Asked in Human Anatomy and Physiology
Human Anatomy and Physiology
What are neuromodulators?
Asked in Nerves
What are neurotransmitters that affect a neuron's response to other neurotransmitters called?
Asked in Nervous System
How do neurotransmitters differ from neuromodulators?
Asked in Psychology, Solid State Physics, Psychiatry
What state of matter is the mind?
The mind is not any state of matter. The mind is an epiphenomenon of the electrobiochemistry happening in the unbelievably complicated network of neurons, myelin, neurotransmitters, neuromodulators, neuroregulators, hormones, etc. that make up the about three pounds of largely fatty tissue enclosed in our bony skull that we refer to as a brain.
What are two possible effects that neurotransmitters may have at synapse?
The two major effects are excitatory and inhibitory. For example ACh leads to the post-synaptic cell's depolarization while GABA or glycine will hyperpolarize the post-synaptic cell. But this is all a simplification. Some synapses have an effect of neuromodulators sometimes released as a co-transmitter (e.g. NPY and epinephrine from sympathetic ganglionic neurons). In some situations the cotransmitter can have a mixture of effects.
Hello Joel-thanks fo?
Hello Joel-thanks for your question. Mal de Debarquement Syndrome (MdDS) is a rare syndrome characterized by a sensation of constant movement like swaying, rocking or bobbing. It occurs after a travel experience involving motion, like a cruise or flight, and can last for weeks to years. Unfortunately, there is no cure for MdDS. However, some people find some relief with exercise, like yoga or walking. Vestibular rehabilitation is a form of physical therapy that helps some people. While traditional medications for dizziness don't work for MdDS, certain medications like benzodiazepines and neuromodulators (e.g. clonazepam, amitriptyline) provide relief for some people with MdDS but not everyone. Your wife's physician can further discuss medication options with you and may also provide a referral for vestibular rehabilitation.
Asked in Medication and Drugs
Hi Joel-I am copying?
Hi Joel-I am copying the answers I provided yesterday, which I believe address your current question. Let me know if you need further information. Mal de Debarquement Syndrome (MdDS) is a rare syndrome characterized by a sensation of constant movement like swaying, rocking or bobbing. It occurs after a travel experience involving motion, like a cruise or flight, and can last for weeks to years. Unfortunately, there is no cure for MdDS. However, some people find some relief with exercise, like yoga or walking. Vestibular rehabilitation is a form of physical therapy that helps some people. While traditional medications for dizziness don't work for MdDS, certain medications like benzodiazepines and neuromodulators (e.g. clonazepam, amitriptyline) provide relief for some people with MdDS but not everyone. Your wife's physician can further discuss medication options with you and may also provide a referral for vestibular rehabilitation. I would not expect it to get worse over time. The symptoms may last for awhile or go away on their own over time.
Asked in Human Anatomy and Physiology
List all the essential neurotransmitters?
Acetylcholine - synthesized from Choline, Lecithin, and panthothenic acid (B5), or Diethylaminoethanol (DMAE) - Arousal and orgasm - voluntary muscular control and proper tone - enhance energy and stamina - memory - long-term planning - mental focus Dopamine - synthesized from amino acid Levodopa - Alertness - Motivation - motor control - immune function - Ego hardening, confidence, optimism - Sexual Desire - Fat gain and loss - lean muscle gain - Bone density - ability to sleep soundly - Inhibits prolactin - thinking, planning, and problem solving - Aggression - Increase psychic and creative ability - Reduction of compulsivety - Salience and paranoia - Processing of pain - Increase sociability Serotonin (5-HT) - Synthesized from amino acid L-tryptophan with co-factor Niacin (B3), through the intermediate 5-hydroxytryptophan (5-HTP) - Decrease thought - Anaesthesize emotions - Decrease Agression and anger - Decrease Anxiety - Promote satiety and decrease appetite - Elevates Pain threshold - Reduces compulsivety/impulsivety - Decrease Sexual Desire - Orgasm - Thermoregulation (5-HT1A) - Stimulate Emesis (5-HT3) - Cerebrospinal fluid secretion (5-HT2C) - Platelate aggregation (5-HT2A) - Smooth muscle contraction, vasoconstriction, and vasodilation (5-HT2A) - Release oxytocin (5-HT1A) - Learning (5-HT2A & 5-HT4) - Memory (5-HT4) - Neuronal excitation (5-HT2A, 5-HT3, & 5-HT4) - GI motility (5-HT4) - Neuronal inhibition (5-HT1A) - Cerebral vasoconstriction (5-HT1D) - Pulmonary vasoconstriction (5-HT1B) - Presynaptic inhbition (5-HT1B) Norepinephrine - Synthesized from Dopamine with co-factor of vitamin C through the intermediate DOPAC. - Increase physical energy - Reduce compulsivety - Increase heart rate - Increase BP - Aggression - Alertness - Wakefulness/sleep cycle - Memory and learning - Orgasm - Decrease blood flow to extremities - Increase heart rate - Maintenance of attention - Orgasm - Cerebral plasticity Epinephrine - Synthesized from Norepinephrine. Also know as adrenaline, acts as both neurotransmitter and hormone. Oxidizes into Adrenochrome. - increases supply of oxygen and glucose to brain and muscles - Surpresses digestion - Increase heart rate and stroke volume - Pupil dilation - constricts arterioles in skin and GI tract - Dilates arterioles in skeletal muscles - Elevates blood sugar levels GABA - synthesized from glutamate - Reduce physical tension - Reduce Anxiety - Reduce Insomnia - Elevates pain threshold - Reduces blood pressure - Decrease heart rate - Reduce compulsivety Prolactin - Inhibition of Dopamine - Decreases sex hormones - estrogen in women, testosterone in men - Stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central nervous system. Nitric oxide - vasodilation, thins blood - reduces platelate stickiness, blood coagulation, wound healing - vasopressin release - stimulation of guanyl cyclase > GTP > cGMP. GMP lays a role in the relaxation of smooth muscle (including penis to facilitate erection), the inhibition of platelet aggregation and participates in signal transduction within the nervous system. Moreover, cGMP is involved in the regulation of the water and electrolyte balance as well as in the metabolism of the bone. cGMP is also involved in retinal phototransduction--that is the conversion of a light signal received by a nerve receptor, to an electrical signal transmitted to the brain. This might help explain transcendental vision, that is the radical increase in visual acuity and sensory perception in general. - involved in apoptosis, and DNA breakage and mutation - enables macrophages to kill tumor cells and bacteria Histamine - synthesized from L-histidine with co-factors folic acid, niacin, and copper. H1 - Vasodilation - Bronchoconstriction - Smooth muscle activation - separation of endothelial cells (responsible for hives) - Pain and itching due to insect stings - Allergic rhinitis - Motion sickness H2 - stimulates gastric acid secretion - Potent stimulant of cAMP production - increases the intracellular Ca2+ concentrations and release Ca2+ from intracellular stores. H3 - presynaptically inhibits the release of a number of other neurotransmitters including, but probably not limited to dopamine, histamine, GABA, acetylcholine, noradrenaline, and 5-HT. It leads to inhibition of the formation of cAMP H4 - H4 Receptors mediate Chemotaxis and Calcium Mobilization of Mast Cells Vasopressin - Water retention - raises blood pressure by inducing moderate vasoconstriction (AVPR1A) - Platellate aggregation (AVPR1A) - involved in aggression, blood pressure regulation and temperature regulation. - It has been implicated in memory formation, including delayed reflexes, image, short- and long-term memory (controversial) - increases peripheral vascular resistance and thus increases arterial blood pressure - adrenocorticotropic hormone secretion in response to stress (AVPR1B) - social interpretation of olfactory cues (AVPR1B) - Gluconeogenesis (AVPR1A) - Social Recognition (AVPR1A) - Increases mental clarity and memory when used as nootropic Oxytocin - spontaneous erections and orgasm - water retention (slight) - inhibition of adrenocorticotropic hormone, cortisol, and vasopressin - bonding - decreased repetitive behaviors and improved interpretation of emotions - Maternal behaviour - increased trust and reduced fear - Affecting generosity by increasing empathy during perspective taking. - inhibition of development of tolerance to various drugs (opiates, cocaine, alcohol), and reduced withdrawals. - impair learning and memory retrieval in certain aversive memory tasks Endocannabinoids - synthesized from an essential fatty acid. Endogenous cannabinoids include anandamine, 2-AG, Noladin Ether, NADA, and OAD - reduce GABA release in interneurons of the basolateral amygdala, thereby helping to extinguish the fear-conditioned response. - Memory - Development of opiate tolerance - control of appetite and food intake - long term potentiation Endogenous opioids - Include Enkephalin, Beta-endorphin, Dynorphin, Endomorphin, Nociceptin, opiorphin, and morphine. Enkephalin is the ligand for delta receptors and also has a high affinity for Mu-opioid receptors. Dynorphin is the ligand for kappa receptors. Beta-endorphin has an affinity for mostly Mu, but also delta and kappa. Endomorphin is the ligand for Mu. Nociceptin for ORL receptors. Opiorphin is found in saliva and inhibits the enzyme that breaks down Enkephalin and B-Endorphin called Enkephalinase. Little is know about the role of Morphine in the body, but speculating from the effects of exogenous morphine, it would bind to Mu-receptors. Mu-1 - Supraspinal Analgesia - Physical dependence Mu-2 - Respiratory depression - Miosis - Euphoria - Reduced GI motility - Physical dependence Kappa - Spinal Analgesia - Sedation - Inhibition of vasopressin release - Miosis Delta - Anti-depressant effects - Analgesia - Physical dependence ORL - Depression - Appetite - Anxiety - Development of tolerance to mu-agonists Sigma Receptors - Little is know about these enigmatic receptors, but possible ligands include DHEA (sigma 1), and endogenous N, N-DMT with slight affinity for both sigma receptors. Effects of sigma receptor stimulation include: - hypertonia (increased muscle tension) - tachycardia - tachypnea (increased breathing rate) - mydriasis (pupil dilation) - Euphoria or dysphoria - anti-depressant effects Other neurotransmitters include Glycine Glutamate and Aspartate - excitatory neurotransmitters that bind to the NMDA receptor. Can be synthesized from L-glutamine, glucose, or lipids. A metabolite of tryptophan in the absence of Niacin may produce kyunerinic acid, is also an NMDA excitatory neurotransmitter. Melatonin - Synthesized from the methylation of serotonin. Regulates circadian rhythms and has powerful anti-oxidant effects. Trace Amines - Include tryptamine, Phenylethylamine, tyramine, octopamine, 3-iodothyronamine, and others. Bind to the TAAR receptors. GHB - bind to GHB receptor(s), and GABAb subunit receptor. Niacin - Also know as vitamin B3, also acts as a neurotransmitter Orexin - Also know as hypocretin. Plays a role in wakefullness and appetite. - Yan Niemczycki Note: There are four criteria by which neurotransmitters are defined. 1. It must be synthesized in the presynaptic cell. 2. It must be released by the presynaptic terminal in sufficient quantities to produce a measurable effect on the postsynaptic cell. 3. When administered artificially, it mimics natural release. 4. A specific, known mechanism exists for it to be removed from the synaptic cleft. Of all the neurochemicals listed here, the following ten actually fit this definition. The remainder are all neuromodulators. 1. Glutamate 2. GABA 3. Glycine 4. Epinephrine (adrenaline) 5. Norepinephrine (noradrenaline) 6. Dopamine 7. Serotonin 8. Acetylcholine 9. Histamine 10. ATP/adenosine
Asked in The Difference Between
The difference between artificial neural network and human neural network?
Difference # 1: Brains are analogue; computers are digital It's easy to think that neurons are essentially binary, given that they fire an action potential if they reach a certain threshold, and otherwise do not fire. This superficial similarity to digital "1′s and 0′s" belies a wide variety of continuous and non-linear processes that directly influence neuronal processing. For example, one of the primary mechanisms of information transmission appears to be the rateat which neurons fire - an essentially continuous variable. Similarly, networks of neurons can fire in relative synchrony or in relative disarray; this coherence affects the strength of the signals received by downstream neurons. Finally, inside each and every neuron is a leaky integrator circuit, composed of a variety of ion channels and continuously fluctuating membrane potentials. Failure to recognize these important subtleties may have contributed to Minksy & Papert's infamous mischaracterization of perceptrons, a neural network without an intermediate layer between input and output. In linear networks, any function computed by a 3-layer network can also be computed by a suitably rearranged 2-layer network. In other words, combinations of multiple linear functions can be modeled precisely by just a single linear function. Since their simple 2-layer networks could not solve many important problems, Minksy & Papert reasoned that that larger networks also could not. In contrast, the computations performed by more realistic (i.e., nonlinear) networks are highly dependent on the number of layers - thus, "perceptrons" grossly underestimate the computational power of neural networks. Difference # 2: The brain uses content-addressable memory In computers, information in memory is accessed by polling its precise memory address. This is known as byte-addressable memory. In contrast, the brain uses content-addressable memory, such that information can be accessed in memory through "spreading activation" from closely related concepts. For example, thinking of the word "fox" may automatically spread activation to memories related to other clever animals, fox-hunting horseback riders, or attractive members of the opposite sex. The end result is that your brain has a kind of "built-in Google," in which just a few cues (key words) are enough to cause a full memory to be retrieved. Of course, similar things can be done in computers, mostly by building massive indices of stored data, which then also need to be stored and searched through for the relevant information (incidentally, this is pretty much what Google does, with a few twists). Although this may seem like a rather minor difference between computers and brains, it has profound effects on neural computation. For example, a lasting debate in cognitive psychology concerned whether information is lost from memory because of simply decay or because of interference from other information. In retrospect, this debate is partially based on the false asssumption that these two possibilities are dissociable, as they can be in computers. Many are now realizing that this debate represents a false dichotomy. Difference # 3: The brain is a massively parallel machine; computers are modular and serial An unfortunate legacy of the brain-computer metaphor is the tendency for cognitive psychologists to seek out modularity in the brain. For example, the idea that computers require memory has lead some to seek for the "memory area," when in fact these distinctions are far more messy. One consequence of this over-simplification is that we are only now learning that "memory" regions (such as the hippocampus) are also important for imagination, therepresentation of novel goals, spatial navigation, and other diverse functions. Similarly, one could imagine there being a "language module" in the brain, as there might be in computers with natural language processing programs. Cognitive psychologists even claimed to have found this module, based on patients with damage to a region of the brain known as Broca's area. More recent evidence has shown that language too is computed by widely distributed and domain-general neural circuits, and Broca's area may also be involved in other computations (see here for more on this). Difference # 4: Processing speed is not fixed in the brain; there is no system clock The speed of neural information processing is subject to a variety of constraints, including the time for electrochemical signals to traverse axons and dendrites, axonal myelination, the diffusion time of neurotransmitters across the synaptic cleft, differences in synaptic efficacy, the coherence of neural firing, the current availability of neurotransmitters, and the prior history of neuronal firing. Although there are individual differences in something psychometricians call "processing speed," this does not reflect a monolithic or unitary construct, and certainly nothing as concrete as the speed of a microprocessor. Instead, psychometric "processing speed" probably indexes a heterogenous combination of all the speed constraints mentioned above. Similarly, there does not appear to be any central clock in the brain, and there is debate as to how clock-like the brain's time-keeping devices actually are. To use just one example, the cerebellum is often thought to calculate information involving precise timing, as required for delicate motor movements; however, recent evidence suggests that time-keeping in the brain bears more similarity to ripples on a pond than to a standard digital clock. Difference # 5 - Short-term memory is not like RAM Although the apparent similarities between RAM and short-term or "working" memory emboldened many early cognitive psychologists, a closer examination reveals strikingly important differences. Although RAM and short-term memory both seem to require power (sustained neuronal firing in the case of short-term memory, and electricity in the case of RAM), short-term memory seems to hold only "pointers" to long term memory whereas RAM holds data that is isomorphic to that being held on the hard disk. (See here for more about "attentional pointers" in short term memory). Unlike RAM, the capacity limit of short-term memory is not fixed; the capacity of short-term memory seems to fluctuate with differences in "processing speed" (see Difference #4) as well as with expertise and familiarity. Difference # 6: No hardware/software distinction can be made with respect to the brain or mind For years it was tempting to imagine that the brain was the hardware on which a "mind program" or "mind software" is executing. This gave rise to a variety of abstract program-like models of cognition, in which the details of how the brain actually executed those programs was considered irrelevant, in the same way that a Java program can accomplish the same function as a C++ program. Unfortunately, this appealing hardware/software distinction obscures an important fact: the mind emerges directly from the brain, and changes in the mind are always accompanied by changes in the brain. Any abstract information processing account of cognition will always need to specify how neuronal architecture can implement those processes - otherwise, cognitive modeling is grossly underconstrained. Some blame this misunderstanding for the infamous failure of "symbolic AI." Difference # 7: Synapses are far more complex than electrical logic gates Another pernicious feature of the brain-computer metaphor is that it seems to suggest that brains might also operate on the basis of electrical signals (action potentials) traveling along individual logical gates. Unfortunately, this is only half true. The signals which are propagated along axons are actually electrochemical in nature, meaning that they travel much more slowly than electrical signals in a computer, and that they can be modulated in myriad ways. For example, signal transmission is dependent not only on the putative "logical gates" of synaptic architecture but also by the presence of a variety of chemicals in the synaptic cleft, the relative distance between synapse and dendrites, and many other factors. This adds to the complexity of the processing taking place at each synapse - and it is therefore profoundly wrong to think that neurons function merely as transistors. Difference #8: Unlike computers, processing and memory are performed by the same components in the brain Computers process information from memory using CPUs, and then write the results of that processing back to memory. No such distinction exists in the brain. As neurons process information they are also modifying their synapses - which are themselves the substrate of memory. As a result, retrieval from memory always slightly alters those memories (usually making them stronger, but sometimes making them less accurate - see here for more on this). Difference # 9: The brain is a self-organizing system This point follows naturally from the previous point - experience profoundly and directly shapes the nature of neural information processing in a way that simply does not happen in traditional microprocessors. For example, the brain is a self-repairing circuit - something known as "trauma-induced plasticity" kicks in after injury. This can lead to a variety of interesting changes, including some that seem to unlock unused potential in the brain (known as acquired savantism), and others that can result in profound cognitive dysfunction (as is unfortunately far more typical in traumatic brain injury and developmental disorders). One consequence of failing to recognize this difference has been in the field of neuropsychology, where the cognitive performance of brain-damaged patients is examined to determine the computational function of the damaged region. Unfortunately, because of the poorly-understood nature of trauma-induced plasticity, the logic cannot be so straightforward. Similar problems underlie work on developmental disorders and the emerging field of "cognitive genetics", in which the consequences of neural self-organization are frequently neglected . Difference # 10: Brains have bodies This is not as trivial as it might seem: it turns out that the brain takes surprising advantage of the fact that it has a body at its disposal. For example, despite your intuitive feeling that you could close your eyes and know the locations of objects around you, a series of experiments in the field of change blindness has shown that our visual memories are actually quite sparse. In this case, the brain is "offloading" its memory requirements to the environment in which it exists: why bother remembering the location of objects when a quick glance will suffice? A surprising set ofexperiments by Jeremy Wolfe has shown that even after being asked hundreds of times which simple geometrical shapes are displayed on a computer screen, human subjects continue to answer those questions by gaze rather than rote memory. A wide variety of evidence from other domains suggests that we are only beginning to understand the importance of embodiment in information processing. Bonus Difference: The brain is much, much bigger than any [current] computer Accurate biological models of the brain would have to include some 225,000,000,000,000,000 (225 million billion) interactions between cell types, neurotransmitters, neuromodulators, axonal branches and dendritic spines, and that doesn't include the influences of dendritic geometry, or the approximately 1 trillion glial cells which may or may not be important for neural information processing. Because the brain is nonlinear, and because it is so much larger than all current computers, it seems likely that it functions in a completely different fashion. (See here for more on this.) The brain-computer metaphor obscures this important, though perhaps obvious, difference in raw computational power.