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Shefa'a's first Prezi

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Shefa'a Shatnawi

on 12 November 2014

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Transcript of Shefa'a's first Prezi

Review about nervous system
watch this video about
sympathetic & parasympathetic
#either ME or PHRMA !
- Chapter 6
nervous system
any nervous tissue outside CNS
brain & spinal cord
Afferent (sensory)
from organ to CNS
Efferent (motor)
from CNS to body ;
muscle ,gland ..etc
bring ur book
write ur note
remember !!
involuntary control of functions
voluntary control of functions

look !

-length of preganglionic
-length of post ganglionic
-site of origin in spinal cord
compare between sympathetic & parasympathetic:
write ur answer
Study smart .. NO Hard ")
challenge PHRMA ")
I 'm coming!
somatic nerve
most parasympathetic postganglionic
few sympathetic postganglionic
ACH = Acetylcholine
to sweat gland
such as:

-semiatonomous part of ANS.
-Located in the gastrointestinal tract.
-Consist of: myenteri plexus & submucous plexus

cholinergic transmission
*Acetylcholine (ACh) *
cotransmitters in cholinergic & adrenergic
Many autonomic nerves have transmitter vesicles that


other transmitter molecules in addition to the primary agents
Adrenegic Transmission
*Norepinephrine (NE) *
include ATP (adenosine triphosphate), enkephalins, vasoactive intestinal peptide, neuropeptide Y, substance P, neurotensin, somatostatin, and others
Synthesis Of "ACH"
#note that !
where AcCoA was made !? .
The transporter of choline ?
The transporter of Ach to vesicle?
the enzyme catalyst the synthesis of ACH

look at : {VAMPs , SNAPs} ")
The greatest question that
how we can inhibit the ACH synthesis !?

Remember it very well !
CHT: sodium-dependent choline transporter.
SNAPs: synaptosome-associated proteins.
VAMPs: vesicle-associated membrane proteins.
ChAT: choline acetyltransferase.
VAT: the vesicle-associated transporter.

#note ")
-ACH dose not eccreted BUT recycled in body
-has short half life
the drugs effect on ACh secretion :
1-heicholinium {block the synthesis}
2-vasamicol {block the storage}
3-botulinum toxin {block release}
are not very useful because their effects are not sufficiently selective
Adrenergic Transmission :
at the sympathetic postganglionic neuron-effector cell synapses in most tissues >>> except :
sweat glands and probably vasodilator sympathetic fibers in skeletal muscle
Dopamine -> vasodilator transmitter in renal blood vessels norepinephrine -> vasoconstrictor of these vessels.

Drug effects on adrenergic transmission-Drugs :
1-metyrosine {block synthesis}
2-resopine {block storage}
3-guanethidine {release}
used in treatment :
Hypertention , pheochromocytoma
look !
VMAT: The vesicular monoamine transporter.

NET: norepinephrine transporter, blocked by what!?

SNAPs: synaptosome-associated proteins.

VAMPs: vesicle-associated membrane proteins.

located primarily on autonomic effector cells (including heart, vascular endothelium, smooth muscle, presynaptic nerve terminals, and exocrine glands).
located on ion channels and respond to acetylcholine and nicotine
M2 , M4
coupled to:
Gi protein
coupled to:
Gq prorine

located on vascular smooth muscle,
presynaptic nerve terminals, blood platelets, fat cells and neurons in the brain
located on most types of smooth muscle, cardiac muscle, some presynaptic nerve terminals, and lipocytes as well as in the brain
alpha -1

alpha -2
coupled with::
coupled with:
beta1,beta2,beta3 :
coupled with Gs
subclass of adrenoceptors but with rather different distribution and function
coupled with Gs
Don't show characteristics of either cholinergic or adrenergic fibers

*Some of these are motor fibers that cause the release of ATP and other purines related to it
**Other fibers have the anatomic characteristics of sensory fibers and contain peptides, such as substance P
***These fibers have been termed "sensory-efferent" or "sensory-local effector" fibers because

#uses modulatory pre- and postsynaptic receptors at the local level and homeostatic reflexes at the systemic level
central integration

Functional organization of autonomic activity:
endocrine system are {integrated with each other}
with: sensory input- with information from higher CNS centers.

ُEarly investigators called:
parasympathetic system ك-> trophotropic one ( leading to growth)
sympathetic system-> ergotropic one ( leading to energy expenditure),
changes in any variable contributing to mean arterial pressure evoke powerful homeostatic secondary response that compensate for the directly evoked change .
sympathetic nerves system
directly influence four major variables : peripheral vascular resistance , heart rate , force and venous tone .
directly modulate renin production .

The net feedback effect
of each loop is to compensate for changes in arterial blood pressure .
decreased blood pressure less firing to baroreceptors increased sympathetic outflow and renin release .
elevated pressure firing to baroreceptors reduce sympathetic out flow reduce renin release increase parasympathetic outflow

Autonomic and hormonal control of cardiovascular function:

Tow feedback loops are present :

1- the autonomic nerves system loop
2- the hormonal loop .
Local lntegration
Presynaptic Regulation
This effect is mediated by αalpha 2 receptors located on the presynaptic nerve membrane.

*Presynaptic receptors that bind the primary transmitter substance and thereby regulate its release are called

*Transmitter release is also modulated by other presynaptic receptors
)= in the case of adrenergic nerve terminals, receptors for acetylcholine, histamine, serotonin,
Local feedback control is best documented of these is the negative feedback of norepinephrine upon its own release from adrenergic nerve terminals.
Postsynaptic Regulation
modulation by previous activity at the primary receptor. Up-regulation and down-regulation are known to occur in response to decreased or increased activation, respectively, of the receptors.

**An extreme form of up-regulation occurs after denervation of some tissues, resulting in denervation supersensitivity of the tissue to activators of that receptor type.

**A pharmacologic supersensitivity related to denervation supersensitivity occurs in autonomic effector tissues after administration of drugs that deplete transmitter stores and prevent activation of the postsynaptic receptors for a sufficient period of time.
The second mechanism involves modulation of the primary transmitter-receptor event by events evoked by the same or other transmitters acting on different postsynaptic receptors


TRY to understand ")
not reaching threshold
suprathreshold -> evokes an action potential
evoked by M2 reseptor activation
"possible dopamine receptor activation"
لBinding of an appropriate ligand to a neuronal nicotinic acetylcholine receptor.
The postganglionic cells are activated
fast excitatory postsynaptic potential (EPSP) evokes a propagated action potential if threshold is reached.
a small and slowly developing but longer-lasting hyperpolarizing afterpotential—a slow inhibitory postsynaptic potential (IPSP).
opening of potassium channels by M2 cholinoceptors
a small, slow excitatory postsynaptic potential caused by closure of potassium channels linked to M1 cholinoceptors
a late, very slow EPSP may be evoked by peptides released from other fibers
Full transcript