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Brain and Behavior Exam 1 > Lec 3 Neurotransmitter Systems I & II > Flashcards

Lec 3 Neurotransmitter Systems I & II Flashcards

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1
Q

What are electrical synapses?

A
  • very rare, neurons directly coupled so no chemical process need to transduce electrical impulse from one neuron to next
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2
Q

7 steps in chemical synaptic transmission

A
  1. nerve impuse reaches presynaptic nerve terminal
  2. activation Ca channel and entry Ca into nerve terminal
  3. Ca triggers neurotransmitter release/exocytosis
  4. neurotransmitter activates pre and postsynaptic receptors
  5. receptor activation regulates ion channels to get postsynaptic currents
  6. neurotransmitter removed from synapse
  7. vesicles involved in exocytosis are recaptured by endocytosis
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3
Q

What types of neurotransmatters involved in the “classic” synapse? What makes it classic?

A

classic = nerve terminal in close approximation to a dendritic spine where receprtors/signaling proteins located
- glutamate

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4
Q

What is role of astrocytes in glutamatergic synapses?

A
  • surround synapse

- buffer extracellular levels of glutamate to protect neurons from excessive excitation (excitotoxicity)

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5
Q

What are the 4 steps of neurotransmitter vesicle formation and recycling in the nerve terminal? [and what mediates]

A
  • neurotransmitter packaged into synaptic vesicle via vesicular transport protein on the vesicle membrane
  • vesicles bind active zone on nerve terminal plasma membrane for docking/priming
  • Ca entry into nerve terminal triggers fusion that allows neurotransmitter release into synaptic cleft
  • vesicle recaptured via clathrin mediated endocytosis
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6
Q

Where on the nerve terminal plasma membrane do vesicles containing neurotransmitters bind?

A

the active zone

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7
Q

What triggers neurotransmitter-containing vesicle to fuse with the nerve terminal plasma membrane and release neurotransmitter into the synapse?

A

Ca comes into nerve terminal

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8
Q

What protein mediates endocytosis that allows for recycling of vesicles after they have released neurotransmitter?

A

clathrin

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9
Q

What is role of neurotransmitters in neuronal plasticity?

A
  • cause some short-lived adaptations in neuronal functon and ion channel regulation
  • also cause phosphorylation cascades that lead to changes in transcription factors and thus stable adaptations
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10
Q

What are the 3 amino acid neurotransmitters?

A
  • glutamate
  • GABA
  • Glycine
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11
Q

What are the 4 types of monamine neurotransmitters?

A
  • catecholamines [dopamine, NE, Epi]
  • indoleamines [serotonin, melatonin]
  • acetylcholine
  • histamine
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12
Q

What are the 3 types of catecholamines?

A
  • dopamine
  • norepinephrine [noradrenaline]
  • epinephrine [adrenaline]
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13
Q

what are the 2 types of indoleamines?

A
  • serotonin

- melatonin [in pineal gland only]

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14
Q

What are the 2 types of nucleoside neurotransmitters we talk about?

A
  • adenosine

- ATP

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15
Q

What are two types of lipid derived neurotransmitters?

A
  • Anandamine

- 2AG

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16
Q

What type of neurotransmitter is NO?

A

gas

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17
Q

What are two main types of neurotransmitter receptors?

A
  • ligand-gated channels (ionotropic)

- G-protein coupled receptors [GPCR] (metabotropic)

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18
Q

What happens in ligand gated neurotransmission?

A
  • neurotransmitter binds to site on a multi-subunit (4-5) ion channel that together form pore
  • each subunit is single polypeptide with 4 transmembrane domains
  • neurotransmitter binds, opens channel to allow ions to flow in/out
  • get rapid post-synaptic current
  • can be excitatory or inhibitory
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19
Q

What are 4 types of neurotransmitters that can pass Na (and sometimes ca) leading to excitatory post-synaptic current?

A
  • glutamate
  • acetylcholine
  • serotonin
  • nucleosides
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20
Q

What are 2 types of neurotransmitters that pass Cl leading to inhibitory post-synaptic current?

A
  • GABA

- glycine

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21
Q

What type of neurotransmission with glutamate (receptor type, excite or inhibit)?

A
  • excitatory NA/Ca channels [AMPA, NMDA]

- metabotropic mGluR autoreceptor

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22
Q

What type of neurotransmission with GABA (receptor type, excite or inhibit)?

A
  • inhibitory ligand-gated Cl channel GABA-A

- metabotropic GABA-B and GABA-C

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23
Q

What type of neurotransmission with nucleosides (receptor type, excite or inhibit)?

A

bind ligand gated Na channel (and sometimes Ca) leading to excitatory post-synaptic current

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24
Q

What type of neurotransmission with acetylcholine (receptor type, excite or inhibit)?

A 
nicotinic = ionotropic excitatory Na channel
muscarinic = metabotropic
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25
Q

What type of neurotransmission with serotonin (receptor type, excite or inhibit)?

A 
5HT3 = ligand gated Na excitatory
5HT = Gi
5HT2 = Gq
5HT4-7 = Gs

modulatory NT

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26
Q

What type of neurotransmission with glycine (receptor type, excite or inhibit)?

A
  • bind ligand gated Cl channel leading to inhibitory post-synaptic current
  • only in spine
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27
Q

What is path of GPCR neurotransmission?

A
  • neurotransmitter binds site on a single polypeptide with 7 transmembrane domains
  • triggers conformational change in associated G protein
  • released G protein subunits directly regulate ion channels + trigger secondary messengers/phosphorylation
  • can be excitatory or inhibitory
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28
Q

How do neutrophic factors undergo neurotransmission?

A
  • bind plasma membrane receptors
  • lead directly or indirectly to activation of protein tyrosine kinases which can directly phosphorylate/regulate ion channels
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29
Q

How do steroid hormones undergo neurotransmission?

A
  • diffuse passively into neuron’s cytoplasm

- bind cytoplasmic nuclear hormone receptors which then transport into nucleus and act as transcription factor

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30
Q

What is the major excitatory neurotransmitter in the brain and spinal cord?

A
  • glutamate

- 40-50% of all neurons use glutamate

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31
Q

What are two major classes of glutamate receptors? purpose of each?

A
  1. ligand gated Na(Ca) – mediate rapid neurotransmission

2. GPCRs – exert more modulatory effect, serve as autoreceptor

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32
Q

What are the 3 types of ligand gated channels that glutamate activates? Differences in each?

A
  • AMPA = most important for rapid neurotransmission, usually flux only Na
  • NMDA = flux Ca/NA , deliver Ca signals into neurons which can trigger many forms of plasticity, require co-activation by glycine
  • Kainate
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33
Q

What is function of glutamate GPCR?

A
  • Gi-linked mGLUR1-8 are autoreceptors

- negative feedback loop

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34
Q

What are autoreceptors? Function?

A
  • expressed on nerve terminal and respond to the neurotransmitter released by those terminals
  • linked to Gi so their activation inhibits the nerve terminal = negative feedback
  • expressed on most nerve terminals
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35
Q

Where does glutamate come from?

A
  • it is an AA part of krebs cycle, derivative of aspartate via transaminase
  • present in every cell in body
  • only small fraction of neuronal glutamate used as neurotransmitter in vesicles
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36
Q

What is function of astrocytes in glutamate neurotransmission?

A
  • most of glutamate that is released as neurotransmitter is taken up by glutamate transporters on astrocytes
  • maintains low level of extracellular glutamte need for neuronal survival
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37
Q

What is the glutamate-glutamine shunt around glutamine synapses?

A
  • astrocyte takes up glutamate
  • in astrocyte: glutamate degraded into glutamine via glutamine synthetase
  • glutamine pumped out of astrocyte by active transport and enters nerve terminal
  • in nerve terminal: glutamine converted to glutamate by glutaminase
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38
Q

What are two NMDA glutamate receptor antagonists?

A
  • phencyclidine (PCP)

- alcohol

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39
Q

What is the major inhibitory neurotransmitter in brain and spinal cord?

A
  • GABA

- 40% of all neurons in brain use GABA as transmiter

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40
Q

What happens if too little GABA-ergic neurotransmission?

A

seizures

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41
Q

What happens if too much GABA-ergic neurotransmission?

A

coma

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42
Q

What type of receptor is GABA-A? Function?

A
  • ligand gated Cl channel

- inhibitory postsynaptic currents

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43
Q

What type of receptor if GABA-B? Function?

A
  • GPCR
  • mediates rapid neurotransmission
  • acts as autoreceptor
  • modulatory effect
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44
Q

Where does GABA come from?

A
  • synthesize from cytoplasmic glutamate via glutamate acid decarboxylase (GAD)
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45
Q

What enzyme degrades GABA?

A
  • GABA transaminase
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46
Q

How is GABA recycled?

A
  • returned to nerve terminal via plasma membrane GABA transporter
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47
Q

Where is GABA synthesized?

A

nucleus acucumbens

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48
Q

What levels of GABA in anxiety?

A

low levels

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49
Q

What levels of GABA in huntington disease?

A

low levels

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50
Q

What is effect of anticonvulsant drugs on GABAergic transmission?

A
  • promote GABA-A transmission
    either:
    – increase GABA synthesis in brain
    – OR block reuptake into nerve terminals
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51
Q

What is effect of sedative-hypnotic drugs (benzos/barbs/EtOH) on GABAergic transmission?

A
  • promote GABA-A receptor function

- increase ability of GABA to activate receptor

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52
Q

What is a potential effect of drugs that block GABA-A?

A

induce seizures

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53
Q

What are the two major inhibitory neurotransmitters in spinal cord?

A

GABA and glycine

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54
Q

Where does glycine mainly function?

A
  • as inhibitory neurotransmitter in spinal cord
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55
Q

What is effect of drugs that block glycine receptors?

A
  • induce seizures (convulsants)
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56
Q

What is the name of the major class of glycine receptor? type of receptor?

A
  • ligand gated Cl channel

- called – strychnine-sensitive glycine receptor [b/c blocked by drug strychnine]

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57
Q

What major drug blocks the glycine ligand gated receptor?

A

strychnine

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58
Q

What is glycine’s function in the brain?

A
  • binds with low affinity to NMDA glutamate receptors + enhances ability of glutamate to active these receptors

= co-agonist for NMDA glutamate receptors

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59
Q

What is role of monamines generally?

A
  • in most cases modulatory
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60
Q

Where does dopamine come from? Where is it synthesized?

A
  • tyrosine hydroxylase: tyrosine –> L-DOPA
  • DOPA decarboxylase: L-DOPA –> dopamine [DA]
  • synthesized in ventral tegmentum [VTA] and Substantia nigra [SN] (midbrain) and arcuate nucleus
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61
Q

Where does norepinephrine come from Where is it synthesized?

A
  • same path as dopamine from tyrosine
  • plus dopamine B-hydroxylase: DA –> NE
  • synthesized in locus ceruleus (pons)
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62
Q

Where does epinephrine come from?

A
  • same path as norepinephrine epinephrine

- synthesized in adrenergic neurons and in adrenal medula

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63
Q

By what two enzymes are catecholamines degraded?

A
  • monoamine oxidases (MAOs)

- catechol-O-methyltransferase (COMT)

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64
Q

What protein mediates catecholamines concentration into synaptic vesicles?

A

VMAT (vesicular monoamine transporter)

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65
Q

What are the 3 major dopaminergic nuclei in the brain?

A
  • in midbrain:
  • – substantia nigra [SN]
  • – ventral tegmental area (VTA)
  • in hypothalamus:
  • – arcuate nucleus
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66
Q

What are the 3 major domainergic pathways?

A
  • nigrostriatal [NS] substantia nigra –> striatum
  • mesoLimbic [ML]: VTA –> forebrain, nucleus accumbens [NAc]
  • tuberoinfundibular [TI]: arcuate nucleus –> anterior pituitary
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67
Q

What is function of nigroStriatal [NS] dopamine pathway?

A
  • modulates extrapyramidal motor function
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68
Q

What is function of mesoLimbic [ML] dopamine pathway?

A
  • emotion, reward, motivation, cognition
69
Q

What is function of arcutate nucleus dopamine neurons?

A
  • inhibit prolactin secretion
70
Q

What type of receptors are dopamine receptors?

A
  • all GPCRs
  • D1 and D5 coupled to Gs
  • D2, D3, D4 coupled to Gi, autoreceptor
71
Q

What is effect of antipsychotic drugs on dopamine receptors?

A
  • antagonists at D2 receptors
72
Q

What is effect of psycho-stimulant drugs [cocaine, meth] on dopamine transmission?

A
  • promote dopamine function

- inhibit re-uptake [coke] or stimulate release [meth]

73
Q

What causes parkinsons disease?

A
  • loss of substantia nigra dopamine neurons
74
Q

What are levels of dopamine in parkinsons?

A

low

75
Q

What are levels of dopamine in huntington disease?

A

high

76
Q

What are levels of dopamine in depression?

A

low

77
Q

What are 2 main treatments for parkinsons?

A
  • L-DOPA [precursor to dopamine]

- D2 dopamine receptor agonists

78
Q

What is function of cocaine on dopamine activity?

A
  • inhibits dopamine reuptake so promotes dopamine activity
79
Q

What is effect of drugs of abuse on mesocorticolimbic dopamine path?

A

all via indirect effect enhance this pathway to reinforce addiction

80
Q

Where is NE synthesized in the brain? Its function?

A
  • locus ceruleus
81
Q

What is effect of noreadrenerginc innervation?

A
  • promotes vigilance and attention
  • major NT of sympathetic NS
  • plays role in regulation of stress response
82
Q

What types of receptors are the 3 norepinephrine receptors?

A

All GPCRs

  • a1 receptors: coupled to Gq
  • a2: coupled to Gi, act as autoreceptors
  • B: coupled to Gs
83
Q

What types of drugs tend to act on NE receptors?

A
  • cardiovascular and upper respiratory (anti-allergy)
84
Q

What are 2 possible actions of antidepressant drugs on NE transmission?

A
  • inhibit NE reuptake

- inhibit MAO

85
Q

Match type of G protein coupled to each of the 3 NE receptors

A

a1 – Gq
a2 –Gi
B – Gs

86
Q

From what amino acid is serotonin/melatonin derived

A

Tryptophan

87
Q

What is the other name for 5HT

A

Serotonin

88
Q

How is serotonin synhtesized?

A

Raphe nucleus (brainstem)

– tryptophan + tryptophan hydroxylase –> 5-hydroxytryptophan + aromatic amino acid decarboxylase –> 5HT

89
Q

Where does serotonin –> melatonin conversion occur

A

Pineal gland only

90
Q

What enzyme can degrade serotonin?

A

MAOs [monamine oxidases]

91
Q

Where is serotonin synthesized?

A
  • raphe nuclei of midbrain
92
Q

What are functions of serotonin neurotransmission?

A
  • regulate stress responses and emotional behavior

- regulate eating and weight control and circadian rhythms

93
Q

How many types of serotonin receptors are there? Which are ligand gated?

A
  1. Only one [5HT3] is ligand-gated. All others GPCRs
94
Q

What type of receptor is 5HT1?

A
  • serotonin GPCR coupled to Gi

- Acts as an autoreceptor

95
Q

What type of receptor is 5HT2?

A

serotonin GPCR coupled to Gq

96
Q

What type of receptor is 5HT3?

A

serotonin ligand gated

97
Q

What type of receptors are 5HT4-7?

A

serotonin GPCRs coupled to Gs

98
Q

What are 2 possible mech of antidepressants on serotonin neurotransmission?

A
  • Most inhibit 5HT reuptake

- Some are MAO inhibtors

99
Q

What are 2 mechs of action that newer antipsychotic drugs usually have?

A
  • Block D2 dopamine receptors AND

- block 5HT2A receptors

100
Q

What is mech of newer anti-migraine drugs [triptans] on 5HT neurotransmission?

A

agonists at 5HT1D receptors

101
Q

What is function of 5HT2C receptors?

Effect of their agonists/antagonists?

A
  • related to control of appetite
  • agonists decrease feeding
  • antagonists increase feeding → obestity
102
Q

Where does acetylcholine come from?

A

brainstem nuclei, basal forebrain

  • derived from choline:
    acetyltransferase: choline + acetyl CoA → acetylcholine
103
Q

What degrades ACh?

A

acetylcholesterase

104
Q

How is Ach recycled?

A

degraded by acetylcholneserase in synapse into choline and acetate
Choline taken up by cholinergic nerve terminals

105
Q

Where are cholinergic neurons located?

A

A small number of neurons in tightly packed nuclei in:

  • Brainstem (dorsolateral tegmentum in pons)
  • forebrain (meynerts nucleus and medial septal nuclei)
  • small number in the striatum
106
Q

What is function of cholinergic brainstem nuclei?

A

innervate widely many regions of brain, important for sleep cycle control

107
Q

What is function of cholinergic forebrain nuclei? What do they innervate?

A

innervate hippocampus, important in learning and memory

108
Q

What is function of striatum cholinergic neurons?

A

modulate striatal-dependent motor function

109
Q

What are functions of Ach in brain? Outside of brain?

A

In brain:
- cognition, regulate sleep cycles, modulate striatal motor function

Out of brain:
-major NT of autonomic NS and neuromuscular junction

110
Q

What are the two main types of Ach receptors?

A

Ligand gated nicotinic receptors and GPCR muscarinic receptors

111
Q

What is mech/function of nicotinic receptors?

A

ligand gated Ach receptors

- Na and Ca channels, create excitatory current

112
Q

What is mech/function of muscarinic receptors?

A

GPCR Ach receptors

  • several types M1-M5, coupled to Gi or Gq
  • serve as auto-receptors
113
Q

What is the relationship between nicotine and ACh neurotransmission?

A
  • nicotine is partial agonist at nicotinic cholinergic receptors
  • activates VTA dopamine neurons to promote reward/addiction
114
Q

What disease can you treat with muscarinic cholinergic antagonists?

A

parkinson’s disease

115
Q

What is mech of action of parkinsons disease drugs on ACh neurotransmission?

A

muscarinic cholinergic antagonists used to treat parkinson’s

- because cholinergic interneurons regulate striatal function

116
Q

What disease can you treat with acetylcholinesterase inhibitors?

A

dementia/alzheimers

117
Q

What is mech of action of dementia drugs on ACh neurotransmission?

A
  • act as acetylcholinesterase inhibitors
118
Q

What is histamine derived from?

A
  • histidine + histidine decarboxylase –> histamine
119
Q

Where is histamine synthesized?

A
  • hypothalamic tuberomammillary nucleus
120
Q

What is function of histamine in brain?

A
  • promote sedation
121
Q

What type of receptors are the 3 histamine receptors? What is the major important one in brain?

A
  • all GPCRs

- major receptor in brain is H1

122
Q

What is function of H1 receptor antagonists? location?

A
  • classic “antihistamines”
  • used as anti-allergy drugs
  • also induce sedation as side effect
  • in brain
123
Q

Where is of H2 receptors? location?

A
  • regulate acid secretion [inhibits acid]

- c in stomach

124
Q

What is function of H3 receptors? Location?

A

autoreceptor in brain

125
Q

What are 4 ways that peptide neurotransmitters different from small molec neurotransmitters?

A
  1. peptides must be synthesized in cell bodies [vs small molec synthesized locally within nerve terminals]
  2. peptides packed to large dense core vesicles in cell bodies and transported to nerve terminals [vs small molec packaged to small clear synaptic vesicles]
  3. peptides once released are enzymatically degraded which is irreversible [vs small molec reuptake / recycled back to presynaptic nerve terminal]
  4. All peptides act solely on GPCRS [vs many small molec act on ligand gated receptors as well]
126
Q

What type of receptors do peptide transmitters act on?

A

solely GPCRs (no ligand gated)

127
Q

What is function of hypothalamic releasing and inhibitory factors? Examples?

A
  • utilized by hypothalamic and extra-hypothalamic neurons as neurotransmitters
  • regulate pituitary hormone release
  • ex: CRF, TRF, GnRF, GHRF, somatostatin
128
Q

What are some [5] examples of feeding and gut-brain peptides?

A
  • NPY (neuropeptide Y)
  • a-MSH
  • cholecystokinin [CCK]
  • glucagon-related peptide [GRP]
  • VIP (vasoactive intestinal polypeptide)
129
Q

What is function of tachykinins? example?

A
  • ex: substance P

- regulate nociception (ability to sense pain)

130
Q

How are peptide neurotransmitters synthesized?

A
  • perpropeptide gene –> mRNA –> protein on RER
  • prepropeptide processed to propeptide –> multiple mature mature peptide
  • peptides packaged to dense core vesicles for transport
131
Q

What 3 peptides come from POMC propeptide?

A
  • ACTH
  • B-endorphin
  • a-MSH [a-melanocyte stimulating hormone]
132
Q

What is the basis of neurons using “co-transmitters”?

A
  • most peptidergic neurons also use a small molec neurotransmitter (glutamate, MAO, etc)
133
Q

What is another name for orexin?

A

hypcretin

134
Q

Where is orexin synthesized?

A

lateral hypothalamus [but have widespread projections throughout brain]

135
Q

What are the two types of orexin receptors?

A
  • both GPCRS

- OX1, OX2

136
Q

What is function of orexin?

A
  • promotes alertness/wakefulness

- also modulate mood, reward, alertness, motivation [via brainstem ACh nuclei]

137
Q

To what 2 places do orexinergic neurons project strongly?

A
  • tuberomammillary nucleus [histamine synthesis site]

- brainstem nuclei [ACh synthesis site]

138
Q

What is cause of human narcolepsy?

A
  • death [autoimmune-mediated] of orexinergic neurons

- characterized by suddenly falling into REM sleep during period of wakefullness

139
Q

What are the 3 main types of opioid peptides?

A
  • enkephalins
  • endorphins
  • dynorphin
140
Q

What are enkephalins derived from? Where synthesized?

A
  • from preproenkephalin

- synthesized throughout brain and spinal cord

141
Q

What are endorphins derived from? Where synthesized?

A
  • from prePOMC

- synthesized primarily in hypothalamus

142
Q

What are dynorphins derived from? Where synthesized?

A
  • from preprodynorphin

- synthesized throughout brain and spinal cord

143
Q

Where are each of the 3 types of opioids synthesized?

A
  • enkephalins and dynorphins throughout brain and spinal cord
  • endorphins primarily in hypothalamus
144
Q

What type of receptors to each of the 3 types of opioids act on?

A
  • enkephalins and endorphins act on μ and δ opioid receptors

- dynorphins act on κ opioid receptors

145
Q

What is function of enkephalins/endorphins?

A
  • promote reward, positive mood, analgesia, sedation
146
Q

What is function of dynorphins?

A
  • promote analgesia and sedation

- generally induce negative mood state

147
Q

What is primary action of all illegal and prescription opiate drugs?

A
  • primarily μ opioid receptor agonists
148
Q

What is function of nucleoside neurotransmitters?

A
  • modulatory function
149
Q

What are steps of ATP as neurotransmitter?

A
  • ATP packaged in synaptic vesicles and released
  • once released can directly activate nucleoside receptors or be converted to adenosine in synaptic space (adenosine can also be released directly from postsynaptic)
150
Q

What types of receptors are nucleoside receptors?

A
  • ~20 types, including ligand and GPCR
151
Q

What is funtion of adenosine neurotransmission?

A
  • regulates alertness and sleep
  • adenosine accumulates during wakefulness to promote sleep
  • sleep (even brief period) reduces adenosine levels = associated with fatigue
152
Q

What is function of adenosine receptor antagonist? main example?

A
  • promote wakefullness

- CAFFEINE!!!!!!

153
Q

What are two well-known lipid-derived neurotransmitters? What are they derived from?

A
  • anandamide [AEA]
  • 2AG [2-arachidonoylglycerol]

arachidonic acid –> AEA + 2AG

154
Q

What are endocannabinoids? Why name?

A
  • endocannabinoids = lipid derived neurotransmitters anandamine and 2AG
  • natural neurotransmitters ligands for GPCRs that are also targeted by cannibus
155
Q

Mech of endocannabinoid action?

A
  • synthesized postsynaptically in response to Ca influx
  • released into synapse and act on cannabinoid CB1 receptors on nerve terminal
  • decrease NT release
  • not stored in vesicles
  • “retrograde” synaptic transmission
156
Q

What are the two types of cannabinoid receptors? Which is most important in brain?

A
  • CB1 and CB2
  • both GPCRs
  • CB1 more improtatn in brain by far
157
Q

What is mech of marijuana action/

A
  • activate CB1 receptors of lipid neurotransmission
158
Q

What is function of endocannabinoids?

A
  • effect brain function, regulate perception, appetite, nociception, reward, and levels of consciousness
159
Q

What is prototypical gas neurotransmitter?

A

NO [nitric oxide]

160
Q

How is NO synthesized? Where?

A
  • NO synthase: arginine –> NO

- synthesized postsynaptically in response to Ca influx into neuron

161
Q

What it the path of NO action?

A
  • NO synthesized post-synaptically in response to CA influx into neuron
  • passively diffuses into nearby nerve terminals
  • activates guanylyl cyclase –> increase cGMP –> modulate release of NTs
162
Q

What is function of NO as neurotransmitter?

A
  • modulatory function in brain
163
Q

What are two examples of retrograde synaptic transmission?

A
  • NO

- lipid derived neurotransmitters [endocannabinoids]

164
Q

What type of receptors are ionotropic receptors?

A

ligand gated [rapid transmission]

165
Q

What type of receptors are metabotropic?

A

GPCRs [slower postsynaptic response]

166
Q

How are lipid NTs degraded?

A

by fatty acid amide hydrolysis in glial cells

167
Q

What is role of lipid neurotransmission in glutamate synapses?

A
  • glutamate synapses have presynaptic CB receptors to protect against excitotoxicity
168
Q

What is function of melatonin?

A

regulate sleep-wake cycles

Brain and Behavior Exam 1 (15 decks)

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