18. The dopamine pathways in schizophrenia In schizophrenia there is an increase in dopamine transmission between the substantia nigra to the caudate nucleus-putamen (neostriatum) compared with normal. While in the other major dopaminergic pathways — to the mesolimbic forebrain and the tubero-infundibular system — dopamine transmission is reduced. The dopamine hypothesis of schizophrenia proposes that increased levels of dopamine or dopamine receptors in the dorsal and or ventral striatum underlie the disorder.
19. The glutamate pathways in a brain affected by schizophrenia In the normal brain the prominent glutaminergic pathways are: the cortico-cortical pathways; the pathways between the thalamus and the cortex; and the extrapyramidal pathway (the projections between the cortex and striatum). Other glutamate projections exist between the cortex, substantia nigra, subthalamic nucleus and pallidum. The glutaminergic pathways are hypoactive in the brains of people diagnosed with schizophrenia and this is thought to cause the confusion and psychosis associated with the disorder.
20. The serotonergic pathway showing the effects of schizophrenia The two key serotonergic pathways in schizophrenia are the projections from the dorsal raphe nuclei into the substantia nigra and the projections from the rostral raphe nuclei ascending into the cerebral cortex, limbic regions and basal ganglia. The up-regulation of these pathways leads to hypofunction of the dopaminergic system, and this effect may be responsible for the negative symptoms of schizophrenia. The serotonergic nuclei in the brainstem that give rise to descending serotonergic axons remain unaffected in schizophrenia.
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32. Neuropeptides Function of Neuropeptides: There are cells in the brain that produce various neuropeptides, and these neuropeptides do just about everything. They can be either pro-inflammatory or anti-inflammatory, with anti-inflammatory being preferred. They are responsible for many functions: They control our mood, energy levels, pain and pleasure reception, body weight, and ability to solve problems; they also form memories and regulate our immune system. These active little messengers in the brain actually turn on cellular function in the skin.
33. Characteristics of Neuropeptides: Peptides are compounds consisting of two or more amino acids (the building blocks of proteins), chained together by what is called a peptide bond. Neuropeptides are peptides released by neurons (brain cells) as intercellular messengers. Some neuropeptides function as neurotransmitters, and others function as hormones. Peptides and neuropeptides, like many substances in our bodies (think cholesterol) can work both for and against us. Anti-inflammatory neuropeptides work for us to reduce inflamation fo the skin.
34. Transmitter names are shown in bold. Norepinephrine (noradrenaline). In neurons of the A2 cell group in the nucleus of the solitary tract ), norepinephrine co-exists with: Galanin Enkephalin Neuropeptide Y GABA Somatostatin (in the hippocampus ) Cholecystokinin Neuropeptide Y (in the arcuate nucleus ) Acetylcholine VIP Substance P - Originally nown as Tachykinins. Because they are rapidly absorbed they now known as neurokinins. They play a key role in modulation of pain and emotions. Hence possibly in the future this could be a source of new antidepresants PEPTIDES
35. Dopamine Cholecystokinin Neurotensin Epinephrine (adrenaline) Neuropeptide Y Neurotensin Serotonin (5-HT) Substance P TRH Enkephalin PEPTIDES
39. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Supersensitivity is a compensatory response of the postsynaptic neuron when it receives too little stimulation. The neuron tries to make up for a lack of stimulation by increasing receptor responsiveness. Over time, the postsynaptic neuron may also compensate for lack of stimulation by synthesizing additional receptor sites. This process is known as up-regulation. Upregulation theory Supersensitivity (up-regulation) Supersensitivity (up-regulation) Supersensitivity (up-regulation) Supersensitivity (up-regulation) Supersensitivity (up-regulation) Supersensitivity (up-regulation) Supersensitivity (up-regulation)
40. By increasing the amount of neurotransmitter in the cleft, you can normalize responsiveness. Increased neurotransmitter increases stimulation of receptor sites, which prompts the postsynaptic neuron to compensate by decreasing receptor sensitivity, a process known as desensitization DESENSITIZATION THEORY
41. The postsynaptic neuron is also thought to compensate for increasing stimulation by decreasing the number of receptor sites, a process known as down-regulation. Downregulation hypothesis
44. “ To study medicine without books and mentors is like a shaman who professes who know everything but deep inside he knows nothing at all. You can shake, rattle, and roll. But at the end of the day, you wish that you have studied hard for the life you are handling in front of you is not a guinea pig at all”.
