nicotinic receptor subunits were decreased in the numbers of a and P2 immunoreactive neurons in the paraventricular nucleus (PV) and nucleus reuniens (NR) in autistic subjects (Ray et al., 2005 Fig. 4). These deficits in nicotinic receptor subunits perhaps result in the failure of the PV and NR (and so the thalamus) to correctly modulate sensory input. This effect would then be transferred throughout the limbic system to other parts of the brain, contributing to the incorrect sensory processing found in autism (Martin-Ruiz et al., 2004). The co-expression of a and glutamic acid decarboxylase (GAD) study indicated that despite the decrease in a7, the expression of GAD in the PV was similar in both autistic and control subjects (Ray et al., 2005). This suggests that the decrease in a7 subunits in the thalamus is not associated with the GABAergic system. 

The cell bodies of neurons that involve NE are located in the brain stem, with projections to the thalamus, cortex,hippocampus, and cerebellum. Other neurotransmitters, such as ACh and some neuropeptides, are broken down while still in the synaptic cleft. In the synapses connecting neurons and muscle cells, the enzyme acetyl cholinesterase performs this task. Excitatory ACh receptors that activate skeletal musdes at the neuromuscular juncture are called nicotinic receptors because they are stimulated by nicotine. 

In 1926, Otto Loewi discovered that acetylcholine was the principal neurotransmitter of the parasympathetic nervous system. As with other neurotransmitters, acetylcholine is synthesized and stored in vesicles within presynaptic neurons. Ninety percent of the cholinergic neurons in the brain are muscarinic, controlling salivation,sweating, dyspnea, diarrhea, vertigo, confusion, weakness and coma. Acetylcholine binds to muscarinic receptors on smooth muscle cells, innervated by post-synaptic fibers of the parasympathetic nervous system. The thalamus and cerebellar cortex have nicotinic receptors, i diile most other regions of the brain have muscarinic neurons. 

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... 

Striatum, Flippocampus, Thalamus Relatively few studies have investigated the expression of AChRs outside the cortex in schizophrenia ( Table 4.2-7). However, studies done in the striatum, the hippocampus, and the thalamus have identified changes similar to those in the cortex including increased (striatum), unaltered (thalamus), or decreased (striatum, hippocampus) binding of [3H] nicotine to 4P2 type nAChRs in schizophrenia (Leonard et al., 1998 Court et al., 1999 Breese et al., 2000 Court et al., 2000). Supporting decreased expression of nicotinic type receptor in the striatum and the hippocampus, [3H]cytosine and [3H]epibatidine were similarly reported decreased in schizophrenia (Freedman et al., 1995 Breese et al., 2000 Durany et al., 2000). Additionally, a7 receptor binding in the hippocampus and the thalamus, as well as a.7 protein expression in the striatum, was reported to be decreased in this illness (Freedman et al., 1995 Leonard et al., 1998 Court et al., 1999). 

Ray MA, Graham AJ, Lee M, Perry RH, Court JA, Perry EK (2005) Neuronal nicotinic acetylcholine receptor subunits in autism an immunohistochemical investigation in the thalamus. Neurobiol Dis 19 366-377... 

Actions of acetylcholine (ACh) are referred to as muscarinic based on the observation that muscarine acts selectively at certain sites and, quahtatively, produces the same effects as ACh. Peripheral muscarinic acetylcholine receptors are found primarily on autonomic effector cells innervated by postganghonic parasympathetic nerves and on some cells that receive little or no cholinergic innervation but express muscarinic receptors e.g., vascular endothelial cells). There are also muscarinic receptors in ganglia and the adrenal meduUa, where muscarinic stimulation seems to modulate the effects of nicotinic stimulation. Within the central nervous system (CNS), the hippocampus, cortex, and thalamus have high densities of muscarinic receptors. 

Cao et uL, 2005), whereas dopamine regulates ACh release in the striatum (Acquas and Di Chiara, 2001 Alcantara ei ai, 2003). Nicotinic [St subunit-receptor knockout mice show markedly less depolarization-induced dopamine release (Picciotto er al 1998). Glutamatergic inputs from the thalamus can also intluence cholinergic intemeurons, increasing striatal ACh release Baldi ei ai, 1995 Console et ai, 1990 Pollack, 2001). 

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