intro and synaptic transmission Flashcards

1
Q

the criteria for chemical mediators?

A
  1. present in the presynaptic terminal
  2. It should be realized in adequate quantities on stimulation.
  3. there must be an adequate way to remove neurotransmitters from the synaptic cleft.
  4. It should have a similar action on the postsynaptic structure, like that of a normal neurotransmitter.
  5. blocking and competitive agents should affect their normal action.
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2
Q

what are the ways to remove chemical mediators or neurotransmitters from the synaptic cleft?

A
  1. by inactivating enzyme Eg: acetylcholinesterase for acetylcholine.
  2. by process of re-uptake. taking them back into the presynaptic terminal using active transport.
  3. transmitter removed by diffusion out of the synaptic cleft into the surrounding fluids
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3
Q

The nervous system comprises two types of cellular elements

A
  1. connective elements - neuroglia
  2. functional elements - nerve cells
  3. Schwann cells - formation of myelin shealth
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4
Q

Three main types of glia are found in CNS

A
  1. microglia: phagocytic role, enters NS from blood.
  2. oligodendrogliocyte: responsible formation of myelin health in CNS.
  3. Astrocytes: the major regulator of energy metabolism in the brain.
    types of astrocytes: I. Protoplasmic: found in grey matter and have many branching processes whose end feet envelop synapses.
    II. Gömöri-positive astrocytes. These are a subset of protoplasmic astrocytes that contain numerous cytoplasmic inclusions, or granules, that stain positively with Gömöri’s chrome-alum hematoxylin stain.
    III. Fibrous: found in white matter and have long thin unbranched processes whose end-feet envelop nodes of Ranvier.
    note: Both types send processes to blood vessels, where they induce capillaries to form the tight junctions that form the blood-brain barrier. They also send processes that envelop synapses and the surface of nerve cells. They produce substances that are trophic to neurons, and they help maintain the appropriate concentrations of ions and neurotransmitters.
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5
Q

why neurons has lost its power of division

A

A nucleus containing a great nucleolus and sometimes two nucleoli, but as a role no centrosome. The absence of a centrosome indicates that the highly specialized nerve cell has lost its power of division

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6
Q

Specific organelles:

A
  1. cytoplasmic organelles, notably mitochondria, a well-developed Golgi apparatus, ribosomes, and endoplasmic reticulum.
  2. I. Nissl bodies: are rough endoplasmic reticulum (with ribosomes) and are the site of protein synthesis.
    ii. neurofibrils: play a role in transporting proteins and other substances within the cytoplasm.
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7
Q

axon hillock

A

is a specialized part of the cell body (or soma) of a neuron that connects it to the axon.

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8
Q

The sheath of Schwann

A

is the outermost nucleated cytoplasmic layer of Schwann cells (also called neurilemmocytes) that surrounds the axon of the neuron.

for more see image in physiology documents.

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9
Q

The sheath of Henle

A

A layer of delicate reticular connective tissue surrounding a nerve fiber. - contain fibrocyte.

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10
Q

Resting membrane potential

A

-90mV

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11
Q

Ionic basis of resting membrane potential

A
  1. K + permeability is greater than Na + permeability.

2. active Na+-K+ pump 3 Na out and 2 K in.

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12
Q

T

A

T

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13
Q

spike potential

A

the initial, very large change in potential of the membrane of an excitable cell during excitation.

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14
Q

after-potential

A

the period following termination of the spike potential.

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15
Q
  1. excitation threshold potential

2. peak potential

A
  1. +15 mV

2. +35mV

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16
Q

why Hyperpolarization

A

prolonged membrane permeability to potassium

17
Q

Latent period

A

Time taken for the stimulus to travel along the nerve

18
Q

Latent period

A

Time taken for the stimulus to travel along the nerve

19
Q

the moving impulse does not depolarize the area behind

A

because the area behind is refractory

20
Q

orthodromic conduction

A

Conduction of the impulse in the normal direction

21
Q

antidromic conduction

A

Conduction in the opposite direction

22
Q

salutatory conduction

A

50 times faster than the fastest unmyelinated fibers

23
Q

Catecholamines

A

are small, chemically similar molecules derived from the amino acid tyrosine. The major catecholamines are dopamine, norepinephrine, and epinephrine (old name: adrenalin).

24
Q

role of calcium ion in synaptic junction

A

simply put: they cause the release of neurotransmitters in the synaptic cleft.

  1. When an action potential depolarizes the presynaptic membrane, voltage-gated calcium channels open and allows large numbers of calcium ions to flow into the terminal.
  2. The quantity of neurotransmitter that is then released from the terminal into the synaptic cleft is directly related to the number of calcium ions that enter.
  3. When the calcium ions enter the presynaptic terminal,
    they bind with special protein molecules on the inside
    the surface of the presynaptic membrane called release sites.
  4. his binding in turn causes the release sites to open
    through the membrane, allowing a few transmitter vesicles to release their transmitter into the cleft after each
    single action potential.
25
Q

major types of synapses

A

(1) chemical and (2) electrical

26
Q

Receptor activation controls the opening of ion channels in the postsynaptic cell in one of two ways:

A

(1) by gating ion channels directly and allowing passage of specified types of ions through the membrane.
- Neurotransmitter receptors that directly gate ion channels are often called ionotropic receptors.

(2) by activating a “second messenger” that is not an ion channel but instead is a molecule that protrudes into the cell cytoplasm and activates one or more substances inside the postsynaptic neuron.
- those that act through second messenger systems are called metabotropic receptors.

27
Q

Which receptor that cause prolonged effect in postsynaptic membrane

A

Second messenger receptor/ metabotropic receptor

Many functions of the nervous system—for instance, the process of memory—require prolonged changes in neurons for seconds to months after the initial transmitter substance is gone. The ion channels are not suitable for causing prolonged postsynaptic neuronal changes because these channels close within milliseconds
after the transmitter substance is no longer present.
However, in many instances, prolonged postsynaptic neuronal excitation or inhibition is achieved by activating a
“second messenger” chemical system inside the postsynaptic neuronal cell itself, and then it is the second messenger that causes the prolonged effect.

28
Q

Effect of Inhibitory Synapses on the Postsynaptic

Membrane

A
  1. both chloride influx and potassium efflux increase the degree of intracellular negativity, which is called hyperpolarization.

This increase inhibits the neuron because the membrane potential is even more negative than the normal intracellular potential.

29
Q

spatial summation.

A

is the effect of summing simultaneous postsynaptic potentials by activating multiple terminals on widely spaced areas of the neuronal membrane.

30
Q

temporal summation.

A

successive discharges from a single presynaptic terminal, if they occur rapidly enough, can add to one another; that is, they can “summate.” hence excite postsynaptic membrane.

31
Q

“Facilitation” of Neurons

A

the neuron is said to be facilitated, if its
membrane potential is nearer the threshold for firing
than normal due to the previous summation but is not yet at the firing level. Consequently, another excitatory signal entering the neuron can then excite the neuron very easily.

32
Q

Fatigue of Synaptic Transmission.

A

the mechanism of fatigue is mainly exhaustion or partial exhaustion of the stores of transmitter substance in the presynaptic terminals.

33
Q

Effect of Acidosis or Alkalosis on Synaptic Transmission.

A
  1. Normally, alkalosis greatly increases neuronal excitability. For instance, a rise in arterial blood pH from the 7.4 norm to 7.8 to 8.0 often causes cerebral epileptic seizures because of increased excitability of some or all of the cerebral neurons.
  2. acidosis greatly depresses neuronal activity; a fall in pH from 7.4 to b below 7.0 usually causes a comatose state. For instance, in very severe diabetic or uremic acidosis, coma almost alwaysdevelops
34
Q

Renshaw cell inhibition

A

Renshaw cells are inhibitory interneurons found in the gray matter of the spinal cord, and are associated in two ways with an alpha motor neuron.

  1. They receive an excitatory collateral from the alpha neuron’s axon as they emerge from the motor root, and are thus “kept informed” of how vigorously that neuron is firing.
  2. They send an inhibitory axon to synapse with the cell body of the initial alpha neuron and/or an alpha motor neuron of the same motor pool.

In this way, the Renshaw cell action represents a negative feedback mechanism. A Renshaw cell may be supplied by more than one alpha motor neuron collateral and it may synapse on multiple motor neurons.

35
Q

interfere with the synthesis of ATP, and therefore block synaptic transmission. ……., and ………

A

dinitrophenol and cyanide