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physiology > neurotransmitter > Flashcards

neurotransmitter Flashcards

1
Q

what is NO associated with?

A 
hypertension
diabetes mellitus
coronary artery disease
pregnancy-induced hypertension
renal failure
neurodegenerative diseases
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2
Q

Features of NO

A

lipid soluble gas

synthesised on demand

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3
Q

What role do epithelial cells of blood vessels in the effect of NO on vascular smooth muscle?

A

epithelial cells present = NO release vasodilator

epithelial cells absent = NO release vasoconstricts

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4
Q

What symptoms are serotonin associated with?

A 
migraine
emesis
appetite
sleep-wake cycle
depression
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5
Q

In what ways does NO differ from other neurotransmitters (ACh, NA, 5-HT)?

A
  • synthesised on demand
  • the catalytic enzyme responsible for its synthesis exists in constitutive forms
  • it does not mediate physiological responses via interactions with a membrane receptor (can diffuse across)
  • can easily diffuse in and out of cells
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6
Q

Can ATP act as a neurotransmitter?

A
  • released along with NA and ACh
  • can act as a co-transmitter
  • many purinergic receptors; excitatory in some tissues (bladder), inhibitory in some tissues (gut)
  • junctional and exntrajunctional
  • metabolised rapidly
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7
Q

How do NA and ATP bring about contraction in the male reproductive tract?

A

= biphasic action potential, first, rapid depolarisation; then second, slower and higher AP

  • alpha-adrenoceptor blocking drug: blocks the second, slow depolarisation
  • beta purinoceptor blocking drug (P2X): blocks the first, rapid depolarisation
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8
Q

What happens in mice with no P2X receptors?

A 
no purinoceptors (P2X), then no extra junctional potentials
= mice are infertile (can produce sperm but lack component of initial contraction of vas deferens - sperm doesn't move to urethra)
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9
Q

Features of nitric oxide (NO)?

A
  • very lipid soluble
  • not stored in vesicles
  • synthesised on demand
  • an increase in cytoplasmic calcium is required
  • readily passes across cell membranes
  • powerful inhibitor of smooth muscle contraction
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10
Q

What are the important steps in nitric oxide synthesis?

A
  • [Ca2+]i increase
  • Ca2+ binds to calmodulin; together activate nitric oxide synthase (NOS)
  • L-arg is converted to NO and L-citrilline
  • NO (lipid soluble) diffuses into the effector cell (from varicosity of nerve terminal) and binds to guanylate cyclase inside the cell
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11
Q

what does ionotrophic mean?

A

once the transmitter binds to the receptor, the receptor becomes the channel
- more like change in force of contraction

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12
Q

Difference between chemical structure of noradrenaline and adrenaline?

A

adrenaline has an extra -CH3 group

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13
Q

What enzyme converts noradrenaline to adrenaline?

A

PNMT: phenethanolamine-N-methyl-transferase

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14
Q

What is the vasodilating transmitter thought to be involved in vaginal secretions?

A

sensory nerves in female reproductive tract release CGRP: calcitonin gene related peptide which causes vasodilation

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15
Q

At rest, what is the dominant branch of the autonomic nervous system in regulating penile vasotone?

A

Sympathetic nervous system. Tonic activity at rest constricts arteries (detumescence).
- Sympathetic NS also contracts tubes (ejaculation), transmitter is likely mainly noradrenaline - these sympathetics are inhibited at rest.

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16
Q

What is the role of the parasympathetic nervous system in the male reproductive system?

A
  • dilates penile arteries (erection)

- transmitter is nitric oxide

17
Q

How does diabetes impact on the ability to maintain an erection?

A

diabetes - increased production of ROS decreases NO availability, achieve a partial erection

18
Q

What is the effect of NO on smooth muscle?

A

relaxation: of blood vessels and penile erectile tissue

- NO released from parasympathetic nerves

19
Q

What occurs after NO binds to guanylate cyclase?

A
  • guanylate cyclase converts GTP to cGMP
  • activates PKG
  • phosphodiesterase removes cGMP: no activation of PKG
  • viagra blocks activity of phosphodiesterase
  • absence of NO then viagra has no effect (impotent - can’t produce NO to get vasodilation of penile artery, infertile - can’t transport sperm to urethra)
20
Q

How is the sex response initiated in males?

A
  • psychogenic: higher centres, cerebrum, in response to sight, memories
  • sensory: tactile stimulation: travels to higher cortical centres via the spinothalamic tract. Synapse with parasympathetic preganglionic neurone in same spinal cord segment to drive reflex response
21
Q

Describe the four stages of the male sex response?

A
  1. engorgement of the penis: parasympathetic mediated increase in blood flow in erectile tissue, main transmitter is NO, down regulation of tonic sympathetic activity to penile artery.
  2. secretion: parasympathetics cause secretions from glands (seminal vesicles, prostate gland, bulbourethral glands), secretions containing nutritive and activating factors for sperm.
  3. emission: postganglionic sympathetic neurons contract tubes (epididymis and vas deferens) to move sperm to urethra. Also constrict smooth muscle tubes of prostate and seminal vesicles to deliver secretions to urethra. Smooth muscle of internal urethral sphincter contract to prevent movement of sperm into the bladder.
  4. ejaculation: ANS component - sympathetic mediated contraction of tubes of smooth muscle. Non-ANS component - somatic motor nerves contract skeletal muscles at base of penis.
22
Q

Where do baroreceptor afferents synapse in the brain when BP is too high?

A

NTS

  • inhibitory interneurons are stimulated and they inhibit cardiovascular excitatory centres and suppress the sympathetic NS = decreased rate and force of contraction and vasodilation of blood vessels
  • excitatory interneurons are stimulated in NTS which stimulates the CV inhibitory centre and increases the parasympathetic nervous system, slowing the heart
23
Q

When do baroreceptors afferents synapse in the brain when BP is too low?

A

NTS

  • excitatory interneurons activates CV excitatory centre, enhancing sympathetic nervous system: increases rate and force of contraction, vasoconstriction of peripheral blood vessels, triggers release of A and NA from adrenal medulla
  • inhibitory interneurons inhibits CV inhibitory centre, suppressing parasympathetic NS, allows as increase in sympathetic NS effects
24
Q

What are the effects of the spinal cord injury between the NTS and T3? Cardiac and GI effects?

A

parasympathetic pathways are still intact (heart can slow if BP increases)

  • lost connection between NTS and sympathetic nerves exiting
  • re blood loss, can’t get increase in HR and heart contractility
  • parasympathetics can contract smooth muscle of GIT, but sympathetics are lost (no relaxation of GIT smooth muscle)
25
Q

What is the effect of sympathetic nervous system activation on the bladder?

A
  • SNS acts on beta 2 receptors in the bladder, relaxes the detrusor muscle of the bladder; at the same time during bladder filling, the sympathetic nervous system contracts the internal urethral sphincter via alpha 1 adrenoceptors
  • sympathetic nerves in the bladder wall inhibit parasympathetic postganglionic transmission
  • signals from the storage centre (pons) in the brain will result in inhibition of signals from sensory nerves to preganglionic parasympathetic nerves; pathway leading to bladder contraction will be inhibited by the pontine storage centre
26
Q

What is the somatic control over micturition?

A

somatic innervation of external (skeletal muscle) urethral sphincter, have conscious control

27
Q

What are the effects of a spinal cord injury between T11-L2 to S2-4?

A
  • as the bladder fills, stretch receptors synapse in the spinal cord at S2-S4 levels
  • in spinal cord injury, there is no inhibition from the brain because it has been severed: therefore the stretch afferents directly stimulate parasympathetics which stimulates contraction - leads to infrequent, involuntary micturition
  • will empty but not properly; as soon as stretch receptors are unloaded by contraction of the bladder, they will stop driving this reflex response, and contraction will stop, and residual urine will be contained in the bladder

physiology (3 decks)

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