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The effect of a neurotransmitter (NT) depends on the kind of channel that opens when the NT binds to a receptor on the post-synaptic cell. |
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NTS that open channels allow positively charged ions in, such as sodium (NA+) or calcium (Ca+). |
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NTS that open channels allow negatively ions to enter the cell, such as cloride (Cl-). |
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neurotransmitter that is produced by the cell and released from the pre-synaptic neuron into the synaptic cleft, or a drug that is artificially introduced into the synaptic cleft. Anthing that binds to a receptor |
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receptors that immediately open channels into the cell to allow positive or negative ions to enter, considered fast-acting. |
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ionotropic receptors example |
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The receptor to which alcohol, benzodiazepines, barbiturates, steroids, and the neurotransmitter GABA bind is ionotropic. It consists of five segments, and each of the above binds to different segments. |
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G coupled or metabotropic receptors |
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This receptor type is formed of a protein chain that crosses the cell membrane seven times. Ligands bind by fitting into the “pockets” on the outside, moving the 3-D structure of the protein, which moves internally and starts a chain of events on the inside of the cell. |
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metabotropic receptors changes |
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After the receptor has been activated, internal events may consist not only of opening a channel further along the membrane (an indirect effect, in other words), but also DNA transcription factors are also initiated (that is, getting certain genetic sequences read out and proteins actively produced). Nitric oxide (NO) may also be released back to the pre-synaptic cell. This in turn initiates certain DNA transcription activities.This can result in more permanent changes in the structure of the receptor itself, such that the synaptic connection between the pre- and post-synaptic neurons is strengthened. |
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Any NT or drug that facilitates the action of a receptor (whether excitatory or inhibitory) |
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Any NT or drug that diminishes the action of a receptor (whether excitatory or inhibitory) |
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ligand that does not fully activate the receptor. In some cases this can have a facilitating effect (some action is better than no action). In other situations, such as when it blocks access to the receptor for a full agonist, the net effect is to reduce the overall activity of the receptor from what it could maximally be. |
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that activates a receptor but produces the opposite effect to that which it normally produces (e.g., hyper-activity versus sedation). |
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receptors to which the same NT can bind. For example, there are at least 5 different types of dopamine receptors (D1, D2, D3, D4, D5) in the body to which the NT dopamine can bind. These different receptors are distributed in different parts of the brain and body in different amounts. This allows the same NT to have different effects depending on which receptors it is binding to. |
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inhibiting the action of inhibitory neurons that release and refers to the action of “taking off the brakes”. |
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mu, delta, and kappa receptors. Each type of receptor has different effects. For example, the mu and delta receptors are involved in reducing the activity of neurons that convey information about pain. They reduce pain by directly inhibiting the neurons that convey pain information (i.e., opening Cl- channels or allowing potassium to exit the cell via K+ channels). |
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reward pathway of the dopamine system |
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Definition
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two areas of dopamine production |
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produced in two areas of the brain (but also in the hypothalamus and retina): The substantia nigra The ventral tegmental area (VTA) |
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mesolymbic dopamine pathway |
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VTA to nucleus accumbens, then to prefrontal cortex. Important for reward and pleasure.Firing of these neurons produces feelings of intense pleasure. Stimulation of either area (VTA or NA) will continue without satiation (the person or mouse never tires of stimulation). There are inhibitory GABA neurons that synapse (connect) with the VTA to regulate their activity. Opioid autoreceptors on the GABA-releasing neurons inhibit the firing of these neurons, thus reducing their braking activity on the DA neurons |
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tuberoinfundibular dopamine pathway |
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Definition
dopamine is released from the hypothalamus into the pituitary gland. Regulates / inhibits production of prolactin (lactogenesis) |
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mesocortical dopamine pathway |
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VTA to prefrontal and other cortical areas directly. Important in thinking. executive functions as inhibition, working memory |
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nigrostriatal dopamine pathway |
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Definition
substatia nigra (in the midbrain) to the striatum (basal ganglia).Involved in regulation of motor functions and procedural learning). |
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disorders of mesolimbic pathway |
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disorders of nigrostriatal pathways |
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neurological disorders affecting movement such as Parkinson’s disease and Huntington’s disease. |
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disorders of mesocortical pathways |
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schizophrenia treated with neuroleptics, or medications that counter-act the effect of DA. These medications have numerous side-effects. ADHD- Reduced production of DA Faster elimination of DA from the synapse (COMT enzyme type – val or met) Fewer receptors for DA |
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front of face vs back of head |
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split brain by ears (face vs back of head), also by lateral fissure |
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split brain by chin to make a caudal and rostral section |
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split on longitudinal fissure or corpus callosum either in middle through whole face |
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front of face vs back of head |
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voluntary movement relays info to and from skeletal muscles and skin; The sensory (AFFERENT) division – transmits impulses from sense organs located in the periphery of the body – such as the ears and taste buds and information about touch, pain, and temperature – to the central nervous The motor (EFFERENT) division- transmits information from the central nervous system to the muscles and glands (effectors). |
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involuntary movement in organs. maintaining homeostasis in the functioning of many organs of the body. control functions of the body that are not under conscious control (although via biofeedback and meditation techniques one can, in fact, develop some control over such functions as blood pressure, skin temperature |
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autonomic nervous system-two areas |
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parasympathetic and sympathetic nervous system |
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parasympathetic nervous system |
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controls organism when at rest |
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sympathetic nervous system |
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controls organism in times of stress |
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five sections of spinal cord |
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the cervical, thoracic, lumbar, sacral, and coccygeal regions. The level of injury determines the extent of paralysis and/or loss of sensation. No two injuries are alike. |
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carries touch and vibration information to the brain |
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Pain and temperature travel along the spinothalamic pathway. Unlike the spinocortical pathway, the nerves carrying pain information cross over at once on entering the spinal cord, and then travel upwards to the thalamus without crossing again higher up. At the thalamus, information is sent to both the emotional processing area of the brain called the cingulate cortex, and also, simultaneously, to the sensory cortex in the parietal lobe |
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emotional processing area of the brain |
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This syndrome dramatically illustrates the disconnection between touch and pain pathways. A lesion of half the spinal cord (on the right or left side) results in a distinctive pattern of sensory loss, such that the person loses the sense of pain on the opposite side of the body below the lesion, and loses the sense of touch on the same side as, and below, the lesion. |
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Motor commands leave the frontal motor area (in the frontal lobe of the brain) where the motor homunculus is located, and descend to the spinal cord, where the nerves synapse on the alpha neurons that project ventrally out of the spinal cord and form the mixed nerve, ending on muscles and other peripheral nerves |
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Dura (outermost, attached to skull) Arachnoid (intermediate, thin and delicate) Subarachnoid space:Filled with fluid/ Site of re-absorption of CSF Pia: follows convolutions of gyri closely |
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Manufactured in all of the ventricles Circulates through the system in a specific pattern, moving from the lateral ventricle to the third, and then from the third to the fourth. From the fourth ventricle, it passes into the subarachnoid space where it circulates around the outside of the brain and spinal cord and eventually makes its way to the superior sagittal sinus via the arachnoid granulations or arachnoid villi. In the superior sagittal sinus, it is reabsorbed into the blood stream. regenerated several times every twenty-four hours |
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Buoyancy: The actual mass of the human brain is about 1400 grams; however the net weight of the brain suspended in the CSF is equivalent to a mass of 25 grams. The brain therefore exists in neutral buoyancy, which allows the brain to maintain its density without being impaired by its own weight, which would cut off blood supply and kill neurons in the lower sections without CSF. Protection: CSF provides limited protection for the brain tissue from injury when jolted or hit. Chemical stability: CSF flows throughout the inner ventricular system in the brain and is absorbed back into the bloodstream, rinsing the metabolic waste from the CNS through the blood-brain barrier. This allows for homeostatic regulation of the distribution of neuroendocrine factors, to which slight changes can cause problems or damage to the nervous system. For example, high glycine concentration disrupts temperature and blood pressure control, and high CSF pH causes dizziness and syncope.[ Prevention of brain ischemia: The prevention of brain ischemia is made by decreasing the amount of CSF in the limited space inside the skull. This decreases total intracranial pressure and facilitates blood perfusion. |
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regions involved in executive functioning |
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Ventral medial prefrontal cortex (VMPFC) Dorsolateral prefrontal cortex (DLPFC) Amygdala and hippocampus Anterior cingulate cortex (ACC) |
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functions of the thalamus |
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Arousal: bilateral lesions affecting the intralaminar nuclei, which can be considered extensions of the brainstem reticular formation, can cause unresponsiveness, but the eyes remain open. This has been called coma vigil or akinetic mutism. Firing patterns affect sleep stages. Memory: Lesions affecting medial thalamic structures (the confluence of mammillothalamic and amygdalofugal tracts, dorsomedial and possibly anterior nuclei) can cause profound amnesia. Other cognitive functions: neglect and visuospatial dysfunction have been described with lesions, and presumably relate to interruption of reciprocal connections with the cerebral cortex. Most ascending sensory information passes through it. |
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functions of hypothalamus |
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Exerts control over the pituitary gland and thus over endocrine function in general Has extensive connections with brainstem autonomic nuclei. |
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amnesia, aphasia, coma vigil or akinetic mutism |
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pathology of hypothalamus |
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Lesions affect appetite, emotional behavior, temperature control, and numerous other autonomic and endocrine-influenced behaviors |
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leave the cerebral cortex |
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Connect cortical areas with each other within one hemisphere |
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connect hemispheres with each other, ie the corpus collosum |
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internal carotid arteries and vertebral arteries. Right & left basilar artery The basilar artery joins the blood supply of the internal carotid arteries in a ring at the base of the brain. This ring of arteries is called the circle of Willis. The circle of Willis provides a safety mechanism...if one of the arteries gets blocked, the "circle" will still provide the brain with blood. |
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