Movement, addiction and Sleep Flashcards
4 forms of analgesics
-Opium
-Morphine
-Heroin
-Opioids
Acetycholine
Procuced by a clsuter of neurons in the basal ganglia and the brainstem. Controls every move you make, relases motor neurons through controlling sketal muscles, contributes to the regulation of attention arousal memory
ACh for Arousal
Important NT for aoursl. two groups: one in pons other in basal forebrain. They produce activation and coritcal desynchrony. There is a third grroup in the medial septum to the hippocampus
ACh Recptors”
(ionotropic– sitmulated by nicotine)
-Nicontinc receptors between motor neurons and muscles, some clearly some are in the CNS
(Metabotropic – stimulate by muscarine)
-Muscarinric recptors, CNS has both receptors but primairlly muscarinic
Adenosine
Accumulation of this chemical inhibits neural activity and causes emotional/cognitive effects seen with sleep deprivation.
Affinity
Drugs vary widely in this, which the readiness by which two moecules attach. For this example, it is between a drug and itss binding site.
Agonists
Facilitate an NT system
Alcohol
A CNS depressant and the second most used psychoactive drug. It has two sites of action: Inderaction agonist for GABA receptor and interct antagonist for NMDA recptors. Both cause apoptosis.
Amino Acids
Most abdunant NT in the CNS. The 3 most common, in the CNS, are:
-Glutamte
-GABA
-Glycine
AMPA receptors
An ionotropic glutaamate receptor with an affinity for alpha-amino-3-hydroxxy-5-methyl-4-isoxazole propronic acid
Amphetamine
A CNS Stimulant that has antiastmatic effects, boost alternetness and produces a feeling of confidence. It is a catecholamine agnost, blocking reuptake and directly stimulating the release of dopamine from the presynpatic terminal.
Antagonists
Repress an NT system
Antagonists muscles
Moving an arm or leg back and forth requires opposing sets of muscles
Anterior corticospinal tract:
Ipsilateral fibers direct primary motor cortect directly to target neurons in spinal cord. Controls the core
Ascending reticular activating system
Wakefulness. Begins from brainstem to hypothalamus to forebrain
Basal Ganglia
Striatum, caudate nucleus and putamen, globus pallidus, substaintia nigra, subthamalmic nucleus, nucleus accumbens. Functions to orchestrating planned movement, smooth intended motor activity, inhibits unintended motor activity.
Behavioral tolerance
Tolerance as modifiied by the enviroment – learning and memory
Botulin
Blocks release of ACh at the neuromuscular junction
Causes of Huntingont’s diseasq
Repeats of CAG on chromosone 4. Graudal damange in the basal ganglia and the cerebral cortex
Causes of parkinson
An impairmenet in intitating spontaneous movement in the absence of stimuli to guide the action. Gradual progressive death of neurons, especially in the substantia nigra
Cells in cortex
Upper motor neurons
Cells in ventral horn in spinal cord
Lower motor neurons
Cocaine
A CNS stimulate that causes a sense of euphoria, increased and heightened mental alerntness. Combats effects of hunger a fatigue. It blocks the reuptake of DA,NE 5-HT
Cocaine and meth elebate activtity at NE synapses.
How do cocaine and meth effect NE synapses
Cocaine and Meth elevates activity at DA synapses. Which interferes with Process of reuptake
How do Cocaine/Meth effect Dopamine?
Competitve binding
Direct agonists and antagonists act directly on the NT binding site
Corticospinal tracts
Paths from cortex to spinal cord. Orginatin in layer V where Betz cells are located. Travels through the corona radiata
Curare
Blocks nictonic recptors at the neuromuscular junction
Decussation
Anterior Corticopsinal tract – Crossing over in spinal cord
Direct agonists
A drug capable of mimicing the effects of an NT
Direct Antagonists
Drugs that can bind with the receptors of a postsynpatic neuron but does not open the ion channel and acts as a receptor blocker
Disorders associate with the dysregulation of DA
Parkinsons
-Huntington’s
-Schizophrenic disorders
-Addictive disorders
Disorders associated with the disregulation of Glutamate:
-Schizophrenia
-Mood Disorders
-Epilepsy
Disorders associated with the dysregulation of NE synapses
Depressive disorders
Disorders associated with the dysregylatuion of serotonin
-Depressive disorders
-OCD’s
-Eating disorders
Disorsders assoicates witht eh dysregulate of ACh
-Alzheimers Disease
Dopamine
Dopaminergic systems originate in the midbrain. Contributes to voluntary movement, attention and learning as well acting as a reward pathway.
Efficacy
Drugs vary widely in this: the ability to produce a desired or intended result.
Endocannabinoid
Lipids found in the cannbinoid receptors stimulated by tetrahydrocannbinol. Anandamide, a natural ligand, stimualtes these receptors.
Endorphines
Peptides involved in the pain and reward processses.
Enzymatic degradation
A specific enzyme changes the structure of the neurotransmitter so it is not recognized by the receptor. For example, acetylcholinesterase is the enzyme that breaks acetylcholine into choline and acetate.
Epinephrine
Hormone produced by the adrenal medulla. A NT in the brain and is referred to colloqiually as “Adrenaline.”
Extrafusal fibers
A skeletal muscle fiber, contracts to shorten a muscle
Four major types of glutamate receptors
(Ionotopic)
-NMDA receptor
-AMPA receptor
-Kainate recptor
(Metabotropic)
-Metbotrpic glutamate recptor (At least 8 subtypes)
GABA
Simialr to glutamte. Has direct excitatory and inhibitpory effects on axons as well as the ability to raise or lower the threshold of excitation. No need for special rceptors, which indicates that these had a modulating effect before specialized receptors.
Gamma-aminobutryic Acid (GABA)
Produced from glutamaitic acid by the action of glutamic acid decarboxylase (GAD)
Glutamate
Specifically involved in the creation of synapses, strengthening of synpases– directly affecting neuroplasticity.
Glutamate
Simialr to GABA. Has direct excitatory and inhibitpory effects on axons as well as the ability to raise or lower the threshold of excitation. No need for special rceptors, which indicates that these had a modulating effect before specialized receptors.
Glycine
Inhibitory NT in spinal cord and lower portions of the brain stem. Iontropic [Cl-] produces IPSPs. Unsure of how Glycine is produced
Glycogen
In times of increased activity, this chemical is converted into fuel and induces prolonged wakefulmess. During the SWS, astrocytes renew their stores of this chemcial